Organisms Responding to Internal and External Changes PDF

ORGANISMS RESPOND TO CHANGES IN THEIR INTERNAL AND EXTERNAL ENVIRONMENTS 3.6 6A: STIMULI AND RESPONSES STIMULUS AND RESPONSE By responding to changes in their environment, organisms increase their chance of survival. Those organisms that survive have a greater chance of raising off...

ORGANISMS RESPOND TO CHANGES IN THEIR INTERNAL AND EXTERNAL ENVIRONMENTS 3.6 6A: STIMULI AND RESPONSES STIMULUS AND RESPONSE By responding to changes in their environment, organisms increase their chance of survival. Those organisms that survive have a greater chance of raising offspring and of passing their alleles to the next generation. There is always, therefore, a selection pressure favouring organisms with more appropriate responses. 1. STIMULUS – detectable change in the internal/external environment of an organism that leads to a response 2. RECEPTOR – detects stimulus, specific to one type of stimulus. 3. COORDINATOR – formulates a suitable response to a stimulus e.g. nervous system / hormonal system 4. EFFECTOR – produces response to a stimulus e.g. muscles / glands 5. RESPONSE – This response may be at the molecular level or involve the behaviour of a whole organism. TAXES A taxis is a simple, directional responses determined by the direction of the stimulus. Used by simple mobile organisms who move towards or away from a stimulus. Positive taxis – move towards a favourable stimulus Negative taxis – move away from an unfavourable stimulus Examples of tactic responses: 1. Positive phototaxis – Single-celled algae will move towards light which increases their chances of survival since, being photosynthetic, they require light to manufacture their food. 2. Negative phototaxis – Earthworms will move away from light which increases their chances of survival because it takes them into the soil, where they are better able to conserve water, find food and avoid some predators. 3. Positive chemotaxis – Some species of bacteria will move towards a region where glucose is more highly concentrated which increases their chances of survival because they use glucose as a source of food. KINESES A kinesis is a non-directional simple response used by simple mobile organisms who change the speed of movement or the rate of direction change, in response to a non-directional stimulus. If an organism moves from an area where there are beneficial stimuli to an area with harmful stimuli, its response will be to increase the rate it changes direction to return to the favourable conditions quickly. If it is surrounded by negative stimuli, the rate of turning decreases to keep it moving in a relatively straight line to increase the chances of it finding a new location with favourable conditions. This type of response tends to bring the organism into a new region with favourable conditions. It is important when a stimulus is less directional: humidity and temperature, do not always produce a clear gradient from one extreme to another. Examples of kinetic responses: 1. Humidity – woodlice lose water from their bodies in dry conditions, need damp conditions to prevent excessive water loss ○ Damp area → a dry one = they move more rapidly and change direction more often. This increases their chance of moving back into the damp area. ○ Once back in the damp area = they slow down and change direction less often. This means they are more likely to stay within the damp area so survival increases. ○ Completely dry area = the turning rate would decrease so that it would move in a straight line to increase the chances of finding a new damp area. TROPISMS A tropism is the growth of part of a plant in response to a directional stimulus. Positive tropism – growth towards stimulus Negative response – growth away from stimulus Examples of tropisms: SHOOTS - so that their leaves are in the most favourable position to capture light for photosynthesis. Positive phototropism - towards light Negative gravitropism - away from gravity ROOTS - increases the probability that roots will grow into the soil, where they are belier able to absorb water and mineral ions Negative phototropism - away from light Positive gravitropism - towards gravity GROWTH FACTORS IN FLOWERING PLANTS Plants respond to changes in both their external and internal environments: LIGHT (PHOTOTROPISM) – Shoots grow towards light (positively phototropic) because light is needed for photosynthesis. GRAVITY (GRAVITROPISM) – Plants need to be firmly anchored in the soil. Roots are sensitive to gravity and grow in the direction of its pull (positively gravitropic). WATER (HYDROTROPISM) – Almost all plant roots grow towards water (positively hydrotropic) in order to absorb it for use in photosynthesis and other metabolic processes, as well as for support. Plant responses to external stimuli involve hormone-like substances called plant growth factors. ➔ They exert their influence by affecting growth ➔ Can be made by cells located throughout the plant rather than in particular organs. ➔ Unlike animal hormones, some plant growth factors affect the tissues that release them rather than acting on a distant target organ. ➔ Plant growth factors are produced in small quantities. An example of a plant growth factor is indoleacetic acid (IAA), which belongs to a group of substances called auxins. ROLE OF IAA IN ELONGATION GROWTH Indoleacetic acid (IAA) is a type of auxin. Controls cell elongation in shoots Inhibits the growth of cells in the roots. It is made in the tip of the roots and shoots but moved by diffusion and active transport over short distances and by the phloem over long distances to other cells. The transport of IAA is in one direction - away from the tip of shoots and roots where it is produced. lAA has a number of effects on plant cells including increasing the plasticity (ability to stretch) of their cell walls. The response only occurs on young cell walls where cells are able to elongate. ○ As the cells mature they develop greater rigidity therefore older parts of the shoot/root will not be able to respond. The proposed explanation of how IAA increases the plasticity of cells is called the acid growth hypothesis: ○ It involves the active transport of hydrogen ions from the cytoplasm into spaces in the cell wall causing the cell wall to become more plastic allowing the cell to elongate by expansion. The elongation of cells on one side only of a stem or root can lead to them bending. ○ This is the means by which plants respond relatively quickly to environmental stimuli like light and gravity. ○ These responses can be explained in terms of the stimuli causing uneven distribution of IAA as it moves away from the tip of the stem or root. CONTROL OF PHOTOTROPISMS BY IAA YOUNG SHOOTS Grow towards unilateral light as it is needed for the LDR. Positive phototropism: 1. Cells in the tip of the shoot produce IAA, which is then transported by diffusion down the shoot. 2. The IAA is initially transported evenly throughout all regions as it begins to move down the shoot. 3. Light causes the movement of lAA from the light side to the shaded side of the shoot where it accumulates. 4. A greater concentration of IAA builds up on the shaded side of the shoot than on the light side. 5. As IAA causes elongation of shoot cells, the cells on the shaded side elongate more. 6. The shaded side of the shoot elongates faster than the light side, causing the shoot tip to bend towards the light. ROOTS Do not require light as they do not photosynthesis, and are more able to anchor the plant if they are deep in the soil away from light. They grow away from light which is negative phototropism: 1. Cells in the tip of the root produce IAA, which is then transported by diffusion down the root. 2. The IAA is initially transported evenly throughout all regions as it begins to move down the root. 3. Light causes the movement of lAA from the light side to the shaded side of the shoot where it accumulates. 4. A greater concentration of IAA builds up on the shaded side of the shoot than on the light side. 5. In roots, a high concentration of IAA inhibits cell elongation. 6. Causing roots cells to elongate more on the lighter side and so the root bends away from light. CONTROL OF GRAVITROPISMS BY IAA HORIZONTALLY GROWING ROOT Positive gravitropism: 1. Cells in the tip of the root produce IAA, which is then transported by diffusion along the root. 2. The IAA is initially transported to all sides of the root. 3. Gravity influences the movement of IAA from the upper side to the lower side of the root. 4. A greater concentration of IAA builds up on the lower side of the root than on the upper side. 5. In root cells, IAA inhibits the elongation so the cells on the lower side elongate less than those on the upper side. 6. The relatively greater elongation of cells on the upper side compared to the lower side causes the root to bend downwards towards the force of gravity. HORIZONTALLY GROWING SHOOT Negative gravitropism: 1. Cells in the tip of the shoot produce IAA, which is then transported by diffusion along the shoot. 2. The IAA is initially transported to all sides of the shoot. 3. Gravity influences the movement of IAA from the upper side to the lower side of the shoot. 4. A greater concentration of IAA builds up on the lower side of the shoot than on the upper side. 5. In shoots, the greater concentration of IAA on the lower side increases cell elongation and causes this side to elongate more than the upper side. 6. As a result, the shoot grows upwards away from the force of gravity. PHOTOTROPISMS GRAVITROPISMS NERVOUS ORGANISATION 2 major parts of the nervous system: Central nervous system ○ Brain and spinal cord ○ The spinal cord is a column of nervous tissue that runs along back and lies inside the vertebral column for protection Peripheral nervous system ○ Pairs of nerves that originate from either brain or spinal cord Peripheral nervous system: Sensory neurones - carry nerve impulses from receptors towards the CNS Motor neurones - carry nerve impulses away from CNS to effectors Intermediate neurones (coordinator) - connect spinal motor and sensory neurons Relay neurones - between sensory and motor neurons in the brain and spinal cord Motor neurons further subdivided: Voluntary nervous system - carries nerve impulses to body muscles and is under voluntary (conscious) control Autonomic nervous system - carries nerve impulses to glands, smooth muscle and cardiac muscle and is not under voluntary control, that is, it is involuntary (subconscious) REFLEX ARC Reflex - involuntary response to a sensory stimulus. Reflex arc - the pathway of neurons involved in a reflex. A spinal reflex is one where one of the neurons involved is in the spinal cord. Spinal reflex: 1. Stimulus 2. Receptor 3. Sensory neuron 4. Coordinator (intermediate neuron) 5. Motor neurone 6. Effector 7. Response IMPORTANCE OF REFLEX ARCS Increases survival, protects the body from harm. Involuntary - do not require brain ○ Brain is not overloaded with situations in which response is always the same. Fast - neuron pathway is short ○ Only one or two synapses where neurons communicate with ○ Synapses are the slowest link in a neuron pathway Absence of decision making - rapid action Effective from birth, do not have to be learnt RECEPTORS Sensory reception - the function of receptors Sensory perception - involves making sense of the information from the receptors, largely brain function. Receptors are specific to a single stimulus Stimulation of a receptor leads to the establishment of a generator potential The Pacinian Corpuscle is a receptor to know in detail. HOW RECEPTORS WORK Receptors in the nervous system convert the energy of the stimulus into the electrical energy used by neurones. Resting potential – the potential difference across the membrane due to a difference in charge between the inside and outside of a cell when it is at rest (inside is negatively charged relative to the outside). Generator potential – change in the potential difference when a stimulus is detected as the cell membrane is excited and becomes more permeable, allowing more ions to move in and out of the cell Threshold level – the level the generator potential reaches to trigger an action potential. Action potential – electrical impulse along a neurone triggered if the generator potential is big enough and reaches the threshold level. Action potentials are all one size, so the strength of the stimulus is measured by the frequency of the action potentials. All stimuli involve a change in some form of energy which is converted into nerve impulses (energy) which is the role of the transducer. FEATURES OF PACINIAN CORPUSCLE What are they? Pacinian corpuscles are mechanoreceptors - they detect mechanical stimuli such as pressure and vibrations. Where are they found? They occur deep in the skin and are most abundant on the fingers, soles of the feet and the external genitalia.They also occur in joints, ligaments and tendons, where they enable the organism to know which joints are changing direction. Structure Contain the end of a sensory neurone (aka sensory nerve ending) wrapped in many layers of connective tissue called lamellae, each separated by a gel. The sensory neuron ending at the centre of the Pacinian corpuscle has a special type of sodium channel in its plasma membrane, a stretch -mediated sodium channel. HOW THE PACINIAN CORPUSCLE FUNCTIONS 1. In its normal (resting) state, the stretch-mediated sodium channels of the membrane around the neurone of a Pacinian corpuscle are too narrow to allow sodium ions to pass along them. in this state, the neurone of the Pacinian corpuscle has a resting potential. 2. When pressure is applied to the Pacinian corpuscle, it is deformed and the membrane around its neurone becomes stretched. 3. This stretching widens the sodium channels in the membrane and sodium ions diffuse into the sensory neurone. 4. The influx of sodium ions changes the potential of the membrane (it becomes depolarised), thereby producing a generator potential. 5. The generator potential in turn creates an action potential (nerve impulse) that passes along the neurone and then, via other neurones, to the central nervous system. THE EYE STRUCTURE ➔ Fovea – area of the retina where there are lots of photoreceptors ➔ Optic nerve – bundle of neurons which carries nerve impulses from photoreceptor cells to the brain ➔ Blind spot – the point where the optic nerve leaves the eye, there are no photoreceptors here so it is not sensitive to light ➔ Bipolar neuron – connects photoreceptors to optic nerve ➔ Rod – a photoreceptor found at the edge of the retina which are very sensitive to light - monochromatic ➔ Cone – a photoreceptor found in the fovea which are less sensitive to light – 3 types, trichromatic ➔ Ganglion neurons – ➔ Retinal convergence – the process by which multiple photoreceptor cells in the retina send signals to a single bipolar cell, which then sends a signal to a single ganglion cell. RECEPTORS IN THE EYE The light receptor cells of the mammalian eye are found on its innermost layer, the retina. The millions of light receptor cells found in the retina are of two main types: rod cells and cone cells. Both rod and cone cells act as transducers by conserving light energy into the electrical energy of a nerve impulse DISTRIBUTION OF ROD AND CONE CELLS: ➔ The distribution of rod and cone cells on the retina is uneven. ➔ Light is focused by the lens on the pan of the retina opposite the pupil (the fovea). ➔ The fovea therefore receives the highest intensity of light. ➔ Therefore cone cells, but not rod cells, are found at the fovea. ➔ The concentration of cone cells diminishes further away from the fovea. ➔ At the peripheries of the retina, where light intensity is at its lowest, only rod cells are found. The distribution of rod and cone cells, and the connections they make in the optic nerve, can explain the differences in sensitivity and visual acuity in mammals. By having different types of light receptor, each responding to different stimuli, mammals can benefit from good all-round vision both day and night. ROD CELLS SENSITIVITY TO COLOUR: Rod cells cannot distinguish different wavelengths of light ○ Therefore lead to images being seen only in black and white. SENSITIVITY TO LIGHT: Rod cells are more numerous than cone cells - there are around 120 million in each eye. Many rod cells are connected to a single sensory neurone in the optic nerve Rod cells are used to detect light of very low intensity. A certain threshold value has to be exceeded before a generator potential is created in the bipolar cells. As a number of rod cells are connected to a single bipolar cell (retinal convergence), there is a much greater chance that the threshold value will be exceeded than if only a single rod cell were connected to each bipolar cell (due to summation). In order to create a generator potential, the pigment in the rod cells (rhodopsin) must be broken down. There is enough energy from low-intensity light to cause this breakdown. VISUAL ACUITY: Due to retinal convergence, light received by rod cells sharing the same neurone will only generate a single impulse travelling to the brain regardless of how many of the neurons are stimulated. This means that, in perception, the brain cannot distinguish between the separate sources of light that stimulated them. Two dots close together cannot be resolved and so will appear as a single blob, so give low visual acuity  If one cone cell has been stimulated for a while, they become CONE CELLS exhausted and stop working, meaning other colour cone cells are stimulated and an afterimage is shown in a different colour. SENSITIVITY TO COLOUR: Cone cells are of three different types, each responding to a different range of wavelengths of light. ○ Blue, red and green. Depending upon the proportion of each type that is stimulated, we can perceive images in full colour. The wavelengths overlap so we can see other colours Each of the three different types of cone cell contains a specific type of iodopsin so each cone cell is sensitive to a different specific range of wavelengths. SENSITIVITY TO LIGHT: Around 6 million cone cells Each cell has its own separate bipolar cell connected to a sensory neurone in the optic nerve. This means that the stimulation of a number of cone cells cannot be combined to help exceed the threshold value and so create a generator potential. As a result, cone cells only respond to high light intensity and not to low light intensity. Cone cells contain different types of pigment from that found in rod cells. The pigment in cone cells (iodopsin) requires a higher light intensity for its breakdown. Only light of high intensity will therefore provide enough energy to break it down and create a generator potential. VISUAL ACUITY: Each cone cell has its own connection to a single bipolar cell This means that, if two adjacent cone cells are stimulated, the brain receives two separate impulses. The brain can therefore distinguish between the two separate sources of light that stimulated the two cone cells. This means that two dots close together can be resolved and will appear as two dots. Therefore cone cells give very accurate vision, that is, they have good visual acuity. ROD CELLS AND CONE CELL SUMMARY FEATURE RODS CONES SENSITIVITY Very sensitive Less sensitive VISUAL ACUITY Low High HOW MANY TO 1 BPN Many 1 LOCATION Edges of retina Fovea COLOUR Monochromatic Trichromatic - red, green, blue AUTONOMIC NERVOUS SYSTEM Peripheral nervous system is split into somatic (conscious)and autonomic (unconscious) The autonomic nervous system controls the involuntary (subconscious) activities of internal muscles and glands. It has two divisions: The sympathetic nervous system – this stimulates effectors and so speeds up any activity. It controls effectors when we exercise strenuously or experience powerful emotions. Helps us to cope with stressful situations by heightening our awareness and preparing us for activity (fight or flight response). The parasympathetic nervous system – this inhibits effectors and so slows down any activity. It controls activities under normal resting conditions. It is concerned with conserving energy and replenishing the body's reserves. (Rest and digest). The actions of these systems are antagonistic ELECTRICAL CONTROL OF HEART RATE Cardiac muscle is myogenic - self stimulation from inside muscle rather than outside (neurogenic). The rate of contraction is controlled by electrical activity. Involving these structures: Sinoatrial node (SAN) (pacemaker) – distinct group of cells within the wall of the right atrium of the heart. It is from here that the initial stimulus for contraction originates. Controls rhythm of heartbeat by sending out regular waves of electrical activity to atrial walls, causing them to contract simultaneously. Atrioventricular node (AVN) – group of cells in walls of right and left ventricle. They receive electrical activity from the SAN. Slight delay so that ventricles cn fill with blood before contraction. The Purkyne fibres – specialised muscle fibres in the walls of the ventricles that convey electrical activity to the apex of the heart. The bundle of His – Purkyne tissue collectively make this up which runs through the septum in the walls of the ventricles that convey electrical activity to the apex of the heart. CONTROL OF HEART RATE 1. The SAN sends a wave of electrical excitation/depolarisation to the atrial walls, causing them to contract simultaneously. 2. A layer of non-conductive collagen tissue (atrioventricular septum) prevents the wave crossing to the ventricles. 3. Instead, the wave of excitation/depolarisation enters the AVN, which will lies between atria. 4. After a short delay (beneficial allowing enough time for the atria to fully pump all the blood into the ventricles before ventricles contract) the AVN passes the wave of electrical excitation/depolarisation between the ventricles along the bundle of His. 5. The bundle of His conducts the wave through the atrioventricular septum to the base of the ventricles, where the bundle branches into smaller fibres of Purkyne tissue in the right and left ventricle walls. 6. The wave of excitation is released from the Purkyne tissue, causing the ventricles to contract quickly and simultaneously from the bottom of the heart upwards. 7. The cells then repolarise, and the cardiac muscle relaxes. Describe how a heartbeat is initiated and coordinated. 5 marks 1. SAN sends wave of electrical activity / impulses (across atria) causing atrial contraction; Accept excitation 2. Non-conducting tissue prevents immediate contraction of ventricles / prevents impulses reaching the ventricles; 3. AVN delays (impulse) whilst blood leaves atria / ventricles fill; 4. (AVN) sends wave of electrical activity / impulses down Bundle of His; 4. Allow Purkyne fibres / tissue 5. Causing ventricles to contract from base up; MODIFYING THE RESTING HEART RATE The resting heart rate or a typical adult human is around 70 beats per minute. It is essential that this rate can be altered to meet varying demands for oxygen like during exercise, the resting heart rate may need to more than double. Changes to the heart rate are controlled by a region of the brain called the medulla oblongata: Sympathetic nervous system - increases heart rate Parasympathetic nervous system - decreases heart rate Which of these centres is stimulated depends upon the nerve impulses they receive from two types or receptor, which respond to stimuli of either chemical or pressure changes in the blood: ➔ pH/O2/CO2 – detected by chemoreceptors – walls of carotid arteries and aorta. ➔ Blood pressure – detected by pressure receptors (baroreceptors) – the aorta and carotid arteries. 1. Electrical impulses are sent from receptors to the medulla along sensory neurons. 2. The medulla then processes the information and sends impulses to the SAN along sympathetic/parasympathetic neurons. 3. These systems secrete neurotransmitters: acetylcholine and noradrenaline which increases, decreases heart rate. CONTROL OF HR IN RESPONSE TO BLOOD pH CHANGES pH is determined by concentrations of CO2 in the blood (CO2 forms carbonic acid in the blood) Response to high blood O2/low blood CO2/high pH levels: 1. Chemoreceptors in carotid arteries detect blood has a lower than normal concentration of CO2. 2. Increase the frequency of nervous impulses along sensory neurone to medulla oblongata. 3. This increases frequency of nervous impulses along the parasympathetic neurones to the SAN. 4. The parasympathetic neurones secrete acetylcholine which binds to receptors on the SAN 5. Less impulses released by SAN 6. Heart rate decreases to return levels back to normal Response to low blood O2/high blood CO2/low pH levels: 1. Chemoreceptors in carotid arteries detect blood has a higher than normal concentration of CO2. 2. Increase the frequency of nervous impulses along sensory neurone to medulla oblongata. 3. This increases frequency of nervous impulses along the sympathetic neurones to the SAN. 4. The sympathetic neurones secrete noradrenaline which binds to receptors on the SAN 5. More impulses released by SAN 6. Heart rate increases to return levels back to normal CONTROL OF HR DUE TO BLOOD PRESSURE CHANGES Response to high blood pressure: 1. Baroreceptors in carotid arteries detect blood has a higher than normal blood pressure. 2. Increase the frequency of nervous impulses along sensory neuron to medulla oblongata. 3. This increases frequency of nervous impulses along the parasympathetic neurones to the SAN. 4. The parasympathetic neurons secrete acetylcholine which binds to receptors on the SAN 5. Less impulses released by SAN 6. Heart rate decreases to return blood pressure back to normal Response to low blood pressure: 1. Baroreceptors in carotid arteries detect blood has a lower than normal blood pressure. 2. Increase the frequency of nervous impulses along sensory neuron to medulla oblongata. 3. This increases frequency of nervous impulses along the sympathetic neurones to the SAN. 4. The sympathetic neurons secrete noradrenaline which binds to receptors on the SAN 5. More impulses released by SAN 6. Heart rate increases to return levels back to normal 6B: NERVOUS COORDINATION PRINCIPLES OF COORDINATION There are two main forms of coordination in animals as a whole: Nervous system: Uses nerve cells to pass electrical impulses along their length. They stimulate their target cells by secreting chemicals (neurotransmitters) directly on to them. This results in rapid communication between specific parts of an organism. The responses produced are often short-lived and restricted to a localised region of the body. Hormonal system: Produces chemicals (hormones) that are transported in the blood plasma to their target cells. The target cells have specific receptors on their cell-surface membranes and the change in the concentration of hormones stimulates them. This results in a slower, less specific form of communication between parts of an organism. The responses are often long- lasting and widespread. NERVOUS VS HORMONAL COMMUNICATION NERVOUS HORMONAL Communication by Nerve impulses Hormones (chemicals) Transmission by By neurons In the blood Transmission speed Rapid Slow Specificity Impulses to specific parts of body travel to all parts of the body, but only target cells respond Response location Localised Widespread Speed of response Rapid Slow Length of response Short lasting as neurotransmitters broken Long lasting as not broken down as quickly down quicker Effect Temporary and reversible Permanent and irreversible NEURONES Neurones are nerve cells which are specially adapted to carry nerve impulses (electrochemical changes) to one part of the body to another. Neurones can be classified based on their function: Sensory neurones – transmit nerve impulses from a receptor to an intermediate or motor neurone. They have one dendron that is often very long. It carries the impulse towards the cell body and one axon that carries it away from the cell body. Motor neurones – transmit nerve impulses from an intermediate or relay neurone to an effector, such as a gland or a muscle. Motor neurones have a long axon and many short dendrites. Intermediate or relay neurones – transmit impulses between neurones, for example, from sensory to motor neurons. They have numerous short processes. STRUCTURE OF A MYELINATED MOTOR NEURON Cell body – which contains all the usual cell organelles, including a nucleus and large amounts of rough endoplasmic reticulum. This is associated with the production of proteins and neurotransmitters Dendrons – extensions of the cell body which subdivide into smaller branched fibres, called dendrites, that carry nerve impulses towards the cell body An axon – a single long fibre that carries nerve impulses away from the cell body Schwann cells – which surround the axon, protecting it and providing electrical insulation. They also carry out phagocytosis to remove cell debris and play a part in nerve regeneration. Schwann cells wrap themselves around the axon many times, so that layers of their membranes build up around it. This forms the myelin sheath. Myelin sheath – a covering to the axon and is made up of the membranes of the Schwann cells. These membranes are rich in a lipid known as myelin. Neurones with a myelin sheath are called myelinated neurones. The myelin sheath is an insulator as the lipid does not allow charged ions to pass through to the axon. Nodes of Ranvier – constrictions (gaps) between adjacent Schwann cells where there is no myelin sheath. The constrictions are 2- 3 µm long and occur every 1- 3 mm in humans. RESTING POTENTIAL AND HOW IT IS MAINTAINED Resting potential – In a neurone's resting state (not stimulated / not conducting an impulse) there is a difference between the electrical charge inside and outside of the neurone - membrane is polarised. - The outside of the membrane is more positively charged than the inside (-70mV) The resting potential is maintained by the sodium-potassium pump and potassium ion channels: 1. 3 Na+ binds to specific receptors on the intracellular side of the protein channel 2. Inside the cell, ATP binds to the protein channel and is hydrolysed into ADP + Pi which causes a change to the shape of the protein channel on the opposite side of the membrane (phosphorylation) 3. Na+ actively transported out of the axon 4. 2 K+ bind to specific receptors on the protein channel 5. The Pi and ADP recombine to form ATP which is released 6. K+ actively transported into the axon 7. The outward active transport of Na+ ions is greater than the inward active transport of potassium ions meaning the inside is more negative than the outside (3 to 2) 8. Also more Na+ in the extracellular tissue fluid than in the intracellular cytoplasm and more K+ in the cytoplasm than in the tissue fluid →creating an electrochemical gradient. 9. The membrane is more permeable to K+ at rest so K+ ions begin to diffuse by facilitated diffusion down the concentration gradient back out of the axon in potassium ion channels a. There are more open potassium leakage channels than sodium leakage channels in the phospholipid bilayer of the axon so only some Na+ diffuse back into the cell by facilitated diffusion 10. As even more positive charge is leaving the cell, the resting potential is maintained as more positive outside than inside the cell. ACTION POTENTIAL An action potential is when a neurons voltage increases beyond the threshold level from the resting potential and gives rise to an electrical impulse. - When a stimulus (which is big enough) is detected by a receptor in the nervous system, sodium ion channels open and there is an influx of positive charge into the axon, increased permeability to Na+ - There is a temporary reversal of the charges either side of this part of the axon membrane, inside the membrane goes from -70 mV → +40 mV (axon membrane depolarised). - This depolarisation occurs because the channels in the axon membrane change shape, and hence open or close depending on the voltage across the membrane. THE ACTION POTENTIAL SEQUENCE OF EVENTS 1. RESTING POTENTIAL ○ At resting potential some K+ voltage-gated channels are open (permanently) but the Na+ voltage-gated channels are closed. 2. STIMULUS ○ The energy of the stimulus causes some Na+ voltage-gated channels in the axon membrane to open and therefore membrane permeability to Na+ ions increases ○ Na+ diffuse into the axon through these channels along their electrochemical gradient. ○ Being positively charged, they trigger a reversal in the potential difference across the membrane. 3. DEPOLARISATION ○ As the Na+ ions diffuse into the axon, if the potential difference reaches the threshold (-55 mV), it causes more sodium ion channels to open, causing an even greater influx of sodium ions by diffusion. 4. REPOLARISATION ○ Once the action potential of around +40 mv has been established: i. the voltage gates on the Na+ ion channels close, preventing further influx of Na+ ions. ii. The voltage gates on the K+ ion channels begin to open, membrane is more permeable to K+ + ○ K diffuse out of the axon through these channels along their electrochemical gradient. ○ The electrical gradient that was preventing further outward movement of potassium ions is now reversed, causing more potassium ion channels to open. This means that yet more potassium ions diffuse out, starting repolarisation of the axon. 5. HYPERPOLARISATION ○ The potassium ion channels are slow to close and as there is the outward diffusion of these K+ ions it causes a temporary overshoot of the electrical gradient. ○ The inside of the axon is more negative (relative to the outside) than at the resting potential of -70 mV 6. RESTING POTENTIAL ○ The voltage-gated ion channels on the K+ ion channels now close and the activities of the Na+-K+ pumps cause sodium ions to be pumped out and potassium ions in to re-establish and maintain the resting potential (-70 mV) until next stimulation.  When the neurone’s voltage increases beyond a set point from the resting potential, this generates a nervous impulse. Depolarisation always peaks at the same point. 5. More voltage gated sodium channels open so 7. Once action potential of +40 mV is there is an even greater reached: influx, causing a reversal in - The voltage gates on the Na+ ion the potential difference channels close across the membrane - The voltage gates on the K+ ion channels begin to open, membrane is more permeable to K+ + 4. For any stimuli that is large K diffuse out of the axon through these enough, the diffusion of positive Na+ channels down their electrochemical ions into the axon causes charge to gradient, starting repolarisation of the axon. increase inside, if it reaches -55 mV (the threshold level) 8. Hyperpolarisation - the K+ ion channels are slow to close and causes a temporary overshoot of the electrical 3. If stimuli is too small, the influx of gradient. sodium is too low to cause enough depolarisation for it to reach the 9. Refractory period is after the action threshold level (all-or-nothing) potential has been generated where the inward movement of sodium ions is prevented because the sodium 2. Stimulus provides energy for voltage-gated channels are closed and voltage gated sodium channels to a further action potential cannot be open to allow influx of Na diffusing generated meaning there is a time into the axon delay between action potentials. 1. Resting potential - outwards movement of K+ 10. Resting potential - the voltage-gated K+ ion channels now close and the ions in permanently open channels, voltage gated activities of the sodium-potassium pumps cause sodium ions to be pumped out and sodium channels are closed potassium ions in to re-establish and maintain the resting potential of -70 mV THE ALL-OR-NOTHING PRINCIPLE FOR IMPULSES If the depolarisation as a result of the stimulus reaches the threshold level an action potential is triggered. Depolarisation below the threshold value (-55mV) - NOTHING No action potential →no impulse generated. So any stimulus, of whatever strength, that is below the threshold value will fail to generate an action potential. Depolarisation above the threshold level (-55mV) - ALL Action potential generated →nerve impulse will travel. All action potentials are more or less the same size so always peak at the same maximum voltage. How can an organism perceive the size of a stimulus if all action potentials are the same size? 1. By the number of impulses passing in a given time (frequency). The larger the stimulus, the more impulses that are generated in a given time 2. By having different neurons with different threshold values. The brain interprets the number and type of neurons that pass impulses as a result of a given stimulus and thereby determines its size. Why is it is important? It makes sure that animals only respond to large enough stimuli Rather than responding to every slight change in the environment which would overwhelm them. PASSAGE OF ACTION POTENTIAL - UNMYELINATED AXON Once an action potential is generated, it moves along the neuron as a wave of depolarisation 1. Generation of action potential: a. Resting potential - conc of Na+ ions outside the axon membrane is high relative to the inside. Conc of K+ ions is high inside the membrane relative to the outside. The overall concentration of positive ions is greater on the outside, making this positive compared with the inside so the axon membrane is polarised. b. A stimulus causes a sudden influx of sodium ions and hence a reversal of charge on the axon membrane, this is the action potential and the membrane is depolarised. 2. Passage of this action potential: a. The localised electrical currents established by the influx of Na+ ions cause the opening of sodium voltage-gated channels and influx of sodium ions a little further along the axon → depolarisation in this region.. b. Behind this new region of depolarisation, the axon enters the refractory (repolarisation) period where the sodium voltage-gated channels close and the potassium ones open and leave the axon. c. So once initiated, the depolarisation moves along the membrane and move away from the refractory period as this cannot generate it. d. The action potential (depolarisation) is propagated in the same way further along the axon. The outward movement of the potassium ions has continued to the extent that the axon membrane behind the action potential has returned to its original charged state (positive outside. negative inside), that is, it has been repolarised. e. Repolarisation of the axon allows sodium ions to be actively transported out, once again returning the axon to its resting potential in readiness for a new stimulus it it comes. PASSAGE OF ACTION POTENTIAL - MYELINATED AXON 1. In myelinated axons, the fatty sheath of myelin around the axon acts as an electrical insulator, preventing action potentials from forming. 2. At intervals of 1- 3 mm there are breaks in this myelin insulation, called nodes of Ranvier. 3. Action potentials can occur at these points as depolarisation can happen here. 4. The localised circuits therefore arise between adjacent nodes of Ranvier and the action potentials jump from node to node in a process known as saltatory conduction. 5. As a result, an action potential passes along a myelinated neurones faster than along the axon of an unmyelinated one of the same diameter. 6. This is because in an unmyelinated neuron, the events of depolarisation have to take place all the way along an axon and this takes more time. THE REFRACTORY PERIOD NATURE OF THE REFRACTORY PERIOD Once an action potential has been created in any region of an axon, there is a period afterwards when inward movement of sodium ions is prevented because the sodium voltage-gated channels are closed (repolarisation) During this time it is impossible for a further action potential to be generated as Na+ channels inactivated During the refractory period ion channels are recovering and cannot be opened. This means there is a time delay between one action potential and the next. THE IMPORTANCE OF THE REFRACTORY PERIOD: No overlap of action potentials - discrete impulses ○ A new action potential cannot be formed immediately behind the first one There is a limit to the frequency at which the nerve impulses can be generated ○ As action potentials are separated from one another, it limits the number of them that can pass along an axon in a given time ○ This limits the strength of the stimulus that can be detected. Action potentials are unidirectional (only in one direction) ○ Can only pass from an active region to a resting region ○ This is because action potentials cannot be created in a region in refractory. FACTORS AFFECTING THE SPEED OF CONDUCTANCE MYELINATION AND SALTATORY CONDUCTION Myelination = myelin sheath Myelin sheath is an electrical insulator preventing an action potential forming in the part of the axon covered in myelin. Sodium ion channels are concentrated at the Ranvier nodes between Schwann cells. In myelinated neuron, depolarisation only happens at nodes of Ranvier (where sodium ions can get through through the membrane). Neurons cytoplasm conducts enough electrical charge to depolarise the next node Action potentials impulse jumps from one node of Ranvier to another - saltatory conduction. This speeds up conductance. In non-myelinated neuron, impulse travels as a wave along the whale length of the axon so depolarisation happens along the whole length of the membrane - slower than statutory conduction. AXON DIAMETER Action potentials are conducted quicker along axons with bigger diameters: because there is less resistance to the flow of ions that are in the cytoplasm of a smaller axon. due to less leakage of ions from a large axon (leakage makes membrane potentials harder to maintain). With less resistance, depolarisation reaches other parts of the neuron cell membrane quicker. TEMPERATURE Speed of conduction increases as temperature increases as ions can diffuse faster Increases up to around 40oC as the proteins begin to denature and impulses fail to be conducted at all Respiration provides ATP for active transport, this is controlled by enzymes STRUCTURE OF A SYNAPSE A Synapse is the gap/junction where one neurone communicates with another or with an effector. Synaptic cleft – the gap between the cells where neurotransmitters diffuse across to the receptors on post synaptic neurone. Pre-synaptic neurone – neurone before synapse which action potential travels along before the synaptic cleft, releases the neurotransmitters Post-synaptic neurone – the neurone after the synapse where the neurotransmitter travels to the dentrites and it integrates all the signals it receives to determine what it does next, for example, to fire an action potential of its own or not. Synaptic knob – swelling at the end of the presynaptic nerve which contains synaptic vesicles, possesses many mitochondria and large amounts of endoplasmic reticulum. These are required in the manufacture of the neurotransmitter which takes place in the axon Synaptic vesicles – in the synaptic knob, contains neurotransmitters Neurotransmitters – chemicals which diffuse across the synaptic cleft, they bind to receptors and might trigger an action potential FUNCTIONS OF SYNAPSES Synapses transmit information from one neurone to another. They allow: A single impulse along one neurone to initiate new impulses in a number of different neurones at a synapse. ○ This allows a single stimulus to create a number of simultaneous responses A number of impulses to be combined at a synapse. ○ This allows nerve impulses from receptors reacting to different stimuli to contribute to a single response. How they work: A chemical (the neurotransmitter) is made only in the presynaptic neurone and not in the postsynaptic neurone. The neurotransmitter is stored in synaptic vesicles. When an action potential reaches the synaptic knob the membranes of these vesicles fuse with the pre-synaptic membrane to release the neurotransmitter. When released, the neurotransmitter diffuses across the synaptic cleft to bind to specific receptor proteins which are found only on the postsynaptic neurone. The neurotransmitter binds with the receptor proteins and this leads to a new action potential in the postsynaptic neurone. Synapses that produce new action potentials in this way are called excitatory synapses. CHOLINERGIC SYNAPSE IMPULSE TRANSMISSION 1. An action potential reaches the synaptic knob of the presynaptic neurone - DEPOLARISATION OF IT 2. This stimulates voltage-gated calcium ion channels in the presynaptic neurone to open 3. Calcium ions diffuse by facilitated diffusion into the synaptic knob 4. This influx of Ca ions causes the synaptic vesicles to move to the presynaptic membrane 5. They fuse with the membrane and releases the neurotransmitter acetylcholine (ACh) into the synaptic cleft by exocytosis. 6. The ACh diffuses down its concentration gradient across the synaptic cleft to the postsynaptic membrane 7. It binds to complementary receptors on sodium ion protein channels on the postsynaptic cell surface membrane 8. This causes sodium ion channels to open and sodium to diffuse rapidly along a concentration gradient into the post-synaptic neurone 9. The influx of sodium ions causes the membrane potential to increase and if threshold is reached, it becomes depolarised so a new action potential is generated in the postsynaptic neurone. 10. Degradation occurs to the ACh which is released from the receptors as acetylcholinesterase AChE hydrolyses ACh into choline and ethanoic acid. 11. They diffuse back across the synaptic cleft to the presynaptic neurone and the products are reabsorbed and recycled to make more ACh. This prevents continuous generation of a new action potential so leads to discrete transfer of information across the synapse 12. In the pre-synaptic neurone, ATP released by mitochondria is used to recombine the chlorine and ethanoic acid → ACh which is stored in synaptic vesicles for further use. 13. The sodium ions channels in the receptor sites close and the resting potential is re-established in the post-synaptic neurone FEATURES OF SYNAPSES - UNIDIRECTIONALITY Synapses only allow information to travel in one direction - pre → post synaptic neurone Neurotransmitters (e.g ACh) can only be generated in the presyanptic neurone and stored in synaptic vesicles Receptors complementary to the neurotransmitter (e.g sodium ion channels) are only on the postsynaptic membranes on dendrites So neurotransmitters can only diffuse across the synaptic cleft from the presynaptic to the postsynaptic neurone FEATURES OF SYNAPSES - SUMMATION If a stimulus is weak, there are low-frequency action potentials which release of insufficient concentrations of neurotransmitter to trigger a new action potential in the postsynaptic neurone as it will not reach the threshold level. Summation is where the effect of neurotransmitters can be added together to trigger an impulse: Spatial summation ○ Many presynaptic neurones connect to one post synaptic neurone ○ They all release a small amount of neurotransmitter ○ Together this is enough to reach the threshold level and trigger action potential Temporal summation ○ A single presynaptic neurone releases neurotransmitter many times over a very short period ○ Nerve impulses arrive from the same presynaptic neurone in quick succession ○ If the concentration of neurotransmitter exceeds the threshold value of the postsynaptic neurone, then a new action potential is triggered. Both these summation types mean synapses accurately process information and finely tune the response FEATURES OF SYNAPSES - INHIBITION Inhibitory synapses work by inducing hyperpolarisation so that the potential increases to -80 mV and trigger of an action potential is far more unlikely. - Cl- ions to move into the postsynaptic neurone - K+ to move out of the postsynaptic neurone 1. The presynaptic neurone releases a type of neurotransmitter that binds to chloride ion protein channels on the postsynaptic neurone 2. The neurotransmitter causes the chloride ion protein channels to open 3. Chloride ions move into the postsynaptic neurone by facilitated diffusion. 4. The binding of the neurotransmitter causes the opening of nearby potassium protein channels. 5. Potassium ions move out of the postsynaptic neurone into the synapse. 6. The combined effect of negatively charged chloride ions moving in and positively charged potassium ions moving out is to make the inside of the postsynaptic membrane more negative and the outside more positive. 7. The membrane potential increases to as much as -80 mV compared with the usual - 70 mV at resting potential. 8. This makes it less likely that a new action potential will be created because a larger influx of sodium ions is needed to produce one. TYPES OF NEUROTRANSMITTERS EXCITATORY Depolarise the postsynaptic membrane Making it fire an action potential is the threshold is reached Acetylcholine at cholinergic synapses in the CNS and neuromuscular junctions INHIBITORY Hyperpolarise the postsynaptic membrane Preventing firing of an action potential Acetylcholine in cholinergic synapses at the heart where potassium ion channels open so hyperpolarisation occurs BOTH Depends on the location and type of receptor that is there Acetylcholine is both STRUCTURE OF A NEUROMUSCULAR JUNCTION This is a synapse that occurs between a motor neurone and a skeletal muscle fibre. There are many of these along the muscle because: If there were only one junction of this type it would take time for a wave of contraction to travel across the muscle, in which case not all the fibres would contract simultaneously and the movement would be slow. As rapid and coordinated muscle contraction is frequently essential for survival there are many neuromuscular junctions spread throughout the muscle. This ensures that contraction of a muscle is rapid and powerful when it is simultaneously stimulated by action potentials. Motor units: All muscle fibres supplied by a single motor neurone act together as a single functional unit and are known as a motor unit. This arrangement gives control over the force that the muscle exerts. ○ lf only slight force is needed, only a few units are stimulated. ○ If a greater force is required, a larger number of units are stimulated. The structure is very similar to a normal synapse. NEUROMUSCULAR JUNCTION IMPULSE TRANSMISSION 1. When a nerve impulse is received at the neuromuscular junction, calcium ion channels open and influx of calcium causes the synaptic vesicles fuse with the presynaptic membrane and release their acetylcholine. 2. The acetylcholine diffuses to the postsynaptic membrane (which is the membrane of the muscle fibre) 3. It binds to nicotinic cholinergic receptors 4. This alters its permeability to sodium ions which enter rapidly, depolarising the membrane. 5. The postsynaptic membrane has lots of folds in it which form clefts 6. The clefts store AChE 7. The acetylcholine is broken down by acetylcholinesterase to ensure that the muscle is not over-stimulated. 8. The resulting choline and ethanoic acid (acetyl) diffuse back into the neurone, where theyare recombined to form acetylcholine using energy provided by the mitochondria found there. COMPARISON OF CHOLINERGIC SYNAPSE AND NEUROMUSCULAR JUNCTION TRANSMISSION NEUROMUSCULAR CHOLINERGIC SIMILARITIES Only excitatory Excitatory or inhibitory Unidirectional as receptors only on post synaptic membrane Connects motor neurone to muscles Links neurones to neurones, or Have neurotransmitters that are neurones to other effector organs transported by diffusion Have receptors, that on binding The action potential ends here (it is the A new action potential may be with the neurotransmitter, cause end of a neural pathway) produced along another neurone (the an influx of sodium ions postsynaptic neurone) Use a sodium-potassium pump to repolarise the axon Acetylcholine binds to nicotinic Acetylcholine binds to receptors on Use enzymes to breakdown the cholinergic receptors on membrane of membrane of post-synaptic neurone on neurotransmitter. muscle fibre sodium channels Only motor neurones are involved Motor, sensory and intermediate neurones may be involved EFFECTS OF DRUGS ON SYNAPSES - There are many different neurotransmitters responsible for the exchange of information across a synapse. - There are also many different types of receptor on the postsynaptic neurone. - Each receptor is a protein that binds specifically to a neurotransmitter because they have complementary shapes. Some of these neurotransmitters and receptors are excitatory (lead to a new action potential) and others are inhibitory (make it less likely that a new action potential will be created in the postsynaptic neurone). - Overall, the action of a specific neurotransmitter depends on the specific receptor to which it binds. Drugs act on synapses in two main ways: They stimulate the nervous system by creating more action potentials in postsynaptic neurones. ○ A drug may do this by mimicking a neurotransmitter, stimulating the release of more neurotransmitter, or inhibiting the enzyme that breaks down the neurotransmitter. ○ The outcome is to enhance the body's responses to impulses passed along the postsynaptic neurone. ○ For example, if the neurone transmits impulses from sound receptors, a person will perceive the sound as being louder. They inhibit the nervous system by creating fewer action potentials in postsynaptic neurones. ○ A drug may do this by inhibiting the release of neurotransmitter or blocking receptors on sodium/potassium ion channels on the postsynaptic neurone. ○ The outcome is to reduce the impulses passed along the postsynaptic neurone. In this case, if the neurone transmits impulses from sound receptors, a person will perceive the sound as being quieter. EFFECTS OF DRUGS ON SYNAPSES STIMULATE NERVOUS SYSTEM - GREATER ACTION POTENTIALS IN POSTSYNAPTIC NEURONE Agonists / mimickers Same shape as neurotransmitters so mimic their action This means receptors are activated ○ Nicotine binds to nicotinic cholinergic receptors in the brain by mimicking acetylcholine Stimulate release of neurotransmitters Stimulate release of neurotransmitters from presynaptic neurone so more receptors are activated ○ Amphetamines Inhibits enzymes Inhibit the enzymes that break down the neurotransmitters so stops them from working More neurotransmitters in the synaptic cleft bind to receptors for longer ○ Nerve gases stop acetylcholine from being broken down so loss of muscle control INHIBIT NERVOUS SYSTEM - FEWER ACTION POTENTIALS IN POSTSYNAPTIC NEURONE Antagonists / blockers Block receptors so they cannot be activated by neurotransmitters Fewer receptors activated ○ Curare blocks the effects of acetylcholine by blocking nicotinic cholinergic receptors at neuromuscular junctions so muscle cells cannot be stimulated and results in paralysis of muscles Inhibit release of neurotransmitters Inhibit release of neurotransmitters from the presynaptic neurone so fewer receptors are activated ○ Alcohol ANTAGONISTIC MUSCLES 3 types of muscle in the body: smooth, cardiac and skeletal. Smooth and cardiac muscle contracts under unconscious, involuntary control. Skeletal muscle is attached to bone and acts under voluntary, conscious control ➔ Pairs of skeletal muscles contract and relax to move bones at a joint. ➔ The bones of the skeleton are incompressible (rigid) so act as levers which give muscles something to pull against ➔ Muscles can only pull, not push ➔ This can be automatic as part of a reflex response or controlled by conscious thought. Muscles that work together to pull a bone are antagonistic pairs The contracting muscle is the agonist The relaxing muscle is the antagonist ○ Bending arm up - bicep agonist, tricep antagonist Skeletal muscles are attached to bones by tendons. Ligaments attach bones to bones to hold them together STRUCTURE OF SKELETAL MUSCLES Skeletal muscles are large bundles of long cells called muscle fibres, structure of a muscle fibre: Sarcolemma - the cell membrane of muscle fibre cells Sarcoplasm - muscle cell cytoplasm Transverse (T) tubules - parts of the sarcolemma which folds inwards across the muscle fibre and stick into the sarcoplasm ○ Help spread electrical impulses throughout the sarcoplasm so they reach all parts of the muscle fibre Sarcoplasmic reticulum - network of internal membranes which store and release the calcium ions that are needed for muscle contractions Muscle fibres have lots of mitochondria - to provide the ATP for muscle contraction Muscle fibres are multinucleate - have many nuclei Muscle fibres contain myofibrils ○ Long, cylindrical organelles that are made up of proteins and highly specialised for contraction Myofibrils are made of myofilaments ○ Myosin, actin, tropomyosin ULTRASTRUCTURE OF MYOFIBRILS Myofibrils constrain bundles of thick and thin myofilaments that move past each other to make muscles contract Thick myofilaments = myosin protein Thin myofilaments = actin protein Under an electron microscope myofibrils appear striped, alternating light and dark bands: Light bands = I-bands (isotropic) ○ Contain only thin actin filaments Dark bands = A-bands (anisotropic) ○ Thick myosin filaments with some overlapping of thin actin filaments Myofibrils are made up of many short units called sarcomeres: The ends of each sarcomere are marked with a Z-line, so the space between Z-lines are sarcomeres Z-lines are at the centre of I-bands In the middle of each sarcomere (middle of the myosin filaments) is an M-line Around the M-line is the H-zone which is in the middle of the A-band The H-zone only contains myosin filaments ROLES OF MYOSIN, TROPOMYOSIN AND ACTIN The three main proteins involved in the process of muscle/myofibril contraction by the sliding filament model: MYOSIN Made of 2 proteins ○ a fibrous protein arranged into a filament made up of several hundred molecules (the tail) ○ a globular protein formed into two bulbous structures at one end (the head). The globular heads that are hinged so can move back and forth Each has a binding site for actin Each has a binding site for ATP ACTIN A globular protein Molecules are arranged into long chains that are twisted around one another to form a helical strand. Have a binding site for myosin heads called actin-myosin binding sites TROPOMYOSIN A protein which forms a long, thin, fibrous strand around actin filaments In a resting muscle the actin-myosin binding site is blocked by tropomyosin So myofilaments cannot slide past each other because the myosin heads cannot bind to the binding sites on actin filaments MUSCLE CONTRACTION Muscle contraction happens through the sliding filament mechanism: Myosin and actin filaments slide over each other to make sarcomeres contract ○ The myofilaments themselves do not contract The simultaneous contraction of lots of sarcomeres means the myofibrils and muscle fibres contract and shorten Overall: 1. At rest, tropomyosin blocks the actin-myosin binding site meaning they cannot slide. 2. Action potential causes depolarisation in sarcolemma, T tubules and to sarcoplasmic reticulum. 3. Sarcoplasmic reticulum releases stored calcium ions into the sarcoplasm as channels open. 4. Calcium binds to protein on tropomyosin, protein changes shape and moves tropomyosin out of the binding site 5. The bulbous heads of the myosin filaments bind to the actin filament in the binding site 6. This forms cross-bridges with the actin filaments by attaching themselves to binding sites on the actin filaments 7. ATP → ADP + Pi by ATP hydrolase, energy released causes myosin heads to bend 8. This pulls the actin filaments along the myosin filaments. 9. They then detach and, using ATP, return to their original angle and re-attach themselves further along actin filament. 10. When stopped being stimulated, calcium ions actively transported back into sarcoplasmic reticulum 11. Tropomyosin blocks actin-myosin binding site so cross bridges cannot form so actin slides back and sarcomere lengthens and muscle is relaxed 1) MUSCLE STIMULATION 1. An action potential from a motor neurone reaches many neuromuscular junctions simultaneously, causing calcium ion protein channels to open and calcium ions to diffuse into the synaptic knob. 2. The calcium ions cause the synaptic vesicles to fuse with the presynaptic membrane and release their acetylcholine into the synaptic cleft. 3. Acetylcholine diffuses across the synaptic cleft and binds with receptors on the muscle cell surface membrane, causing the sarcolemma to depolarise. 2) MYOFIBRIL / MUSCLE CONTRACTION 1. The action potential causes depolarisation of the sarcolemma, this depolarisation travels deep into the fibre through T-tubules which spread into the sarcoplasm and to the sarcoplasmic reticulum 2. The action potential opens the calcium ion protein channels on the sarcoplasmic reticulum and calcium ions diffuse into the sarcoplasm down a concentration gradient. 3. Calcium ions bind to a protein attached to tropomyosin, causing the protein to change shape. 4. This pulls the attached tropomyosin out of the actin-myosin binding site on the actin filament, exposing the binding site which allows the myosin head to bind 5. The bond formed when a myosin head binds to the actin filament is an actin-myosin cross bridge. 6. Calcium ions also activate the enzyme ATPase which hydrolyses ATP → ADP + Pi to provide the energy needed for muscle contraction 7. The energy released from ATP causes the myosin head to bend which pulls the actin filament along 8. Another ATP molecule provides the energy to break the actin-myosin cross bridge so the myosin head detaches from the actin filament after it has moved 9. The myosin head then reattaches to a different binding site further along the actin filament, forming new actin-myosin bridge, the process is repeated. 10. Many cross bridges form and break very rapidly which pulls the actin filament along, shortening the sarcomere and causing the muscle to contract. 3) MUSCLE RELAXATION 1. When nervous stimulation ceases, calcium ions are actively transported back into the sarcoplasmic reticulum using energy from the hydrolysis of ATP. 2. This reabsorption of the calcium ions allows tropomyosin to block the actin-myosin binding sites again. 3. Myosin heads are now unable to bind to actin filaments so there are no cross bridges. 4. The actin filaments slide back to their relaxed position which lengthens the sarcomere. EVIDENCE FOR THE SLIDING-FILAMENT MECHANISM Myofibrils appear darker in colour where the actin and myosin filaments overlap and lighter where they do not. - If the sliding filament mechanism is correct, then there will be more overlap of actin and myosin in a contracted muscle than in a relaxed one. When a muscle contracts, the following changes occur to a sarcomere: The I-band becomes narrower. The Z-lines move closer together or, in other words, the sarcomere shortens. The H-zone becomes narrower. The A-band remains the same width. - As the width of this band is determined by the length of the myosin filaments, it follows that the myosin filaments have not become shorter. - This discounts the theory that muscle contraction is due to the filaments themselves shortening. ENERGY SUPPLY DURING MUSCLE CONTRACTION A lot of energy is required for muscle contract which is supplied by the hydrolysis of ATP → ADP + Pi The energy released is needed for: The movement or the myosin heads Breaking of the actin-myosin cross bridge The reabsorption of calcium ions into the endoplasmic reticulum by active transport. ATP needs to be continually regenerated which happens in 3 main ways: 1. Aerobic respiration ○ Most energy is generated via oxidative phosphorylation in the mitochondria ○ Aerobic respiration only works when there is lots of oxygen ○ Good for long periods of low-intensity exercise 2. Anaerobic respiration ○ ATP is made rapidly in glycolysis ○ Pyruvate is converted to lactate by lactate fermentation ○ Lactate quickly builds up and causes muscle fatigue ○ Good for short periods of high-intensity exercise 3. ATP-phosphocreatine (PCr) system ○ ATP is made by phosphorylating ADP by using a phosphate group from phosphocreatine ○ PCr cannot supply energy directly to the muscle, so instead it regenerates ATP rapidly ○ Phosphocreatine is stored in muscle and acts as a reserve supply of phosphate, which is available immediately to combine with ADP and so re-form ATP. ○ PCr runs out after a few seconds so it is used in short bursts of vigorous exercise ○ The ATP-PCr system is anaerobic and alactic (does not form lactate) ○ The phosphocreatine store is replenished using phosphate from ATP when the muscle is relaxed. ○ Some of the creatine gets broken down into creatinine which is removed from the body via the kidneys, levels are high in TYPES OF MUSCLE FIBRES Skeletal muscles are made up of two types of muscle fibres - slow twitch and fast twitch. Different muscles have different proportions of the two fibres. SLOW TWITCH FAST TWITCH STRUCTURE Large store of myoglobin (red protein stores oxygen) Thicker and more myosin filaments AND Rich blood supply (to deliver glucose and oxygen) Large store of glycogen ADAPTATIONS Lots of mitochondria (to produce ATP) Store of phosphocreatine High concentration of enzymes for anaerobic resp Don't have much myoglobin so can’t store much O2 LOCATION Calf muscles, muscles in back for posture Biceps, eye movement CONTRACTION Slower and less powerful Faster and more powerful RESPIRATION Aerobic - prevent build up of lactate Anaerobic and ATP-phosphocreatine system LENGTH Long period of time without fatiguing Only for short period of time as fatigue quickly EXERCISE Endurance - marathons Intense - weightlifting 6C: HOMEOSTASIS HOMEOSTASIS Homeostasis is the maintenance of a constant internal environment within restricted limits in organisms via physiological control systems. The internal environment is the blood and tissue fluid that surrounds cells. Homeostasis ensures that the cells of the body are in an environment that meets their requirements and allows them to function normally despite external changes: - This does not mean that there are no changes as there are continuous fluctuations brought about by variations in internal and external conditions, such as changes in temperature, pH and water potential. - These changes occur around an optimum point and homeostasis is the ability to return to that optimum point and so maintain organisms in a balanced equilibrium. THE IMPORTANCE OF HOMEOSTASIS IN MAINTAINING A STABLE CORE TEMPERATURE AND BLOOD pH Temperature and pH affect enzyme activity and enzymes control the rate of metabolic reactions. ➔ They also affect proteins and channels in membranes. ➔ Any changes to these factors reduces the rate of reaction of enzymes or may even prevent them working altogether. ➔ Even small fluctuations in temperature or pH can impair the ability of enzymes to carry out their roles effectively. ➔ Maintaining a fairly constant internal environment means that reactions take place at a suitable rate. Temperature: If too high (40oC) enzymes become denatured. The enzyme’s molecules vibrate too much which breaks the hydrogen bonds holding them in shape, this alters the tertiary structure of the enzyme’s active site so E-S complexes cannot form as no longer complementary. Enzyme cannot function as a catalyst and metabolic reactions are less efficient. If too low, enzyme activity is reduced and the rate of metabolic reactions are too slow The highest rate of enzyme activity happens at optimum temperature (37oC in humans) pH: If too high or too low, enzymes become denatured. The hydrogen bonds holding them in shape are broken, this alters the tertiary structure of the enzyme’s active site so E-S complexes cannot form as no longer complementary. Enzyme cannot function as a catalyst and metabolic reactions are less efficient. The highest rate of enzyme activity happens at an optimum pH (usually 7 neutral, pepsin 2 stomach) THE IMPORTANCE OF HOMEOSTASIS IN MAINTAINING STABLE BLOOD GLUCOSE CONCENTRATIONS The concentration of glucose in the blood is important because cells need glucose as a respiratory substrate and to maintain a constant water potential of the blood. ➔ Cells need glucose in order to release energy through respiration ➔ Changes to the water potential of the blood and tissue fluids may cause cells to shrink and expand (even to bursting point) as a result of water leaving or entering by osmosis. Water potential: High blood glucose: Water potential of blood is reduced Water molecules move by osmosis out of cells into the blood Causes them to shrivel up and die Low blood glucose: Water potential of blood is increased Water molecules move by osmosis into cells from the blood Causing them to swell and burst (cytolysis) Respiratory substrate: If blood glucose is too low then cells are unable to carry out normal activities because there is not enough glucose for respiration to provide energy. HOMEOSTATIC CONTROL MECHANISMS Self-regulating homeostatic systems involve receptors, a communication system (coordinator) and effectors. Receptor - detects any deviation from the optimum point by a stimulus and informs the coordinator. Coordinator - coordinates information from receptors and sends instructions to an appropriate effector Effector - often a muscle or gland, which brings about the changes instructed by coordinator A feedback mechanism is set up - by which a receptor responds to a stimulus created by the change to the system brought about by the effector. There are two types of feedback mechanisms: Positive feedback (not involved in homeostasis as it does not keep the internal environment stable) Negative feedback (counteracts a change to return the system to the optimum to maintain stability) POSITIVE FEEDBACK Positive feedback amplifies the effect of a change, enhancing it further away from the normal level. This can occur also when a homeostatic system breaks down. It is useful as it rapidly activates something Examples: 1. Blood clot after an injury a. Platelets become activated and release a chemical which triggers activation of more platelets b. They rapidly form a blood clot at the injury site c. The process ends with negative feedback when the body detects the blood clot has been formed 2. Hypothermia a. Hypothermia is low body temperature below 35oC when heat is lost faster than can be produced b. As body temperature falls the brain does not work properly and shivering stops, making it fall more c. Positive feedback takes the body temperature further from the normal level d. This will continue to decrease until action is taken  ENDOTHERMS (inside heat) TEMPERATURE CONTROL Animals (birds and mammals) get most of their heat from metabolic activities inside their bodies. Body temperature remains relatively constant despite fluctuations in the external ECTOTHERMS (outside heat) temperature. Endothermic animals use behaviour to maintain a Reptiles gain heat from the environment, so their body constant body temperature but also use a wide range of temperature fluctuates with the environment. They therefore physiological mechanisms to regulate their temperature. control their body temperature by adapting their behaviour to changes in the external temperature. Cold environments: Vasoconstriction - diameter of arterioles near skin They control their body temperature by: narrower to reduce volume of blood reaching surface so Exposing themselves to the sun - In order to gain heat less heat transfer lizards orientate themselves so that the maximum surface Shivering - involuntary rhythmic contractions to produce area of their body is exposed to the warming rays of the metabolic heat Sun. Hair raising - layer of still, insulating air Taking shelter - Lizards will shelter in the shade to Increased metabolic rate - respiration up, more heat prevent overheating when the Sun's radiation is at its Hot environments: peak. At night they retreat into burrows in order to reduce Vasodilation - diameter of arterioles near skin wider to heat loss when the external temperature is low. increase volume of blood reaching surface so more heat Gaining warmth from the ground - Lizards will press transfer their bodies against areas of hot ground to warm Sweating - To evaporate water from the skin surface themselves up. When the required temperature is requires energy in the form of heat. reached, they raise themselves off the ground on their Lowering of hairs - no insulating layer of air legs. NEGATIVE FEEDBACK Negative feedback is when there is a deviation from the normal values and restorative systems are put in place to counteract the change, decreasing its effects and returning this back to the original level. This involves the nervous system and often hormones. It only works within certain limits as if the change is too big the effectors cannot counteract it. Example: 1. Control of body temperature ○ If the temperature of the blood increases, thermoreceptors in a region of the brain called the hypothalamus send more nerve impulses to the heat loss centre, which is also in the hypothalamus. ○ This in turn sends impulses to the skin (effector organ). ○ Vasodilation, sweating and lowering of body hairs all lead to a reduction in blood temperature. ○ If the fact that blood temperature has returned to normal is not fed back to the hypothalamus, it will continue to stimulate the skin to lose body heat. ○ Blood temperature will then fall below normal and may continue to do so causing hypothermia and the death of the organism or another negative feedback cycle happens. ○ The cooler blood returning from the skin passes through the hypothalamus and the thermoreceptors send fewer impulses to the heat loss centre. ○ This in turn stops sending impulses to the skin and so vasodilation, sweating, etc. cease, and blood temperature remains at its normal level rather than continuing to fall. The blood, having been cooled to its normal temperature, has resulted in turning off the effector (the skin) that was correcting the rise in temperature. BENEFIT OF SEPARATE FEEDBACK MECHANISMS Having separate negative feedback mechanisms that control departures from the norm in either direction gives a greater degree of homeostatic control. Control systems normally have many receptors and effectors. This allows them to have separate mechanisms that each produce a positive movement towards an optimum. This allows a greater degree of control of the particular factor being regulated. Having separate mechanisms that controls departures in different directions from the original state is a general feature of homeostasis. It is important to ensure that the information provided by receptors is analysed by the coordinator before action is taken. For example: - Temperature receptors in the skin may signal that the skin itself is cold and that the body temperature should be raised. However, information from regions in the hypothalamus in the brain may indicate that blood temperature is already above normal (this situation might arise during strenuous exercise when blood temperature rises but sweating cools the skin). - By analysing the information from all detectors, the brain can decide the best course of action - in this case not to raise the body temperature further. - In the same way, the control centre must coordinate the action of the effectors so that they operate harmoniously. For example, sweating would be less effective in cooling the body if it were not accompanied by vasodilation. WHY DOES BLOOD GLUCOSE NEED REGULATING? Glucose is a substrate for respiration, providing the source of energy for almost all organisms. It is therefore essential that the blood of mammals contains a relatively constant concentration of glucose for respiration. ➔ If the concentration falls too low, cells will be deprived of energy and die - brain cells are especially sensitive in this respect because they can only respire glucose. ➔ If the concentration rises too high, it lowers the water potential of the blood and creates osmotic problems that can cause dehydration and be equally dangerous. HOW IS BLOOD GLUCOSE REGULATED? It is controlled by the self-regulating hormonal system through negative feedback. The regulation of blood glucose is an example of how different hormones interact in achieving homeostasis. The hormones involved in regulation of blood glucose are: insulin and glucagon. Insulin and glucagon and proteins. These two hormones work in opposite direction, antagonistic. The interaction between these two hormones allows highly sensitive control of blood glucose concentration. ○ This is because it is only when the concentration falls below the set point that insulin secretion is reduced which leads to a rise in blood glucose concentration again. Glucagon secretion is only reduced when it rises and exceeds the set point. One mechanism of hormone action is the second messenger model used by glucagon (and adrenaline) in the regulation of blood glucose concentration. THE FACTORS INFLUENCING BLOOD GLUCOSE CONCENTRATION The normal concentration of blood glucose is 5 mmoldm-3. Blood glucose comes from three sources: Directly from the diet in the form of glucose absorbed following hydrolysis of other carbohydrates such as starch, maltose, lactose, and sucrose From the hydrolysis in the small intestine of glycogen = glycogenolysis stored in the liver and muscle cells From gluconeogenesis, which is the production of glucose from sources other than carbohydrate. Blood glucose fluctuates in animals. Increases after eating food containing carbohydrates Decreases when not eating and after exercise as glucose is used in respiration to release energy ROLE OF THE PANCREAS IN REGULATING BLOOD GLUCOSE CONCENTRATION The pancreas produces enzymes (protease, amylase and lipase) for digestion and hormones (insulin and glucagon) for regulating blood glucose concentration. When examined microscopically, the pancreas is made up largely of the cells that produce its digestive enzymes. Scattered throughout these cells are groups of hormone-producing cells known as islets of Langerhans. The cells of the islets of Langerhans include: ɑ-cells - which are larger and produce the hormone glucagon ꞵ-cells - which are smaller and produce the hormone insulin NEGATIVE FEEDBACK CYCLE OF BLOOD GLUCOSE Too high (hyperglycaemia) 1. Receptors on ꞵ-cells in the pancreas detects stimulus that blood glucose concentration is too high 2. ꞵ cells of islets of Langerhans secrete insulin 3. ɑ cells of islets of Langerhans stop secreting glucagon 4. Insulin binds to receptors on liver and muscle cells (effectors) 5. Cells take up more glucose, glycogenesis is activated and cells respire more glucose 6. Blood glucose concentration lowers in the blood Too low (hypoglycaemia) 7. Receptors on ɑ-cells in the pancreas detects stimulus that blood glucose concentration is too low 8. ꞵ cells of islets of Langerhans stop secreting insulin 9. ɑ cells of islets of Langerhans secrete glucagon 10. Glucagon binds to receptors on liver cells (effector) 11. Glycogenolysis is activated, gluconeogenesis is activated and cells respire less glucose 12. Blood glucose concentration lowers in the blood ROLE OF THE LIVER IN REGULATING BLOOD SUGAR The liver is is made up of cells called hepatocytes. While the pancreas produces the hormones insulin and glucagon, it is in the liver where they have their effects. There are three important processes associated with regulating blood sugar which take place in the liver: GLYCOGENESIS - the conversion of glucose into glycogen. ➔ When blood glucose concentration is higher than normal the liver removes glucose from the blood and converts it to glycogen. ➔ It can store 75-100g of glycogen, which is sufficient to maintain a human's blood glucose concentration for about 12 hours when at rest, in the absence of other sources. GLYCOGENOLYSIS - the breakdown of glycogen to glucose. When blood glucose concentration is lower than normal, the liver can convert stored glycogen back into glucose which diffuses into the blood to restore the normal blood glucose concentration. GLUCONEOGENESIS - the production of glucose from sources other than carbohydrate. ➔ When its supply of glycogen is exhausted, the liver can produce glucose from noncarbohydrate sources such as glycerol and amino acids. ACTION OF INSULIN Insulin lowers blood glucose concentration. The beta-cells of the islets of Langerhans in the pancreas have receptors that detect the stimulus of a rise in blood glucose concentration and respond by secreting the hormone insulin directly into the blood plasma. Insulin is a globular protein made up of 51 amino acids. How does it decrease blood glucose? 1. Attaches to specific receptors on the cell surface membranes of liver and muscle cells. ○ This causes a change in the tertiary structure of the glucose transport carrier proteins, causing them to change shape and open, allowing more glucose into the cells by facilitated diffusion. The cell membrane is more permeable to glucose. 2. Inclusion of protein channels into cell membranes ○ GLUT4 is a glucose transporter channel protein which is stored in vesicles when insulin is low. ○ When insulin binds to receptors on cell surface membrane, it triggers the movement of vesicles containing GLUT4 to the membrane where it fuses and increases the number of glucose transport channels. Glucose can then be transported into the cell through GLUT4 by facilitated diffusion from the blood. 3. Activating enzymes involved in the conversion of glucose to glycogen in liver and muscle cells (glycogenesis) ○ The cells are able to store glycogen in their cytoplasm as an energy source. 4. Increasing the rate of respiration of cells ○ This therefore uses up more glucose, thus increasing their uptake of glucose from the blood ACTION OF GLUCAGON Glucagon raises blood glucose concentration. The alpha-cells of the islets of Langerhans in the pancreas have receptors that detect the stimulus of a drop in blood glucose concentration and respond by secreting the hormone glucagon directly into the blood plasma. How does it increase blood glucose? 1. Attaches to specific receptors on the cell surface membranes of liver cells. ○ Liver cells are the target cells. 2. Activating enzymes involved in the conversion of glycogen to glucose in liver cells (glycogenolysis) ○ This happens through a second messenger model as when glucagon binds it causes a protein to be activated into adenylate cyclase which catalyses the conversion of ATP into a molecule called cyclic AMP (cAMP). cAMP activates an enzyme, protein kinase, that can hydrolyse glycogen into glucose. 3. Activating enzymes involved in the conversion of glycerol and amino acids into glucose (gluconeogenesis) ○ These are non-carbohydrate components that form glucose 4. Decreases the rate of respiration in cells ○ So less glucose is being broken down to release energy so there are greater concentrations in the blood. ACTION OF ADRENALINE Adrenaline raises blood glucose concentration It is a hormone secreted from adrenal glands It is secreted when there is a low concentration of glucose in the blood when excited, stressed or exercising. It gets the body ready for action by making more glucose available for muscles to respire. How does it increase blood glucose? 1. Attaches to specific receptors on the cell surface membrane of liver cells ○ This causes a protein (G protein) to be activated and to convert ATP into cAMP. cAMP activates an enzyme that can hydrolyse glycogen into glucose, therefore activating glycogenolysis. 2. Activates glycogenolysis ○ Activated by the cAMP when adrenaline binds to receptors on liver cells, the second messenger mechanism 3. Inhibits glycogenesis ○ Preventing the synthesis of glycogen from glucose 4. Activates glucagon secretion and inhibits insulin secretion THE SECOND MESSENGER MODEL The second messenger model is the process by which the hormones activate glycogenolysis (glycogen →glucose) inside a cell even though they bind to receptors on the outside of the cell on the cell-surface membrane. This mechanism is used by glucagon and adrenaline in the regulation of blood glucose concentration. 1. Adrenaline/glucagon binds to a specific complementary transmembrane protein receptor within the cell-surface membrane of a liver cell. 2. The binding of adrenaline/glucagon causes the protein to change shape on the inside of the membrane. 3. This change in tertiary structure leads to the activation of an enzyme called adenylate cyclase. 4. The activated adenylate cyclase converts ATP to cyclic AMP (cAMP). 5. The cAMP acts as a second messenger 6. cAMP binds to an enzyme called protein kinase A, changing its shape and therefore activating it. 7. The active protein kinase A enzyme catalyses the conversion of glycogen to glucose (glycogenolysis) 8. Glucose moves out of the liver cell by facilitated diffusion and into the blood, through channel proteins. TYPE I DIABETES MELLITUS Diabetes is a disease when blood glucose concentration cannot be controlled naturally due to a lack of the hormone insulin or a loss of responsiveness to insulin. TYPE I DIABETES WHAT IS IT? Body is unable to produce its own insulin. The immune system attacks the beta-cells on the islets of Langerhans so they cannot produce any insulin. After eating, blood glucose concentration stays high (hyperglycaemia). The kidneys cannot reabsorb all the glucose, so some is excreted in urine. CAUSES May be as a result of an autoimmune response where body attacks self beta-cells. Some people have a genetic predisposition. Usually develops in childhood. Develops quickly usually over a few weeks, and the signs and symptoms are normally obvious. CONTROL: Insulin therapy - injecting insulin throughout the day or using insulin pump. Insulin cannot be taken by mouth INSULIN because, being a protein, it would be digested in the alimentary canal. This needs to be monitored carefully as too much insulin will cause a dangerous drop in blood glucose (hypoglycemia). To ensure the correct dose, blood glucose concentration is monitored using biosensors. CONTROL: Eating regularly and controlling simple carbohydrate intake helps to avoid sudden rises in glucose. DIET TYPE II DIABETES MELLITUS TYPE II DIABETES WHAT IS IT? Beta-cells do not produce enough insulin or when the body cells do not respond properly due to receptors on the target cells losing their responsiveness to insulin. This means cells do not take up enough glucose and blood glucose concentration stays high. CAUSES Usually acquired later in life and is linked with obesity, lack of exercise, age and poor diet. It is more likely in people with a family history of type II diabetes. It develops slowly, and the symptoms are normally less severe and may go unnoticed. CONTROL: Injections of insulin or use of drugs that stimulate insulin production - metformin. INSULIN Other drugs can slow down the rate at which the body absorbs glucose from the intestine. Stimulate kidneys to make you wee out extra sugar. CONTROL: Treated by eating a healthy, balanced diet, losing weight and exercising regularly. DIET Reduced sugar intake (carbs) in diet / eat food with low glycaemic index → Less sugar absorbed into blood Reduced fat intake → Less fat converted to glucose More (regular) exercise → Uses glucose / fats by increasing respiration Lose weight→ Increased sensitivity of cells to insulin / increased uptake of glucose by cells EVALUATING THE POSITIONS OF HEALTH ADVISORS AND FOOD INDUSTRY IN RELATION TO RISING INCIDENCE OF TYPE II DIABETES Type II diabetes is becoming increasingly common in the UK. - Increasing levels of obesity, more unhealthy diets and low levels of physical activity. Type II diabetes can cause additional health problems. - Visual impairments and kidney failure Health advisors are keen to educate people about risks and reduce incidence of type II diabetes. Recommending people: - Eat diet low in fat, sugar, salt with plenty of whole grains, fruit and vegetables - Take regular exercise and lose weight if necessary Some people think the food industry has a role in tackling the problem. - Need to reduce advertising of junk food particularly to children - Sweetener alternatives and reduce sugar, fat, salt content in products But companies want to increase profits so industry may only respond in long term when healthy eating changes. OSMOREGULATION Osmoregulation is the homeostatic control of the water potential of the blood. - In the blood an optimum concentration of water and salts is maintained to ensure a fairly constant water potential of blood plasma and tissue fluid. Osmoregulation is carried out by the kidneys, specifically the nephron: The nephron is the structure in the kidney where the blood is filtered, and useful substances are reabsorbed into the blood. The kidneys excrete waste products (e.g urea) As the blood passes through the capillaries in the cortex of the kidneys, substances are filtered out of the blood and into long tubules that surround the capillary - ultrafiltration. Useful substances (e.g. glucose) and the right amount of