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1QQ# 13 for 10:30 1.Why is action potential conduction velocity slower in a non-myelinated axon compared to a myelinated axon? 2.In what ways do voltage-gated.

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Presentation on theme: "1QQ# 13 for 10:30 1.Why is action potential conduction velocity slower in a non-myelinated axon compared to a myelinated axon? 2.In what ways do voltage-gated."— Presentation transcript:

1 1QQ# 13 for 10:30 1.Why is action potential conduction velocity slower in a non-myelinated axon compared to a myelinated axon? 2.In what ways do voltage-gated Na+ channels differ from voltage-gated K+ channels?

2 1QQ# 13 for 11:30 1.Why are myelinated axons considered more energy-efficient that non-myelinated axons? 2.In what ways do voltage-gated Na+ channels differ from voltage-gated K+ channels?

3 Figure 6.27 Vesicle release proportional to Ca++ influx (High f AP leads to residual Ca++ in terminal) Fates of neurotransmitters: 1)Bind to receptor on Post- synaptic cell 2)Diffusion away from synapse 3)Enzymatic degradation e.g. Acetylcholinesterase (AChE) and Monoamine Oxidase (MAO) 4)Uptake by astrocytes 5)Reuptake into presynaptic terminal (e.g. SSR) S 7 Most neurotransmitters are synthesized in the axon terminal. Exceptions: Peptide NTs originate in cell body, move in vesicles by fast orthograde axonal transport to axon terminal. Tetanus toxin & Botulinum toxin disrupt SNARE function.

4 Figure 6.33 Presynaptic Facilitation Presynaptic Inhibition Who Cares? Mechanism: vary Ca++ entry in presynaptic terminal B. Size of PSP is Variable! S 8

5 Figure 6.25 Unidirectional Release, diffusion, binding, Post-synaptic Receptor Types: Inotropic or Metabotropic Classification: Excitatory (closer to threshold for AP) Or Inhibitory (stabilizes or hyperpolarizes) S 1

6 Inotropic receptorMetabotropic receptor Types of Acetylcholine Receptors so named for agonist: Nicotinic AChR and Muscarinic AChR Types of Ligand-Gated Receptors S 2 Agonist = NicotineAgonist = Muscarine Antagonist = CurareAntagonist = Atropine = ACH = Acetylcholine

7 Priority by proximity To axon hillock! S 3

8 Figure 6.28 EPSPs :which ion moving in which direction? Duration of PSP vs AP Synaptic delay Some ion Channels that allow flux of Na+ and K+ simultaneously e.g. nicotinic Acetylcholine Receptor (nAChR) S 4

9 Figure 6.29 IPSPs :which ion moving in which direction? Some IPSPs result in no change in membrane potential by opening Chloride channels that stabilize membrane potential at resting value (Nernst Potential for Cl- = -70mV) or in cells that actively transport Cl- out. E K+ S 5

10 Figure 6.31 Summation and Synaptic Integration Different timesDifferent locations Challenge question: Suppose each IPSP hyperpolarizes by 5 mV and each EPSP depolarizes by 5 mV. If 4 inhibitory synapses are active at the same time, how many excitatory synapses must be active simultaneously to exceed threshold (-55 mV) if the resting membrane potential is -70mV? S 6

11 Synapses named for NT used: -ergic Examples: Cholinergic Adrenergic Serotonergic GABAergic Peptidergic S 7


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