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 closing Ion 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. Know these: Representative NTs NTsCircuit involvementEffects AcetylcholineNMJ, Autonomic ganglia+/- (Ach)Brain DopamineVTA, Subst. Nigra+/- (DA)accumbens NorepinephrineRAS, many brain+/- (NE)regions SerotoninRaphe, Ctx,+/- (5-HT)many regions Gama-Amino-Ubiquitous- Butyric acid (GABA) GlutamateUbiquitous+ (Glu) EndorphinPAG, VTA, +/- Enkephalin (End/Enk)

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

25. Neurotransmitters bind to receptor sites to produce postsynaptic effects

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

27. Two General Types of Receptor: Ionotropic receptors: the receptor is an ion channel Metabotropic receptors: Activation of the receptor will in turn activate a “second” messenger chemical that may open or close ion channels

28. IONOTROPIC RECEPTORS-

29. Metabotropic Receptors

30. 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. ACH release in the somatic branch of the PNS activates the “Nicotinic” ACH receptor (nACHr). An ionotropic receptor type. Activation of the mACHr leads to an inhibitory response. Activation of the nACHr leads to an excitatory response.

31. NT-receptor interactions must stop! Enzymatic degradation

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

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

34. 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

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

36. Drugs may affect neural transmission in many different ways

37. 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.