Nerve function'

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Chapter 11
Lecture 28 pages 641-654

• Nerve function.

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The function of nerves relies on various features
that control the action potential.
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Myelination increases the speed and efficiency of
action potential propagation.
Glial cells (diagrammed in red) surrounding the
axon produce an electrical insulation rich in
glycolipids. Nodes of Ranvier
located at regular intervals are openings in the
insulation where Na channels are concentrated.
Influx of Na at one node results in
depolarization at the next node due to the rapid
diffusion of Na in the cytoplasm. This triggers
an action potential that leads to
rapid depolarization of the next node.
The action potential jumps from node to node
by a process called saltatory conduction.
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• The threshold potential required to initiate an
  action potential is affected by inhibitory and
  excitatory neurotransmitters acting upon distinct
  transmitter-gated (ligand-gated) ion channels.
• Excitatory neurotransmitters open ligand-gated
  ion channels that depolarize the membrane towards
  the threshold potential.
• Acetylcholine, glutamate and serotonin open
  distinct cation channels that allow influx of
  Na.
• Inhibitory neurotransmitters open ligand-gated
  ion channels that resist depolarization of the
  membrane towards the threshold potential.
• Gamma-aminobutyric acid (GABA) and glycine open
  distinct Cl- channels.
• Psychoactive Drugs alter specific ligand-gated
  ion channels.

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To understand the action of neurotransmitters,
begin by considering the resting state of a cell.
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The graph shows the impact that opening different
channels will have on the membrane potential.
Recall that channels transport ions much faster
than carrier proteins so the ATPases below are
insignificant when considering what happens when
channels are opened.
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A single nerve cell combines the excitatory and
inhibitory signals received from numerous other
neurons to control the frequency with which
action potentials are generated.
The presynaptic terminals are derived from
numerous other neurons. Ligand-gated ion
channels are concentrated at the synapses on the
postsynaptic cell (colored yellowish-brown). Some
of the presynaptic neurons make synapses that are
excitatory and others make synapses are
inhibitory. Neurotransmitters released into each
synapse will generate a postsynaptic potential
(PSP). The voltage-gated Na channels are
concentrated at the axon hillock. An action
potential is initiated at the axon hillock when
the sum of excitatory and inhibitory PSP
depolarize the axon hillock to the threshold
potential.
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• Additional channels located in the axon hillock
  fine tune the control of action potentials.
• Voltage-gated K channels that open after opening
  of the voltage-gated Na channels accelerate the
  repolarization of the membrane so the action
  potentials fire with high frequency. Rapid
  repolarization of the membrane is necessary
  because Na channels can not initiate a second
  action potential until they have been reset by
  the polarized membrane.
• 2. Voltage-gated Ca channels and Ca -
  activated K channels provide an adaptive
  response that desensitizes a nerve.
• Voltage-gated Ca channels open briefly when
  there is an action potential allowing influx of
  Ca.
• Repeated action potentials cause a buildup in
  cytoplasmic Ca.
• Ca causes opening of Ca - activated K
  channels.
• Efflux of K inhibits depolarization to the
  threshold potential.

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The keys to understanding the behavior of the
nerve is to remember 1. Relative distributions
of Na, K, Cl-, and Ca. 2. The resting
potential is negative on the inside and positive
on the outside. 3. Will the movement of a
particular ion promote or inhibit depolarization
of the membrane to the threshold required for an
action potential?
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The neuromuscular junction is an example of how
the action potential from the nerve triggers a
response in another cell.
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1. When the action potential reaches the end of
the axon, it triggers opening of voltage-gated
Ca channels. Influx of Ca triggers the
release of the neurotransmitter, acetylcholine,
into the synaptic cleft. 2. Acetylcholine binds
the acetylcholine-gated cation channel - influx
of Na begins to depolarize the muscle
membrane. 3. At a threshold, many voltage-gated
Na channels open to generate an action
potential. 4 5. The action potential causes
opening of voltage-gated Ca channels in the
plasma membrane and gated Ca release channels
located in the sarcoplasmic reticulum. Increase
in cytoplasmic Ca triggers contraction by
associating with a Ca binding protein.