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Action Potential Skeletal Muscle

A skeletal muscle action potential is generated when the motor endplate potential raises the sarcolemmal potential above the threshold to activate voltage-gated sodium channels in the sarcolemma. This causes rapid depolarization towards the sodium Nernst potential, reaching around +30 mV. The peak is limited by sodium channel inactivation and activation of rectifying potassium channels, which also cause repolarization. Once generated, the action potential spreads as a wave through invaginations called t-tubules to trigger calcium release and contraction.

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Mian Talha Kamal
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58 views1 page

Action Potential Skeletal Muscle

A skeletal muscle action potential is generated when the motor endplate potential raises the sarcolemmal potential above the threshold to activate voltage-gated sodium channels in the sarcolemma. This causes rapid depolarization towards the sodium Nernst potential, reaching around +30 mV. The peak is limited by sodium channel inactivation and activation of rectifying potassium channels, which also cause repolarization. Once generated, the action potential spreads as a wave through invaginations called t-tubules to trigger calcium release and contraction.

Uploaded by

Mian Talha Kamal
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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MIAN TALHA KAMAL, 20-47, BATCH

B
ACTION POTENTIAL SKELETAL
MUSCLE:
The resting membrane potential in skeletal muscle cells is similar to that in neurons, i.e. −70 to −90 mV.
Unlike nerve cells, where the resting membrane potential is predominantly a result of K+ permeability,
skeletal muscle cell resting membrane potential receives a significant contribution from Cl−
conductance. The importance of this Cl− current became apparent when the excitability associated with
myotonia congenita was found to be a result of chloride channel mutations. The physiological relevance
of the Cl− current stems from a need to maintain muscle activity during repeated stimulation. When
muscle contracts, there is leakage of K+ from the cell. With repeated activity there is run-down of the K+
concentration gradient across the sarcolemma. Without the Cl− current to maintain resting membrane
potential, the muscle would not repolarize sufficiently to regenerate the active state of the channels
responsible for generation of succeeding action potentials.

A skeletal muscle action potential is generated when the motor endplate potential is sufficient to raise
the surrounding sarcolemmal potential above the threshold for activation of the voltage gated Na+
channels that are abundant throughout the sarcolemma. When these channels are activated, the
membrane is rapidly depolarized towards the Nernst potential for Na+ (Table 1). However, the peak
potential achieved is approximately +30 mV. The Nernst potential is not achieved for two main reasons.
First, just as the Na+ channels are activated by membrane voltage changes, a process of inactivation is
also initiated as the membrane potential becomes less negative. Inactivation is a slower mechanism
than activation, so the Na+ current continues to flow for a short period after the onset of inactivation,
but not sufficiently to reach the Nernst potential. The second factor limiting the upstroke of the action
potential is the voltage activation of rectifying potassium channels. Their activation is initiated also
during the upstroke of the action potential but (in a similar way to Na+ channel inactivation) there is a
slight delay in channel opening. The resulting K+ current, in addition to limiting the peak of the action
potential, is also principally responsible for repolarization.

Once an action potential has been generated, it spreads as a wave over the sarcolemma. Skeletal muscle
sarcolemma is characterized by invaginations called transverse- or t-tubules that run perpendicular to
the surface of the cell deep into its body. By passing down the t-tubular membrane, the action potential
is carried to the structures responsible for transducing an electrical into a chemical signal that will
trigger activation of the contractile elements

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