Human Physiology BIOL3205 PDF

Human Physiology BIOL3205 Neuronal communication Prof. Chi Bun Chan School of Biological Sciences 5N10 Kadoorie Biological Sciences Building [email protected] 39173823  Lecture outline Membrane potential Formation...

Human Physiology BIOL3205 Neuronal communication Prof. Chi Bun Chan School of Biological Sciences 5N10 Kadoorie Biological Sciences Building [email protected] 39173823  Lecture outline Membrane potential Formation and conduction of action potential Synapse and neurotransmitter Neural integration and networking  Structure of a neuron Dendrites – receiving signals from other neurons toward the cell body Dendritic spine – formation of the synapse (can also be found in the cell body) Cell body – nucleus and organelles, Integrate the signals Input zone Axon – conducts action potential that terminates at other cells Variable in length Action potentials are triggered by axon hillock Axon terminals  Membrane potential Membrane potential is the voltage difference across a cell membrane Resting membrane potential of a neuron cell is Extracellular Intracellular ~ -70 mV No membrane Expressed as negative values because the potential intracellular fluid has a slight excess of anions and the extracellular fluid has a slight excess of cation (polarized) Na+ and K+ are responsible for generating the membrane resting membrane potential Potential developed Maintained by the Na+-K+ pump at the expense of energy Channels always open for K+ (Leaky channel) (https://www.studyblue.com)  Change of membrane potential Only nerve and muscle are excitable tissues Membrane potential can be changed Polarization - more charges are separated by the membrane Depolarization – fewer charges are separated by the membrane Repolarization –returns to resting membrane potential Hyper-polarization – becomes more polarized Ion movement can only be mediated by channels (https://ib.bioninja.com.au/standard-level/topic-6-human-physiology/65-neurons-and-synapses/action-potential.html)  Ion channels (https://hubpages.com/education /Ion-Channels-Definition-Types- Description-of-Sodium-Calcium- Potassium-and-Chloride-Ion- channels) Pores that open and close in an all-or-nothing fashion to provide aqueous channels through the plasma membrane that ions can traverse Leaky Gated channels Voltage gated Chemically gated Mechanically gated Thermally gated  Generation of electoral signals in neuron Electrical signals occur in neurons via changes in Graded membrane potential potential Brought about by changes in ion movement Two basic forms of electrical signals Graded potential Action potential Action potential  Depolarization of membrane in a small and specialized region of the Graded potential total membrane Provoked by Na+ entry Ions flow from active site to inactive site, causing a current along the membrane Bi-directional over a very short distance (detrimental or gradually decrease) → current loss by K+ out flux Function as a signal for a very short distance Change of potential depends on the magnitude of triggering event  Action potential (AP) A brief, rapid, large changes in membrane potential GP Initiated when the membrane potentials reach threshold potential Generated at the axon hillock Propagated throughout the entire membrane nondecrementally Serve as long-distance signals Fixed threshold and magnitude All-or-none  Conformations of voltage-gated Na+ and K+ channels Resting Depolarized Resting Depolarizing Depolarized membrane potential membrane potential  Caused by rapid fluxes of Na+ and K+ Formation of AP Opening and closing of voltage-gated Na+ channels and voltage-gated K+ channels Graded potential activates: Opening of Na+ channel (fast) Closing mechanism of Na channel (slow) Opening of K channel (slow) Positive feedback of Na+ channel – rapid depolarization K+ rushes out of the cell because of channel opening, charges from repelling interior, and the concentration gradient) → rapid repolarization Hyperpolarization is caused by the slow closure of K+ channel Graded potential vs action potential GP AP  A toxin that attacks the nervous system Tetrodotoxin (TTX) Neurotoxins Highly enriched in liver and gonad of pufferfish and also salamanders, octopus and goby Cannot be destroyed by cooking Blocks voltage-gated Na+ channel and thus AP generation Occur 10-45 minutes after eating the pufferfish poison and begin with numbness and tingling around the mouth, salivation, nausea, and vomiting Symptoms may progress to paralysis, loss of consciousness, and respiratory failure, and can lead to death Can be used as analgesic  Propagation of nerve impulse Once AP is imitated, no further triggering event is necessary to activate the remainder of the nerve fiber Conducted through contiguous conduction or saltatory conduction Depends on the axon structure (myelinated or non-myelinated) (http://slideplayer.com/slide/8543338/)  Contiguous conduction Active Inactive Resting membrane Occurs in non-myelinated neurons area area potential Spread of the action potential along every patch of membrane down the length of an axon Active and inactive areas Once initiated, a self-perpetuating cycle is initiated so that the AP is prorogated along the rest of the fiber Resting Resting Membrane Active Inactive The original action potential does not potential area area Membrane potential travel along the member; new action potential is formed The last action potential is identical to the original one Refractory period The time period when a new AP cannot be initiated in a region that has just undergone an AP Absolute refractory vs relative refractory  Myelinate fibers are axons Myelination covered with myelin along ↳ For long Traumation their length ↳ Long necrone A thick layer composed primarily of lipids Nodes of Ranvier Produced by oligodendrocytes o (CNS) and Schwann cells (PNS) Prevent leakage of current (insulation) In between myelinated regions are called nodes of Ranvier (concentrated with Na+ and K+ channels) 50 times faster than unmyelinated fibers Conserve energy Why not all neurons are myelinated? Saltatory conduction AP is only produced at the nodes of Ranvier Not changed membrane potential Currents move under the myelin sheath but diminish in amplitude Na+ entry at the node reinforces the depolarization and keeps the => X action potential generated magnitude to the threshold for the next AP Jump of AP Graded potential vs action potential Voltage GP Voltage Time Voltage AP Voltage Time  Multiple sclerosis An autoimmune disease that attacks the nervous system Loss of myelin Combination of genetic and environmental factors (toxins, virus, smoking, vitamin D) Slows the transmission of nerve impulse (may block the propagation of AP) Symptoms depend on the location of axon degeneration No cure  Structure of a neuron post-synaptic neuron Cell body – nucleus and organelles, Integrate the signals Pre-synaptic neuron Input zone Axon – conducts action potential that terminates at other cells Variable in length Action potentials are triggered by axon hillock Axon terminals Dendrites – receiving signals from other neurons toward the cell body Dendritic spine – formation of the synapse (can also be found in (https://www.semanticscholar.org/paper/Epigenetic-regulation-of- neuronal-dendrite-and-Smrt- the cell body) Zhao/ba6aeb57c781295dd06de39a32ff09bb6321c0c5)  Synapse Axon terminal A neuron may terminate on a (synaptic knob) Synaptic muscle (neuromuscular vesicle junction), a gland (neuroeffector junction), or another neuron (synapse) permits a neuron to pass an Dendritic spine electrical (electrical synapse) or chemical (chemical synapse) signal to another neuron Synaptic knob Synaptic vesicle that contains the neurotransmitter Space between the presynaptic and postsynaptic neuron is called synaptic cleft Operates in one direction  Synaptic transmission Differential localization of synaptic vesicles and neurotransmitter receptors (one way transmission)  Termination of synaptic transmission Endocytosis with the receptor by post-synaptic neuron Re-uptake by the presynaptic terminal (re-use) Destroyed by the enzyme at the synaptic cleft Diffused out => Stop signal transmition  Blocking of neurotransmitter reuptake Cocaine (coke) – a psychostimulatnt First extracted from coca leaves Sigmund Freud (psychologist), who used the drug himself, was the first to broadly promote cocaine as a tonic to cure Cocaine depression and sexual impotence Competitor of dopamine transporter Higher concentration of dopamine in the synaptic cleft Prolonged activation of neural pathways (feeling pleasure)  Types of neurotransmitter Endogenous chemicals that transmit the signal across a synapse Each presynaptic neuron releases only one neurotransmitter Different neurons vary in neurotransmitter release Types of synaptic transmission Binding of neurotransmitter causes a membrane potential change of postsynaptic neuron Can be excitatory (excitatory synapse) or inhibitory (inhibitory synapse) Excitatory postsynaptic potential (EPSP) – a change in the postsynaptic potential occurs at an excitatory synapse (small depolarization) Less => negative membrane potential Inhibitory postsynaptic potential (IPSP) – a change in the postsynaptic potential occurs at an inhibitory synapse (small hyperpolarization) potential membrane Negative of => More Graded potential EPSP cannot depolarize the postsynaptic neuron to bring to the threshold (i.e. AP firing)  Determination of the post- synaptic potential Postsynaptic neuron can be brought to threshold by temporal summation or spatial summation Temporal summation – several EPSP occurring close together in time because of a successive firing of a single presynaptic neuron Spatial summation – EPSPs originated simultaneously from several presynaptic inputs Cancellation of EPSP by IPSP Neuronal integration to control physiological activity (e.g. urination)  Integration of information transfer between neurons Convergent pathway Complex computational network Divergent pathway Divergent pathway – a presynaptic neuron branches to affect a large number of postsynaptic neurons Convergent pathway – many pre-synaptic neurons input to influence of a postsynaptic neuron Number of neurons ~ 100 billion (109) A single neuron connects to 5000 to 10000 other neurons Number of synapses ~ 1014 (100 quadrillions)  What determines the strength of a stimulus? Every AP is identical Loo f Frequency of AP > - Neurotransmitter release may decrease in high transmitter station > - neww frequency → > - High f > - more desensitization  Memory Memory is the storage of acquired knowledge for later recall Short-term memory (seconds to hours) Long-term memory (Days to years) Consolidation – a process that transfers and fixes a short-term areopsis memory into long-term memory 3 No single memory center in the brain – cerebellum, prefrontal cortex, hippocampus => Formation of Memory Structural (branching, elongation of dendrites, formation of new synapse) and functional (long-term potentiation) alternation Long-term potentiation Nervous system is endowed with connector plasticity – the ability to alter its strengthen synaps anatomy and function in response to shmulation - changes in its activity pattern repetitive Long-term potentiation (LTP) – ↑ repetitive stimulation of a particular synapse eventually leads to an increase in the strength of synaptic connection i.e. triggering the AP in the postsynaptic cell Different from a temporal summation Important for the consolidation of long- term memory formation (https://courses.washington.edu/conj/bess/memory/cellular-memory.html) LTP and memory formation NMDAR: N-methyl-D-aspartate receptor (https://slideplayer.com/slide/694474/)  After the lecture, you should be able to explain Membrane potential, graded potential and action potential The formation and transmission of GP The formation and transmission of AP Transmission of information between neurons What is neural integration