Nervous System Lecture Notes PDF

True& false Nervous System There are two control systems in the body which coordinate activities: - (1) Nervous system (2) Endocrine system connected together by hypothalamus...

True& false Nervous System There are two control systems in the body which coordinate activities: - (1) Nervous system (2) Endocrine system connected together by hypothalamus - which coordinates activities that which coordinate rapid activities en -- mm sijos need duration rather than speed · muscle contraction e.g. · - e.g. body growth. Both systems affect their target cells by releasing chemical messengers. munreleasing factor inhibiting factor - sbi act in a complimentary mannerOne- Both systems - e.g. nervous system can control endocrine secretion as in case of hypothalamic control to pituitary is i - --- secretion. voild - it - -d  Functionally NS is divided into 3 main divisions: Sensorv division Motor division: Integrating center: receptors upper & integration of afferents lower motor information tracts neurons → occur in CNS effector at 3 levels center. organs (2) Lower brain level: brain stem & (3) Higher brain level: (1) Spinal cord: for diencephalon i.e cortex responsible immediate automatic Responsible for: for sensory function, day to day activities autonomic regulation, motor activities, e.g. flexor withdrawal, unconscious control of language & memory walking, micturition. respiration, equilibrium & posture.  Synaptic transmission Synapse: is the site of junction Transmission at the synapses is between two neurons. chemical by release of chemical transmitter. Synaptic transmission: is transmission of impulse (action potential) from one neuron to another.  Functional anatomy: Types of synapses: Axodendritic. Axosomatic. Axoaxonic Axon the onlyhave neurotransmitter and riscles  (3) Postsynaptic (1) Synaptic knobs (2) Synaptic cleft: membrane: which contains: Contain receptors formed of: a)Clear vesicles 1- Binding protein to containing rapidly acting 1- 30 - 50 nm width unite with the transmitter e.g. acetyl transmitter. choline. 2- contains extracellular fluid (ECF) (Nat, cl). 2- Ligand channels: b)Mitochondria. 1- Na+ channels allow Na+ entry. Depolarization (stimulate) 2- Cl channels: allow cl entry. hyperpolarization (inhibite) 3- K+ channels: allows K+ exit. hyperpolarization  Mechanism of synaptic transmission At Herve terminal  Mechanism of synaptic transmission: (1) Release of chemical transmitter: The action potential in Ca++ enter the knob the presynaptic nerve according to reaches the terminal concentration & electric knob & opens the voltage gradient gated Ca channels. at nerve terminal from outside to inside. 4 cations 4 resides rapture eg inter : > - The amount of The vesicles rupture with transmitter released is release of chemical directly proportional with transmitter in synaptic amount of Ca++ entered. cleft. (2)Union of chemical transmitter with its receptors. This changes the permeability of postsynaptic membrane to one or more ions. (3) Synaptic potential: Changes in ion fluxes through membrane lead to change in resting membrane potential of postsynaptic membrane to become: a/less negative causing excitatory postsynaptic potential. b/More negative causing inhibitory postsynaptic potential.  & Logging) (4) Removal of neurotransmitters and termination of response in one of these ways: 1- Inactivation 3- Active re- of transmitter 2- Passive uptake of by specific diffusion away transmitter by 4- Removal by enzymes at from synaptic axon terminal glial cell post synaptic cleft. to be stored or membrane destroyed Types of postsynaptic potential 1- Excitatory post-synaptic potential 2-Inhibitory post-synaptic potential 3-Grand post-synaptic potential:  Summation of inhibitory & excitatory post-synaptic potential. (A) Post-synaptic potential: 1/Excitatory post-synaptic potential EPSP 2/Inhibitory post-synaptic potential, IPSP 1) It is a state of local partial depolarization of 1) It is a state of partial hyperpolarization of post synaptic membrane. post-synaptic membrane. 2) Produced as 2) Produced as a result of combination of excitatory chemical a result of combination of inhibitory chemical transmitter (e.g. acetyl choline) with its transmitter (e.g. GABA) with it specific specific receptor. receptor. 3) the membrane is facilitated i.e. needs 3) the membrane is inhibited i.e. needs weaker stimulus to be excited (high higher stimulus to be excited (low excitability) excitability). because the potential is away from firing level 4) It is caused by: -Opening of ligand gated Na+ channels which allow: Na+ entry according to concentration & electric gradients. -Opening of ligand gated Ca++ channels. 5) EPSP is a local excitatory state 4) It is caused by: &to reach the threshold value, it -Opening of ligand gated cl & K + must be summated channels a/Temporal (time) summation: -Closure of ligand gated Na +& One pre-synaptic knob is Ca++ channels. stimulated repetitively 5) It is a local state that can be b/Spatial (space) summation: summated (temporal or spatial). Several pre-synaptic knobs are stimulated simultaneously. -When excitation reaches firing level, action potential starts. -Up to 50 EPSPs have to summate to reach the threshold value  (3) Grand Post-synaptic potential GPSP : It is the sum of all EPSPs and IPSPs occurring at the same time in one post synaptic neuron. 1- If excitatory & inhibitory input are equal GPSPis zero 2-If excitatory is slightly greater than inhibitory input GPSP will be depolarization not reach firing level 3-If excitatory is much. greater than inhibatory input GPSP is depolarization reach firing level 4- If inhibitory is greater than excitatory GPSP is hyper polarization  ·S - -fl 9+ Post-synaptic potential Action potential 1) Not obey all or non law 1) Obey all or non law 2) Graded 2) Can not be graded 3) No absolute refractory period 3) there is absolute refractory period 4) Summated 4)Can not be summated 5)Propagated. 5) Not propagated 6) Always make the membrane less negative 6) make the membrane more or less negative.  (3) Characters of synaptic transmission: 2. Synaptic delay: 1. Forward direction: it is the time taken by an impulse to be conducted through synapse. It equals 0.5 msec Impulses are conducted from pre- It is taken by: synaptic to post-synaptic neuron 1-Release of chemical transmitter because neurotransmitter is 2- Union with receptors. released from pre-synaptic 3-Opening ionic gates neuron. 4- Building post-synaptic potential. Number of synapses in reflex arc = Central delay / 0.5 msec Central delay: time of conduction of impulse along the synapses.  3. Fatigue: 4. Synaptic plasticity: It is decrease rate of discharge of impulse from post-synaptic neuron Change in functions according to after long period of high frequency stimulation of pre-synaptic neuron. demand placed on synapse. So, synaptic transmission can be Cause: - exhaustion of vesicles in pre- strengthened or weakened for synaptic terminals short or long duration. Benefit: it stops over excitation in CNS, as in epileptic fits where fatigue stops convulsions.  Factors affecting synaptic transmission: (1) Changes in composition of internal environment: a/pH of blood: 2/Acidosis: → decreases excitability→ 1/Alkalosis: → increases excitability→ decreases synaptic transmission, e.g increases synaptic transmission→ diabetes→Acids (B-hydroxybutyric Convulsions, e.g. Hyperventilation a)→coma Mechanism: In alkalosis, protein carry more negative charge→ combine with ionized Ca→ decrease ionized Ca→ open Na+ channels→ depolarization. b/Hypoxia: Hypoxia means decrease 02 supply→ Accumulation of acid (pyruvate & lactic acid) → decrease synaptic transmission. Interruption of cerebral circulation for 3 - 5 sec→ unconsciousness c/Hypoglycemia decrease synaptic transmission because glucose is the only fuel for brain for energy production & energy is needed for formation of transmitter & active re-uptake. d/Hormones may inhibit or facilitate synaptic transmission e.g. thyroid hormones facilitate synaptic transmission e/H20 & electrolytes: low Ca++ facilitate synaptic transmission. (2)Drugs: may affect mechanism of synaptic transmission Theophylline & caffeine: Strychnine: Anaesthesia & hypnotic: facilitate synaptic competes with inhibitory decrease synaptic transmission because low chemical transmitter transmission. threshold of excitability & (glycine) leaving excitatory -I.V. anesthesia & hypnotic depolarize post-synaptic pathway unaffected → stabilizing cell membrane (convulsions & spasm( membrane → hyperpolarizatior Or interfere with synthesis of the transmitter. (3) Diseases : Tetanus: Parkinsonism: decrease release of inhibitory chemical disease of basal ganglia: decrease release transmitter (GABA) leaving excitatory of inhibitory chemical transmitter chemical transmitter → muscle spasm → (Dopamine) leaving excitatory chemical lock jaw & asphyxia. transmitter (acetyl choline) → muscle spasm & rigidity.  Botulism toxin: Myathenia gravis: block the release of acetylcholine in autoimmune disease: antibody against neuromuscular junction leading to acetyl choline receptors in flaccid paralysis. neuromuscular junction → severe muscle weakness.