Editing Acetylcholine (section)

===Neuromuscular junction===
[[File:The Muscle Contraction Process.png|thumb|400px|Muscles contract when they receive signals from motor neurons. The neuromuscular junction is the site of the signal exchange. The steps of this process in vertebrates occur as follows: (1) The action potential reaches the axon terminal. (2) Calcium ions flow into the axon terminal. (3) Acetylcholine is released into the [[synaptic cleft]]. (4) Acetylcholine binds to postsynaptic receptors. (5) This binding causes ion channels to open and allows sodium ions to flow into the muscle cell. (6) The flow of sodium ions across the membrane into the muscle cell generates an action potential which induces muscle contraction. Labels: A: Motor neuron axon B: Axon terminal C: Synaptic cleft D: Muscle cell E: Part of a Myofibril]]
{{main|Neuromuscular junction}}
Acetylcholine is the substance the nervous system uses to activate [[skeletal muscle]]s, a kind of striated muscle. These are the muscles used for all types of voluntary movement, in contrast to [[smooth muscle tissue]], which is involved in a range of involuntary activities such as movement of food through the gastrointestinal tract and constriction of blood vessels. Skeletal muscles are directly controlled by [[motor neuron]]s located in the [[spinal cord]] or, in a few cases, the [[brainstem]]. These motor neurons send their [[axons]] through [[motor nerve]]s, from which they emerge to connect to muscle fibers at a special type of [[chemical synapse|synapse]] called the [[neuromuscular junction]].

When a motor neuron generates an [[action potential]], it travels rapidly along the nerve until it reaches the neuromuscular junction, where it initiates an electrochemical process that causes acetylcholine to be released into the space between the presynaptic terminal and the muscle fiber. The acetylcholine molecules then bind to nicotinic ion-channel receptors on the muscle cell membrane, causing the ion channels to open. Sodium ions then flow into the muscle cell, initiating a sequence of steps that finally produce [[muscle contraction]].

Factors that decrease release of acetylcholine (and thereby affecting [[P-type calcium channel]]s):<ref name="Miller">{{cite book|veditors = Miller RD, Eriksson LI, Fleisher LA, Wiener-Kronish JP, Young WL|title=Miller's Anesthesia| edition = 7th |date=1 January 2009|publisher=Elsevier Health Sciences|isbn=978-0-443-06959-8|pages=343–47}}</ref>

# [[Antibiotics]] ([[clindamycin]], [[polymyxin]])
# Magnesium:&nbsp;antagonizes P-type calcium channels
# [[Hypocalcemia]]
# [[Anticonvulsant]]s
# [[Diuretic]]s ([[furosemide]])
# [[Eaton-Lambert syndrome]]: inhibits P-type calcium channels
# [[Myasthenia gravis]]
# [[Botulinum toxin]]: inhibits SNARE proteins

[[Calcium channel blocker]]s (nifedipine, diltiazem) do not affect P-channels. These drugs affect [[L-type calcium channel]]s.