Answer
Resting membrane potential.
When a myofiber is unstimulated there is naturally a voltage difference between the outside and inside of the sarcolemma ( or cell). This is a negative difference of about -90mV.
A myofiber is stimulated when acetylcholine molecules bind to acetylcholine receptors (ACHRs) in the sarcolemma of the postsynaptic motor end plate . The binding of ACH causes ligand-gated ion channels to open in the sarcolemma. First, Na+ ions diffuse from the ECF down their electrochemical gradient through the Na+ channels into the cell. This has the immediate effect of depolarizing the myocyte. As small amounts of ACH are released from the synaptic vesicles into the synaptic cleft and bind with ACHRs, depolarizations are generated: but these are, at first, low peak voltage depolarizations referred to as miniature end plate potentials (MEPPs) which may summate to form an end plate potential (EPP). If the EPP reaches threshold voltage it is able to trigger an action potential (AP).
Work Step by Step
When the action potential is triggered, voltage-gated Na + channels open, and Na+ ions diffuse theough the sarcolemma into the cytosol. The accumulation of Na+ ions result in depolarization of the cell and may at peak raise the membrane potential to about +30 mV.
Na+ channels are open only briefly; soon they close and the slower K+ channels open. As the K+ ions pour out down their concentration gradient the cell recovers its polarity and may hyperpolarize (+100 mV). But soon the Na+/K+ ATPase pump gets to work, kicking out excess Na+ ions. This action restores the resting membrane potential. Though Na+ ions leak back in slowly, and K + ions leak out slowly The N+/K+ ATPase pump kicks out three Na+ ions for every two K+ ions that it brings in, so the RMP is maintained in the unstimulated muscle cell.
