1 / 11

1QQ# 13 for 10:30

1QQ# 13 for 10:30. Why is action potential conduction velocity slower in a non-myelinated axon compared to a myelinated axon? In what ways do voltage-gated Na+ channels differ from voltage-gated K+ channels?. 1QQ# 13 for 11:30.

judith
Download Presentation

1QQ# 13 for 10:30

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

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

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

  3. S 7 Figure 6.27 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. Vesicle release proportional to Ca++ influx (High f AP leads to residual Ca++ in terminal) • Fates of neurotransmitters: • Bind to receptor on Post-synaptic cell • Diffusion away from synapse • Enzymatic degradation e.g. Acetylcholinesterase (AChE) and Monoamine Oxidase (MAO) • Uptake by astrocytes • Reuptake into presynaptic terminal (e.g. SSR) Tetanus toxin & Botulinum toxin disrupt SNARE function.

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

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

  6. Types of Ligand-Gated Receptors S 2 = ACH = Acetylcholine Inotropic receptor Metabotropic receptor Agonist = Nicotine Agonist = Muscarine Antagonist = Curare Antagonist = Atropine Types of Acetylcholine Receptors so named for agonist: Nicotinic AChR and Muscarinic AChR

  7. S 3 Priority by proximity To axon hillock!

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

  9. S 5 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. EK+

  10. S 6 Figure 6.31 Summation and Synaptic Integration Different times Different 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?

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

More Related