- Key People:
- Otto Loewi
- Sir Henry Dale
- Sir Bernard Katz
- Related Topics:
- botulism
- ester
- end-plate potential
- acetic acid
- Choline
- On the Web:
- National Center for Biotechnology Information - Acetylcholine (Oct. 16, 2026)
Acetylcholine
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What is acetylcholine?
Acetylcholine is a neurotransmitter and an ester of choline and acetic acid that operates in both the central and peripheral nervous systems. Within the autonomic nervous system, acetylcholine acts as a vasodilator, decreases heart rate and heart muscle contraction, and increases peristalsis in the stomach and the amplitude of digestive contractions. It is the primary transmitter of nerve impulses within the parasympathetic nervous system, which slows the heart rate, contracts smooth muscles, dilates blood vessels, and increases bodily secretions.
Acetylcholine is stored in vesicles at the ends of acetylcholine-producing neurons. When a nerve impulse arrives at the terminal of a motor neuron, acetylcholine is discharged into the neuromuscular junction. There, it bonds with a receptor molecule in the postsynaptic membrane of a muscle fiber. This bonding alters the membrane's permeability, which causes channels to open that allow positively charged sodium ions to flow into the muscle cell, resulting in muscle cell contraction if the frequency is high enough. The enzyme acetylcholinesterase rapidly destroys acetylcholine; thus, it is only briefly effective.
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Where is acetylcholine found in the human body?
Acetylcholine is a neurotransmitter in both the central and peripheral nervous systems. Within the autonomic nervous system, it impacts various bodily functions, such as vasodilation, decreased heart rate, increased peristalsis in the stomach, and stimulation of bodily secretions. It is also present at the neuromuscular junction, where motor nerves contact muscles. In the central nervous system, acetylcholine plays a role in memory and learning.
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What role does acetylcholine play in nerve communication?
Acetylcholine is a neurotransmitter that facilitates communication between nerve cells in the central and peripheral nervous systems. Released from vesicles at the ends of cholinergic neurons, acetylcholine transmits nerve impulses to muscle fibers at the neuromuscular junction. It binds to receptor molecules on the postsynaptic membrane of the muscle fiber, which increases the membrane's permeability and allows positively charged sodium ions to flow into the muscle cell. This process, if repeated at a high enough frequency, fully activates sodium channels, resulting in muscle cell contraction. Acetylcholine can either stimulate or block responses, leading to either excitatory or inhibitory effects. After acetylcholine binds to receptors, it is rapidly broken down by the enzyme acetylcholinesterase or diffuses out of the primary cleft, which prevents constant stimulation of acetylcholine receptors.
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How does acetylcholine affect muscle movement?
Acetylcholine is a neurotransmitter that affects muscle movement. When a nerve impulse reaches a motor neuron's terminal, acetylcholine is released into the neuromuscular junction.
Acetylcholine then binds to receptor molecules on the muscle fiber's end-plate membrane. This binding alters the membrane's permeability, opening channels for positively charged sodium ions to flow into the muscle cell, leading to muscle cell contraction if nerve impulses occur frequently enough. After release, acetylcholine is either broken down by the enzyme acetylcholinesterase or diffuses out of the synaptic cleft.
Myasthenia gravis, a disease of the neuromuscular junction, occurs when antibodies block acetylcholine molecules, preventing muscle fiber depolarization and contraction.
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What happens when there is not enough acetylcholine in the brain?
When there is an insufficient supply of acetylcholine in the brain, it can have significant implications, especially concerning memory and learning. Notably, an abnormally short supply of acetylcholine is associated with Alzheimer's disease, where reduced transmission of acetylcholine contributes to the disease's neuropathology.
In the context of Parkinson's disease, abnormal activity of acetylcholine, mediated by muscarinic acetylcholine receptors, can produce certain symptoms of parkinsonism.
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How do some medicines or toxins change the way acetylcholine works?
Several medicines and toxins can influence acetylcholine's function by blocking its release, mimicking its effects, or affecting its breakdown.
Botulinum toxin can block acetylcholine release, leading to muscle paralysis; however, it can also treat muscle spasms or reduce wrinkles. Pilocarpine mimics acetylcholine, and is used in eyedrops for glaucoma. Drugs such as atropine and scopolamine act as antagonists, suppressing the parasympathetic system and are used to dry secretions during anesthesia. Nicotine affects nicotinic receptors, while nicotinic-receptor antagonists can paralyze the autonomic nervous system and relax muscles during surgery. Additionally, acetylcholinesterase inhibitors like neostigmine and pyridostigmine prolong acetylcholine's action at the neuromuscular junction by inhibiting its breakdown.
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Acetylcholine, an ester of choline and acetic acid that serves as a neurotransmitter within the central and peripheral nervous systems. Acetylcholine is the chief neurotransmitter of the parasympathetic nervous system, the part of the autonomic nervous system (a branch of the peripheral nervous system) that contracts smooth muscles, dilates blood vessels, increases bodily secretions, and slows heart rate. Acetylcholine can stimulate a response or block a response and thus can have excitatory or inhibitory effects.
Storage and release
Acetylcholine is stored in vesicles at the ends of cholinergic (acetylcholine-producing) neurons. In the peripheral nervous system, when a nerve impulse arrives at the terminal of a motor neuron, acetylcholine is released into the neuromuscular junction. There it combines with a receptor molecule in the postsynaptic membrane (or end-plate membrane) of a muscle fiber. This bonding changes the permeability of the membrane, causing channels to open that allow positively charged sodium ions to flow into the muscle cell (see end-plate potential). If successive nerve impulses accumulate at a sufficiently high frequency, sodium channels along the end-plate membrane become fully activated, resulting in muscle cell contraction.
Actions and breakdown
Within the autonomic nervous system, acetylcholine behaves in a similar manner, being discharged from the terminal of one neuron and binding to receptors on the postsynaptic membrane of other cells. Its activities within the autonomic nervous system affect a number of body systems, including the cardiovascular system, where it acts as a vasodilator, decreases heart rate, and decreases heart muscle contraction. In the gastrointestinal system, it acts to increase peristalsis in the stomach and the amplitude of digestive contractions.
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In the urinary tract, acetylcholine activity decreases the capacity of the bladder and increases voluntary voiding pressure. It also affects the respiratory system and stimulates secretion by all glands that receive parasympathetic nerve impulses. In the central nervous system, acetylcholine appears to have multiple roles. It is known to play an important role in memory and learning and is in abnormally short supply in the brains of persons with Alzheimer disease.
Acetylcholine is rapidly destroyed by the enzyme acetylcholinesterase and thus is effective only briefly. Inhibitors of the enzyme (drugs known as anticholinesterases) prolong the lifetime of acetylcholine. Such agents include physostigmine and neostigmine, which are used to help augment muscle contraction in certain gastrointestinal conditions and in myasthenia gravis. Other acetylcholinesterases have been used in the treatment of Alzheimer disease.
Historical developments
Naturally occurring acetylcholine was first isolated in 1913 by English chemist Arthur James Ewins, at the urging of his colleague, physiologist Sir Henry Dale, who in 1914 described the chemical’s actions. The functional significance of acetylcholine was first established about 1921 by German physiologist Otto Loewi. Loewi demonstrated that acetylcholine is liberated when the vagus nerve is stimulated, causing slowing of the heartbeat. Subsequently he and others showed that the chemical is also liberated as a transmitter at the motor end plate of striated (voluntary) muscles of vertebrates. It later was identified as a transmitter at many neural synapses and in many invertebrate systems as well. Owing to Dale’s and Loewi’s work, acetylcholine became the first neurotransmitter to be identified and characterized. For their work, the two men shared the 1936 Nobel Prize for Physiology or Medicine.