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Galala University

Dr. Ramadan Saad

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synapse physiology neurotransmitter biology

Summary

This document details the physiology of synapses, a critical juncture in the nervous system. Synaptic transmission is explained, and the roles of neurotransmitters and postsynaptic potentials are addressed. The document covers the mechanism of synaptic transmission, outlining the steps involved in neurotransmitter release and action on postsynaptic receptors. Various potentials, including EPSPs and IPSPs, are also explained, along with factors influencing synaptic transmission.

Full Transcript

PHYSIOLOGY OF Synapse Dr. Ramadan Saad Objectives At the end of this lecture the student should: (1) Describe the parts of a synapse & what does each part contain. (2) Differentiate between different types of synapses. (3) Define synaptic transmitters, give example...

PHYSIOLOGY OF Synapse Dr. Ramadan Saad Objectives At the end of this lecture the student should: (1) Describe the parts of a synapse & what does each part contain. (2) Differentiate between different types of synapses. (3) Define synaptic transmitters, give examples of excitatory & inhibitory ones ; explain how they are released (4) Explain ionic channels that mediate actions on synaptic receptors. (5) Explain EPSP, IPSP. (6) Explain how acidosis and alkalosis can affect synaptic transmission. Synaptic transmission Synapse: Specialized junction where one part of a neuron contacts and communicates with another neuron or cell type (such as a muscle or glandular cell). Information tends to flow in one direction, from a neuron to its target cell. The first is said to be presynaptic and the target is said to be postsynaptic. Chemical Synapses Physiological anatomy: Presynaptic Postsynaptic Synaptic cleft small round or oval Show a thickening directly opposite knobs→ terminal buttons the synaptic knob (active zone) or synaptic knobs Contains vesicles and Contains receptors for mitochondria neurotransmitters Mechanism of Synaptic Transmission It involves 3 steps: 1) Release of neurotransmitter into synaptic cleft. 2) Action of the neurotransmitter on postsynaptic membrane. 3) Termination of synaptic transmission. Release of Neurotransmitter Stimulation of presynaptic neuron → generation of AP → AP reaches the synaptic knob→ transient opening of the voltage gated Ca++ channels → Ca++ influx Ca++ activates proteins in the vesicle and active zone. Activated proteins causes synaptic vesicles to fuse with membrane. Vesicles release the transmitter by exocytosis in cleft The number of vesicles ruptured depends upon the concentration of Ca2+ within the active zone of the Neurotransmitter Release Postsynaptic Potentials Postsynaptic potentials (PSPs) are 2 major types: Excitatory Postsynaptic Potentials (EPSPs) Inhibitory Postsynaptic Potentials (IPSPs) Excitatory Postsynaptic Potentials (EPSPs) 1) Def. It is a state of partial depolarization which occurs in the postsynaptic membrane due to single presynaptic impulse Excitatory Postsynaptic Potentials (EPSPs) 2) Mechanism: When the excitatory chemical transmitter bind to and open ligand-gated cation channels→ allow much Na influx than K efflux→ depolarization of postsynaptic membrane → brought the postsynaptic membrane potential close to the threshold for excitation → called EPSP. Excitatory Postsynaptic Potentials (EPSPs) When the summated EPSPs reach the firing level, This will generate an action potential at the initial segment of the axon (axon hillock). Inhibitory Postsynaptic Potentials (IPSPs) 1)Def. It is a state of partial hyperpolarization which occurs in the postsynaptic membrane due to single presynaptic impulse Inhibitory Postsynaptic Potentials (IPSPs) 2)Mechanism: When the inhibitory chemical transmitter bind to and open ligand-gated anion channels→ allow much Cl influx → hyperpolarization of postsynaptic membrane → brought the postsynaptic membrane potential away from the threshold for excitation → called IPSP. Termination of synaptic transmission It occurs when the transmitter is removed from the synaptic cleft by one or more of the following ways: i) Active reuptake of the transmitter into the presynaptic terminal. ii) Enzymatic degeneration e.g.: hydrolysis or oxidation….etc. iii) Diffusion to the interstitial fluid. NT NT Neuronal DIFFUSION Uptake AND URINE EXCRETIO NT ENZYME N HYDROLYSIS 16 ANS, Abdelaziz Hussein General Properties of Synaptic Transmission 1. One-way conduction Synapse allow conduction of the impulses in one direction only; from the presynaptic to the postsynaptic neurons → Bell- Magendie law. This is because transmitter is present in the presynaptic neuron not the postsynaptic neuron 2. Synaptic Delay Def., It is the time that passes between arrival of an action potential to the synaptic knob and the occurrence of response in the postsynaptic neuron Time: 0.5 msec Cause: This represents the time required; 1. Release and diffusion of the neurotransmitter 2. Its binding with its postsynaptic receptors and generation and summation of EPSPs. 3. Synaptic Fatigue Def., Rapid and intense stimulation of synapse→ progressive decline in synaptic transmission and the synapse may in severe conditions, stop functioning Cause: It results mainly from depletion of the neurotransmitter stores the in the synaptic knobs→ because in intensive stimulation the resynthesis and reuptake mechanisms that fill these stores are unable to provide all the demands for the transmitter Significance Protective mechanism against excessive neuronal mechanism e.g. in epileptic fit 3. Synaptic Fatigue Rate of release Rate of reuptake Ca ions...........Ach................. 5. Effects of Hypoxia -Normal function of the neuron is highly dependent upon an adequate O2 supply - Marked hypoxia for a very short period, (a few seconds), causes loss of excitability of many neurons and stop of synaptic transmission. - When the blood supply to the brain is markedly reduced→ coma occurs within less than 7 seconds. 6. Effects of pH Alkalosis→ ↑es excitability of neurons→ at pH 7.8 to 8.0 severe convulsions occurs. Acidosis→ ↓es excitability of neurons→ at pH around 7.0 coma occurs. This latter condition is always seen in severe uremic or diabetic acidosis. 7. Effects of Drugs i) Caffeine and theophylline→↑ neuronal excitability by ↓ing the threshold for excitation of the postsynaptic neurons. ii) Anesthetics and hypnotics →↑ threshold for excitation of the neurons→↓ synaptic transmission. https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcTPXydhxyxxiXIJoktNNdYNG6p7lDKl7Xv_tozlUl1C1dZF4rOIzw THANKS

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