1. Section B: Membrane Potentials Section C: Synapses
30 September 2011
Section B: Membrane Potentials
Section C: Synapses
Test Monday:
Turn in Take-Home Portion at beginning.
All personal materials on floor at front of room.
At least one vacant seat to nearest neighbor.
Coverage up to and including Ch 6 B
Check your Multiple Choice Grade on Moodle Site Tuesday
Wednesday 1QQ on Synapses.

2. 1QQ # 11 for 8:30 class Why doesn’t an action potential reach + 60 mV?
Voltage- gated Na+ channels open and spontaneously close quickly
Voltage-gated K+ channels open a little later than the Na+ channels
Na+ K+ ATPase quickly pumps out the Na+ that enters during an AP
As the membrane approaches +60 mV, the driving force for Na+ entry is weaker
Na+ is not the only permeable ion.
Which are the accurate statements regarding V-gated K+ channels?
The more the membrane is depolarized, the more K+ channels will open, and the membrane will depolarize even more, generating a positive feedback cycle.
These channels inactive after a short open time and can only reopen if the membrane potential returns to negative values.
These channels are “blocked” by lidocaine, xylocaine, and novocaine.
These channels close as the membrane repolarizes.

3. 1QQ # 11 for 9:30 class Why doesn’t an action potential reach + 60 mV?
Voltage- gated Na+ channels would be forced “shut” at + 60 mV
Voltage-gated K+ channels open a little sooner than the Na+ channels.
Na+ K+ ATPase quickly pumps out the Na+ that enters during an AP
As the membrane approaches +60 mV, the driving force for Na+ entry is weaker
Na+ channels open only briefly and then quickly inactivate.
Which are the accurate statements regarding V-gated K+ channels?
The more the membrane is depolarized, the more K+ channels will open, and K+ will leave the cell, contributing to repolarization.
These channels inactive after a short open time and can only reopen if the membrane potential returns to negative values.
These channels are “blocked” by lidocaine, xylocaine, and novocaine.
These channels open shortly after the V-gated Na+ channels open.

4. How does an action potential move along the axon?
The Questions:
How does an action potential move along the axon?
Why doesn’t the amplitude get smaller with distance?
Why is the conduction of an action potential unidirectional?
Axon Hillock of interneuron or efferent neuron
Axon
Trigger Zone of Sensory Neuron

5. S 2
In unmyelinated axons, action potential must be generated at each point along the membrane, a relatively slow process that involves influx of Na+ which sets up positive feedback cycle.
In myelinated axons, action potential must be generated only at the nodes of Ranvier, which allows AP to be conducted much faster and with fewer ions moving, and thus less energetically expensive.

6. Clustering of V-gated channels at Nodes of Ranvier
Saltatory Conduction
S 3
What’s at the end of an axon?
Figure 6.23
AP CV (up to 100 m/s)
Location of channels
Energy Requirements
Axon diameter
Clustering of V-gated channels at Nodes of Ranvier
Reminder: influx of Na+ is very quickly followed by efflux of K+ (not shown above)

7. Section C: Synapses and Synaptic Transmission
Figure 6.24
Section C: Synapses and Synaptic Transmission

8. Anatomy of an Electrical Synapse (aka Gap Junction)
Comparison to Chemical Synapses
Directionality
Response time
Sign inversion?
Uncommon in human CNS. Common in cardiac muscle and some smooth muscle.

9. Anatomy of a Chemical Synapse
Presynaptic cell
Postsynaptic cell

10. Fates of neurotransmitters: Bind to receptor on Post-synaptic cell
Figure 6.27
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.
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.

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