The nerve terminal membrane or pre-synaptic membrane contains numerous vesicles that contain the neurotransmitter, in this case most commonly [[Neurotransmitters_-_Anatomy_%26_Physiology#Other_SMTs|acetylecholine (ACh)]]. Once released from the vesicles the ACh diffuses across the synaptic cleft and binds to receptors in the post-synaptic membrane. This binding causes ligand-gated ion channels to open which are permeable to both Na<sup>+</sup> and K<sup>+</sup>. The movement of potassium is relatively small due to there being only a small electrochemical gradient between the extra and intracellular environment. However there is a large influx of sodium into the cell and consequently this causes depolarisation in the nerve thus propagating the impulse. Within the neuromuscular junction the release of vesicles is facilitated by an influx of calcium into the pre-synaptic nerve just prior to exocytosis. The calcium enters the pre-synaptic nerve via voltage-gated Ca<sup>2+</sup> channels. There are several mechanisms that reduce the intracellular concentration of calcium once vesicles begin to be released to ensure that the neurotransmitter release is brief to prevent hyperpolarisation.
+
The nerve terminal membrane or pre-synaptic membrane contains numerous vesicles that contain the neurotransmitter, in this case most commonly [[Neurotransmitters_-_Anatomy_%26_Physiology#Other_SMTs|acetylecholine (ACh)]]. Once released from the vesicles the ACh diffuses across the synaptic cleft and binds to receptors in the muscle cell membrane. This binding causes ligand-gated ion channels to open which are permeable to both Na<sup>+</sup> and K<sup>+</sup>. The movement of potassium is relatively small due to there being only a small electrochemical gradient between the extra and intracellular environment. However there is a large influx of sodium into the cell and consequently this causes depolarisation in the muscle cell thus propagating the impulse into mechanical movement. Within the neuromuscular junction the release of vesicles is facilitated by an influx of calcium into the pre-synaptic nerve just prior to exocytosis. The calcium enters the pre-synaptic nerve via voltage-gated Ca<sup>2+</sup> channels. There are several mechanisms that reduce the intracellular concentration of calcium once vesicles begin to be released to ensure that the neurotransmitter release is brief to prevent hyperpolarisation.
<br />
<br />
<br />
<br />
−
The particular neurotransmitter ACh is heavily recycled within the synaptic cleft via endocytosis and over time the levels of endocytosis and exocytosis balance one-another resulting in a stable pre-synpatic membrane. Depolarisation within the post-synaptic nerve will last as long as the ACh is present in sufficient quantities within the synaptic cleft.
+
The particular neurotransmitter ACh is heavily recycled within the synaptic cleft via endocytosis and over time the levels of endocytosis and exocytosis balance one-another resulting in a stable pre-synpatic membrane. Depolarisation within the muscle cell will last as long as the ACh is present in sufficient quantities within the synaptic cleft. In reality this only lasts a few milliseconds as the synaptic cleft also contains the enzyme '''acetylcholinesterase''' which hydrolyses the ACh into acetate and choline. Due to this mechanisms, the calcium restriction and the endocytosis, only one action potential is generated within the muscle fibre.