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2018 ; 150
(1
): 7-18
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A perspective on Na and K channel inactivation
#MMPMID29233885
Armstrong CM
; Hollingworth S
J Gen Physiol
2018[Jan]; 150
(1
): 7-18
PMID29233885
show ga
We are wired with conducting cables called axons that rapidly transmit electrical
signals (e.g., "Ouch!") from, for example, the toe to the spinal cord. Because of
the high internal resistance of axons (salt water rather than copper), a signal
must be reinforced after traveling a short distance. Reinforcement is
accomplished by ion channels, Na channels for detecting the signal and
reinforcing it by driving it further positive (to near 50 mV) and K channels for
then restoring it to the resting level (near -70 mV). The signal is called an
action potential and has a duration of roughly a millisecond. The return of
membrane voltage (V(m)) to the resting level after an action potential is
facilitated by "inactivation" of the Na channels: i.e., an internal particle
diffuses into the mouth of any open Na channel and temporarily blocks it. Some
types of K channels also show inactivation after being open for a time. N-type
inactivation of K channels has a relatively fast time course and involves
diffusion of the N-terminal of one of the channel's four identical subunits into
the channel's inner mouth, if it is open. This mechanism is similar to Na channel
inactivation. Both Na and K channels also display slower inactivation processes.
C inactivation in K channels involves changes in the channel's outer mouth, the
"selectivity filter," whose normal function is to prevent Na(+) ions from
entering the K channel. C inactivation deforms the filter so that neither K(+)
nor Na(+) can pass.
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