Essential Cell Biology 5th edition

Ion Channels and Nerve Cell Signaling
419
TABLE 12–3 SOME EXAMPLES OF ION CHANNELS
Ion Channel Typical Location Function
K + leak channel
Voltage-gated Na +
channel
Voltage-gated K +
channel
Voltage-gated Ca 2+
channel
Acetylcholine receptor
(acetylcholine-gated
cation channel)
Glutamate receptor
(glutamate-gated
cation channel)
GABA receptor
(GABA-gated
Cl – channel)
Glycine receptor
(glycine-gated
Cl – channel)
Mechanically-gated
cation channel
plasma membrane of
most animal cells
plasma membrane of
nerve cell axon
plasma membrane of
nerve cell axon
plasma membrane of
nerve terminal
plasma membrane
of muscle cell (at
neuromuscular junction)
plasma membrane of
many neurons
(at synapses)
plasma membrane of
many neurons
(at synapses)
plasma membrane of
many neurons
(at synapses)
auditory hair cell in
inner ear
maintenance of resting
membrane potential
generation of action
potentials
return of membrane to
resting potential after
initiation of an action
potential
stimulation of
neurotransmitter release
excitatory synaptic signaling
excitatory synaptic signaling
inhibitory synaptic signaling
inhibitory synaptic signaling
detection of sound
vibrations
Toxins that bind to any of these excitatory or inhibitory neurotransmitter
receptors can have dramatic effects on an animal—or a human. Curare,
for example, causes muscle paralysis by blocking excitatory acetylcholine
receptors at the neuromuscular junction. This drug was used by South
American Indians to make poison arrows and is still used by surgeons
to relax muscles during an operation. By contrast, strychnine—a common
ingredient in rat poisons—causes muscle spasms, convulsions, and
death by blocking inhibitory glycine receptors on neurons in the brain
and spinal cord.
The locations and functions of the ion channels discussed in this chapter
are summarized in Table 12–3.
Most Psychoactive Drugs Affect Synaptic Signaling by
Binding to Neurotransmitter Receptors
Many drugs used in the treatment of insomnia, anxiety, depression, and
schizophrenia act by binding to transmitter-gated ion channels in the
brain. Sedatives and tranquilizers such as barbiturates, Valium, Ambien,
and Restoril, for example, bind to GABA-gated Cl – channels. Their binding
makes the channels easier to open by GABA, rendering the neuron
more sensitive to GABA’s inhibitory action. By contrast, the antidepressant
Prozac blocks the Na + -driven symport responsible for the reuptake
of the excitatory neurotransmitter serotonin, increasing the amount of
serotonin available in the synapses that use it. This drug has changed the
lives of many people who suffer from depression—although why boosting
serotonin can elevate mood is still unknown.
QUESTION 12–7
When an inhibitory neurotransmitter
such as GABA opens Cl – channels
in the plasma membrane of a
postsynaptic neuron, why does this
make it harder for an excitatory
neurotransmitter to excite the
neuron?