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Neural transmission

Neural transmission. The Reticular theory vs the Synaptic theory. The “resting Membrane Potential”. Ions are responsible for the Resting membrane potential. Hyperpolarization Moves potential away from zero (more negative) Depolarization Moves the potential toward zero (less negative).

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Neural transmission

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  1. Neural transmission

  2. The Reticular theory vs the Synaptic theory

  3. The “resting Membrane Potential”

  4. Ions are responsible for the Resting membrane potential

  5. Hyperpolarization • Moves potential away from zero • (more negative) • Depolarization • Moves the potential toward zero • (less negative)

  6. “Threshold”

  7. What is special about “threshold?”

  8. The forces of Diffusion

  9. The Neurons membrane separates the different ions

  10. The membrane controls diffusion

  11. By opening or closingIon channels

  12. If ion channels are open; diffusion across concentration and electrostatic gradients will occur

  13. Threshold Depolarization activates Na+ ion channels….and then Na+ influx will occur NA+ influx makes the potential more positive…K+ channels then open and K+ efflux occurs…the neuron moves back toward the RMP

  14. Once triggered, the AP is all or none, and “one-way.”

  15. Action potential arrives at terminals

  16. Causing the release of neurotransmitters into the synapse

  17. The action potential at the terminals causes Neurotransmitter release into the synapse.

  18. NTs bind to post-synaptic receptors

  19. EFFECTS OF NTs? • IPSPs: inhibitory post synaptic potentials • Hyperpolarization • Decrease probability of action potential • EPSPs: excitatory post synaptic potentials • Depolarization • Increase probability of action potential

  20. Ways that receptor activation can lead to IPSPs or EPSPs

  21. Neural Integration:if enough EPSPs occur threshold depolarization will activate Na= ion channels

  22. EFFECTS OF NTs? • EPSP or IPSP • Depends on the type of Neurotransmitter

  23. NTsCircuit involvementEffects Acetylcholine NMJ, Autonomic ganglia +/- (Ach) Brain Dopamine VTA, Subst. Nigra +/- (DA) accumbens Norepinephrine RAS, many brain +/- (NE) regions Serotonin Raphe, Ctx, +/- (5-HT) many regions Gama-Amino- Ubiquitous - Butyric acid (GABA) Glutamate Ubiquitous + (Glu) Endorphin PAG, VTA, +/- Enkephalin (End/Enk) Know these: Representative NTs

  24. Ex: Why is ACH sometimes excitatory and other times inhibitory?Receptor subtypesEffects depend on receptor subtype

  25. Neurotransmitters bind to receptor sites to produce postsynaptic effects

  26. A given NT substance will only activate specific receptor proteins, and can not activate receptors for other NTs NT-Receptor Specificity • Lock & Key Model • NT = key • Receptor = lock Activation of a receptor will lead to either Excitation or Inhibition.

  27. One Neurotransmitter may activate any of a “family” of receptor subtypes ACH in the ANS can activate the “Muscarinic” ACH receptor (mACH), a metabotropic receptor type. Activation of the mACHr leads to an inhibitory response. ACH release in the somatic branch of the PNS activates the “Nicotinic” ACH receptor (nACHr). An ionotropic receptor type. Activation of the nACHr leads to an excitatory response.

  28. NT-receptor interactions must stop!Enzymatic degradation

  29. Nerve gases block ACHE-preventing breakdown of Acetylcholine.

  30. Different nerve gas compounds; allchemically related to Diisoflourphosphate (DFP) common in low concentrations in insecticides and some pesticides.

  31. The effects of nerve gas poisoning reflect normal functions of ACH mostly in the PNS Functional paralysis of muscle activity is a result of poisoning. Death is most often due to anoxia, because you can not respire. Antidotes involve drugs that block the effects of ACH

  32. The effects of other NTs are terminated by Reuptake. E.g. the serotonin transport protein recycles 5 Ht from synapse.

  33. Drugs may affect neural transmission in many different ways

  34. Agonism and Antagonism • Agonism- drug effects that are in the direction of or promote the natural effects of a given NTs at its synapse. • Antatgonism- drug effects that are in the opposing direction of or inhibit the natural effects of a given NTs at its synapse.

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