n.
A white crystalline derivative of choline, C7H17NO3, that is released at the ends of nerve fibers in the somatic and parasympathetic nervous systems and is involved in the transmission of nerve impulses in the body.
acetylcholine
Dictionary:
a·ce·tyl·cho·line (ə-sēt'l-kō'lēn')  |
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| Britannica Concise Encyclopedia: acetylcholine |
For more information on acetylcholine, visit Britannica.com.
| Sci-Tech Encyclopedia: Acetylcholine |
A naturally occurring quaternary ammonium cation ester, with the formula CH3(O)COC2H4N(CH)3+, that plays a prominent role in nervous system function. The great importance of acetylcholine derives from its role as a neurotransmitter for cholinergic neurons, which innervate many tissues, including smooth muscle and skeletal muscle, the heart, ganglia, and glands. The effect of stimulating a cholinergic nerve, for example, the contraction of skeletal muscle or the slowing of the heartbeat, results from the release of acetylcholine from the nerve endings.
Acetylcholine is synthesized at axon endings from acetyl coenzyme A and choline by the enzyme choline acetyltransferase, and is stored at each ending in hundreds of thousands of membrane-enclosed synaptic vesicles. When a nerve impulse reaches an axon ending, voltage-gated calcium channels in the axonal membrane open and calcium, which is extremely low inside the cell, enters the nerve ending. The increase in calcium-ion concentration causes hundreds of synaptic vesicles to fuse with the cell membrane and expel acetylcholine into the synaptic cleft (exocytosis). The acetylcholine released at a neuromuscular junction binds reversibly to acetylcholine receptors in the muscle end-plate membrane, a postsynaptic membrane that is separated from the nerve ending by a very short distance. The receptor is a cation channel which opens when two acetylcholine molecules are bound, allowing a sodium current to enter the muscle cell and depolarize the membrane. The resulting impulse indirectly causes the muscle to contract.
Acetylcholine must be rapidly removed from a synapse in order to restore it to its resting state. This is accomplished in part by diffusion but mainly by the enzyme acetylcholinesterase, which hydrolyzes acetylcholine.
Acetylcholinesterase is a very fast enzyme: one enzyme molecule can hydrolyze 10,000 molecules of acetylcholine in 1 s. Any substance that efficiently inhibits acetylcholinesterase will be extremely toxic.
| World of the Body: acetylcholine |
Acetylcholine is a neurotransmitter released from nerve endings (terminals) in both the peripheral and the central nervous systems. It is synthesized within the nerve terminal from choline, taken up from the tissue fluid into the nerve ending by a specialized transport mechanism. The enzyme necessary for this synthesis (choline acetyltransferase) is formed in the nerve cell body and passes down the axon to its end, carried in the axoplasmic flow, the slow movement of intracellular substance (cytoplasm). Acetylcholine is stored in the nerve terminal, sequestered in small vesicles awaiting release.
When a nerve action potential reaches and invades the nerve terminal, a shower of acetylcholine vesicles is released into the junction (synapse) between the nerve terminal and the ‘effector’ cell which the nerve activates. This may be another nerve cell or a muscle or gland cell. Thus electrical signals are converted to chemical signals, allowing messages to be passed between nerve cells or between nerve cells and non-nerve cells. This process is termed ‘chemical neurotransmission’ and was first demonstrated, for nerves to the heart, by the German pharmacologist Loewi in 1921. Chemical transmission involving acetylcholine is known as ‘cholinergic’.
Acetylcholine acts as a transmitter between motor nerves and the fibres of skeletal muscle at all neuromuscular junctions. At this type of synapse, the nerve terminal is closely apposed to the cell membrane of a muscle fibre at the so-called motor end plate. On release, acetylcholine acts almost instantly, to cause a sequence of chemical and physical events (starting with depolarization of the motor endplate) which cause contraction of the muscle fibre. This is exactly what is required for voluntary muscles in which a rapid response to a command is required. The action of acetylcholine is terminated rapidly, in around 10 milliseconds; an enzyme (cholinesterase) breaks the transmitter down into choline and an acetate ion. The choline is then available for re-uptake into the nerve terminal.
These same principles apply to cholinergic transmission at sites other than neuromuscular junctions, although the structure of the synapses differs. In the autonomic nervous system these include nerve-to-nerve synapses at the relay stations (ganglia) in both the sympathetic and the parasympathetic divisions, and the endings of parasympathetic nerve fibres on non-voluntary (smooth) muscle, the heart, and glandular cells; in response to activation of this nerve supply, smooth muscle contracts (notably in the gut), the frequency of heart beat is slowed, and glands secrete. Acetylcholine is also an important transmitter at many sites in the brain at nerve-to-nerve synapses.
To understand how acetylcholine brings about a variety of effects in different cells it is necessary to understand membrane receptors. In post-synaptic membranes (those of the cells on which the nerve fibres terminate) there are many different sorts of receptors and some are receptors for acetylcholine. These are protein molecules that react specifically with acetylcholine in a reversible fashion. It is the complex of receptor combined with acetylcholine which brings about a biophysical reaction, resulting in the response from the receptive cell. Two major types of acetylcholine receptors exist in the membranes of cells. The type in skeletal muscle is known as ‘nicotinic’; in glands, smooth muscle, and the heart they are ‘muscarinic’; and there are some of each type in the brain. These terms are used because nicotine mimics the action of acetylcholine at nicotinic receptors, whereas muscarine, an alkaloid from the mushroom Amanita muscaria, mimics the action of acetylcholine at the muscarinic receptors.
— Alan W. Cuthbert
See also autonomic nervous system; neurotransmitters.
| Food and Nutrition: acetylcholine |
The acetyl derivative of choline, produced at cholinergic nerve endings both in the brain, where it acts as a chemical transmitter, and at the junctions between nerves and muscles, where it stimulates muscle contraction.
| Dental Dictionary: acetylcholine |
(as′ətilkō′lēn, əsē′til)
n
n
1. an acetate ester of choline that serves as a neurohumoral agent in the transmission of an impulse in autonomic ganglia, parasympathetic postganglionic fibers, and somatic motor fibers. n 2. an ester of choline actively involved as a chemical mediator at the neuromuscular junction, at autonomic ganglia, and between parasympathetic nerve endings and visceral effectors.
| Sports Science and Medicine: acetylcholine |
A neurotransmitter synthesized from acetic acid and choline in the synaptic knobs of some nerve endings. It is released by all neurones that stimulate skeletal muscles, and neurones of the parasympathetic nervous system. ACh elicits action potentials in nerve and muscle cells by making them more permeable to sodium ions. Its effect is short-lived because it is destroyed by acetylcholinesterase. Acetylcholine was the first neurotransmitter to be identified.
Acetylcholine
| Columbia Encyclopedia: acetylcholine |
acetylcholine (əsēt'əlkō'lēn), a small organic molecule liberated at nerve endings as a neurotransmitter. It is particularly important in the stimulation of muscle tissue. The transmission of an impulse to the end of the nerve causes it to release neurotransmitter molecules onto the surface of the next cell, stimulating it. After such release, the acetylcholine is quickly broken into acetate and choline, which pass back to the first cell to be recycled into acetylcholine again. The poison curare acts by blocking the transmission of acetylcholine. Some nerve gases operate by preventing the breakdown of acetylcholine causing continual stimulation of the receptor cells, which leads to intense spasms of the muscles, including the heart. Acetylcholine is often abbreviated as Ach. See nervous system.
| World of the Mind: acetylcholine |
(Ach)
An important neurotransmitter, liberated at nerve endings, that transmits nervous impulses to muscles or to other nerve cells. Once released, acetylcholine has a very short existence as it is quickly broken down by the enzyme cholinesterase.
(Published 1987)
An important neurotransmitter, liberated at nerve endings, that transmits nervous impulses to muscles or to other nerve cells. Once released, acetylcholine has a very short existence as it is quickly broken down by the enzyme cholinesterase.
(Published 1987)
| Veterinary Dictionary: acetylcholine |
The acetic acid ester of choline, normally present in many parts of the body and having important physiological functions. It is a neurotransmitter at cholinergic synapses in the central, sympathetic and parasympathetic nervous systems. It is not used clinically but it is the classical cholinergic agonist. Abbreviated ACh.
- a. receptors — structures located at the endorgans, e.g. at the skeletal muscle fibers. The myofibers are stimulated to contract by the interaction of acetylcholine with acetylcholine receptors which are located on the motor end plate or postsynaptic sarcolemma. See also neuromuscular junction.
| Wikipedia: Acetylcholine |
| Acetylcholine | |
|---|---|
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|
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| IUPAC name |
2-Acetoxy-N,N,N-trimethylethanaminium
|
| Identifiers | |
| Abbreviations | ACh |
| CAS number | 51-84-3  |
| PubChem | 187 |
| DrugBank | EXPT00412 |
| ATC code | S01 |
| SMILES |
O=C(OCC[N+](C)(C)C)C
|
| InChI |
1/C7H16NO2/c1-7(9)10-6-5-8(2,3)4/h5-6H2,1-4H3/q+1
|
| InChI key | OIPILFWXSMYKGL-UHFFFAOYAY |
| ChemSpider ID | 182 |
| Properties | |
| Molecular formula | C7H16NO2 |
| Molar mass | 146.21 g mol−1 |
| Pharmacology | |
| Elimination half-life |
approximately 2 minutes |
| (what is this?) (verify) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) |
|
| Infobox references | |
The chemical compound acetylcholine (often abbreviated ACh) is a neurotransmitter in both the peripheral nervous system (PNS) and central nervous system (CNS) in many organisms including humans. Acetylcholine is one of many neurotransmitters in the autonomic nervous system (ANS) and the only neurotransmitter used in the motor division of the somatic nervous system. (Sensory neurons use glutamate and various peptides at their synapses.) Acetylcholine is also the principal neurotransmitter in all autonomic ganglia.
Contents |
History
Acetylcholine (ACh) was first identified in the year 1914 by Henry Hallett Dale for its actions on heart tissue. It was confirmed as a neurotransmitter by Otto Loewi who initially gave it the name vagusstoff because it was released from the vagus nerve. Both received the 1936 Nobel Prize in Physiology or Medicine for their work. Acetylcholine was also the first neurotransmitter to be identified.
Chemistry
Acetylcholine is an ester of acetic acid and choline with chemical formula CH3COOCH2CH2N+(CH3)3. This structure is reflected in the systematic name, 2-acetoxy-N,N,N-trimethylethanaminium.
Function
| Acetylcholine | |
|---|---|
| Abbreviation | ACh |
| Sources | many |
| Targets | many |
| Receptors | nicotinic; muscarinic |
| Agonists | nicotine, physostigmine |
| Antagonists | curare, atropine |
| Precursor | choline |
| Synthesizing enzyme | Choline acetyltransferase (ChAT) |
| Metabolizing enzyme | Acetylcholinesterase (AChE) |
Acetylcholine has functions both in the peripheral nervous system (PNS) and in the central nervous system (CNS) as a neuromodulator.
In the PNS, acetylcholine activates muscles, and is a major neurotransmitter in the autonomic nervous system.
In the CNS, acetylcholine and the associated neurons form a neurotransmitter system, the cholinergic system, which tends to cause excitatory actions.
In PNS
In the peripheral nervous system, acetylcholine activates muscles, and is a major neurotransmitter in the autonomic nervous system. When acetylcholine binds to acetylcholine receptors on skeletal muscle fibers, it opens ligand gated sodium channels in the cell membrane. Sodium ions then enter the muscle cell, stimulating muscle contraction. Acetylcholine, while inducing contraction of skeletal muscles, instead inhibits contraction in cardiac muscle fibers. This distinction is attributed to differences in receptor structure between skeletal and cardiac fibers.
In the autonomic nervous system, acetylcholine is released in the following sites:
- all pre- and post-ganglionic parasympathetic neurons
- all preganglionic sympathetic neurons
- preganglionic sympathetic fibers to suprarenal medulla, the modified sympathetic ganglion; on stimulation by acetylcholine, the suprarenal medulla releases epinephrine and norepinephrine
- some postganglionic sympathetic fibers
- sudomotor neurons to sweat glands.
In CNS
In the central nervous system, ACh has a variety of effects as a neuromodulator upon plasticity, arousal and reward. ACh has an important role in the enhancement of sensory perceptions when we wake up[1] and in sustaining attention.[2]
Damage to the cholinergic (acetylcholine-producing) system in the brain has been shown to be plausibly associated with the memory deficits associated with Alzheimer's disease[3].
Structure
Acetylcholine and the associated neurons form a neurotransmitter system, the cholinergic system from the brainstem and basal forebrain that projects axons to mainly areas of the brain. In the brainstem it originates from the Pedunculopontine nucleus and dorsolateral tegmental nuclei collectively known as the mesopontine tegmentum area or pontomesencephalotegmental complex.[4][5] In the basal forebrain, it originates from the basal optic nucleus of Meynert and medial septal nucleus:
- The pontomesencephalotegmental complex acts mainly on M1 receptors in the brainstem, deep cerebellar nuclei, pontine nuclei, locus ceruleus, raphe nucleus, lateral reticular nucleus and inferior olive[5] It also projects to the thalamus, tectum, basal ganglia and basal forebrain[4]
- Basal optic nucleus of Meynert acts mainly on M1 receptors in the neocortex.
- Medial septal nucleus acts mainly on M1 receptors in the hippocampus and neocortex.
In addition, ACh acts as an important "internal" transmitter in the striatum, which is part of the basal ganglia. It is released by a large set of interneurons with smooth dendrites, known as tonically active neurons or TANs.
Plasticity
ACh is involved with synaptic plasticity, specifically in learning and short-term memory.
Acetylcholine has been shown to enhance the amplitude of synaptic potentials following long-term potentiation in many regions, including the dentate gyrus, CA1, piriform cortex, and neocortex. This effect most likely occurs either through enhancing currents through NMDA receptors or indirectly by suppressing adaptation. The suppression of adaptation has been shown in brain slices of regions CA1, cingulate cortex, and piriform cortex, as well as in vivo in cat somatosensory and motor cortex by decreasing the conductance of voltage-dependent M currents and Ca2+-dependent K+ currents.
Excitability and inhibition
Acetylcholine also has other effects on neurons. One effect is to cause a slow depolarization[citation needed] by blocking a tonically-active K+ current, which increases neuronal excitability. An effect upon postsynaptic M4-muscarinic ACh receptors is to open inward-rectifier potassium ion channel (Kir) and cause inhibition.[6]
These two effects happen upon neurons in different neuron layers. For instance, the excitation effect acts on intrinsic and associational fibers in layer Ib of piriform cortex, but has no effect on afferent fibers in layer Ia. Similar laminar selectivity has been shown[citation needed] in dentate gyrus and region CA1 of the hippocampus.
In the cerebral cortex, ACh inhibits layer 4 medium spiny neurons, the main targets of thalamocortical inputs while exciting pyramidal cells in layers 2/3 and layer 5.[6] This filters out weak sensory inputs in layer 4 and amplifies inputs that reach the layers 2/3 and layer L5 excitatory microcircuits. As a result, these layer-specific effects of ACh might function to improve the signal noise ratio of cortical processing.[6]
Another theory[citation needed] interprets acetylcholine neuromodulation in the neocortex as modulating the estimate of expected uncertainty, acting counter to norepinephrine (NE) signals for unexpected uncertainty. Both modulations would then decrease synaptic transition strength, but ACh would then be needed to counter the effects of NE in learning, a signal understood to be 'noisy'.
Synthesis and degradation
Acetylcholine is synthesized in certain neurons by the enzyme choline acetyltransferase from the compounds choline and acetyl-CoA.
The enzyme acetylcholinesterase converts acetylcholine into the inactive metabolites choline and acetate. This enzyme is abundant in the synaptic cleft, and its role in rapidly clearing free acetylcholine from the synapse is essential for proper muscle function. Certain neurotoxins work by inhibiting acetylcholinesterase, thus leading to excess acetylcholine at the neuromuscular junction, thus causing paralysis of the muscles needed for breathing and stopping the beating of the heart.
Receptors
Main article: Acetylcholine receptor
There are two main classes of acetylcholine receptor (AChR), nicotinic acetylcholine receptors (nAChR) and muscarinic acetylcholine receptors (mAChR). They are named for the ligands used to activate the receptors.
Nicotinic
Nicotinic AChRs are ionotropic receptors permeable to sodium, potassium, and chloride ions. They are stimulated by nicotine and acetylcholine. They are of two main types, muscle type and neuronal type. The former can be selectively blocked by curare and the latter by hexamethonium. The main location of nicotinic AChRs is on muscle end plates, autonomic ganglia (both sympathetic and parasympathetic), and in the CNS.[7]
Myasthenia gravis
The disease myasthenia gravis, characterized by muscle weakness and fatigue, occurs when the body inappropriately produces antibodies against acetylcholine nicotinic receptors, and thus inhibits proper acetylcholine signal transmission. Over time, the motor end plate is destroyed. Drugs that competitively inhibit acetylcholinesterase (e.g., neostigmine, physostigmine, or primarily pyridostigmine) are effective in treating this disorder. They allow endogenously-released acetylcholine more time to interact with its respective receptor before being inactivated by acetylcholinesterase in the gap junction.
Muscarinic
Muscarinic receptors are metabotropic, and affect neurons over a longer time frame. They are stimulated by muscarine and acetylcholine, and blocked by atropine. Muscarinic receptors are found in both the central nervous system and the peripheral nervous system, in heart, lungs, upper GI tract and sweat glands. Extracts from the plant Deadly nightshade included this compound (atropine), and the blocking of the muscarinic AChRs increases pupil size as used for attractiveness in many European cultures in the past. Now, ACh is sometimes used during cataract surgery to produce rapid constriction of the pupil. It must be administered intraocularly because corneal cholinesterase metabolizes topically-administered ACh before it can diffuse into the eye. It is sold by the trade name Miochol-E (CIBA Vision). Similar drugs are used to induce mydriasis (dilation of the pupil), in cardiopulmonary resuscitation and many other situations.
Drugs acting on the acetylcholine system
Blocking, hindering or mimicking the action of acetylcholine has many uses in medicine. Drugs acting on the acetylcholine system are either agonists to the receptors, stimulating the system, or antagonists, inhibiting it.
ACh receptor agonists / antagonists
Acetylcholine receptor agonists can either have an effect directly on the receptors (agonist) or exert their effects indirectly (antagonist), e.g., by affecting the enzyme acetylcholinesterase, which degrades the receptor ligand.
Associated disorders
ACh Receptor Agonists are used to treat myasthenia gravis and Alzheimer's disease.
Alzheimer's disease
Since a shortage of acetylcholine in the brain has been associated with Alzheimer's disease, some drugs that inhibit acetylcholinesterase are used in the treatment of that disease.
Direct acting
- Acetylcholine
- Bethanechol
- Carbachol
- Cevimeline
- Pilocarpine
- Suberylcholine
- Nicotine (in small doses)
- Acetyl l-carnitine[8]
Cholinesterase inhibitors
Main article: Cholinesterase inhibitors
Most indirect acting ACh receptor agonists work by inhibiting the enzyme acetylcholinesterase. The resulting accumulation of acetylcholine causes continuous stimulation of the muscles, glands, and central nervous system.
They are examples of enzyme inhibitors, and increase the action of acetylcholine by delaying its degradation; some have been used as nerve agents (Sarin and VX nerve gas) or pesticides (organophosphates and the carbamates). In clinical use, they are administered to reverse the action of muscle relaxants, to treat myasthenia gravis, and to treat symptoms of Alzheimer's disease (rivastigmine, which increases cholinergic activity in the brain).
Reversible
The following substances reversibly inhibit the enzyme acetylcholinesterase (which breaks down acetylcholine), thereby increasing acetylcholine levels.
- Many medications in Alzheimer's disease
- Edrophonium (differs myasthenic and cholinergic crisis)
- Neostigmine (in myasthenia gravis)
- Physostigmine (in glaucoma and anticholinergic drug overdoses)
- Pyridostigmine (in myasthenia gravis
- Carbamate insecticides (e.g., Aldicarb)
- Huperzine A
Irreversible
Semi-permanently inhibit the enzyme acetylcholinesterase.
- Echothiophate
- Isofluorophate
- Organophosphate Insecticides (Malathion, Parathion, Azinphos methyl, Chlorpyrifos, among others)
- Organophosphate-containing nerve agents (e.g., Sarin, VX)
Victims of organophosphate-containing nerve agents commonly die of suffocation as they cannot relax their diaphragm.
Reactivation of acetylcholine esterase
ACh receptor antagonists
Antimuscarinic agents
Ganglionic blockers
- Mecamylamine
- Hexamethonium
- Nicotine (in high doses)
- Trimethaphan
Neuromuscular blockers
- Atracurium
- Cisatracurium
- Doxacurium
- Metocurine
- Mivacurium
- Pancuronium
- Rocuronium
- Succinylcholine
- Tubocurarine
- Vecuronium
- Hemicholine
Synthesis inhibitors
- Organic mercurial compounds have a high affinity for sulfhydryl groups, which causes dysfunction of the enzyme choline acetyltransferase. This inhibition may lead to acetylcholine deficiency, and can have consequences on motor function.
Release inhibitors
- Botulin acts by suppressing the release of acetylcholine; where the venom from a black widow spider (alpha-latrotoxin) has the reverse effect.
Other / uncategorized / unknown
References
- ^ Jones BE. (2005). From waking to sleeping: neuronal and chemical substrates. Trends Pharmacol Sci. Nov;26(11):578-86. PMID 16183137
- ^ Himmelheber AM, Sarter M, Bruno JP. (2000). Increases in cortical acetylcholine release during sustained attention performance in rats. Brain Res Cogn Brain Res. 9(3):313-25. PMID 10808142
- ^ http://www.biopsychiatry.com/alzheim.htm
- ^ a b Woolf NJ, Butcher LL. (1986). Cholinergic systems in the rat brain: III. Projections from the pontomesencephalic tegmentum to the thalamus, tectum, basal ganglia, and basal forebrain. Brain Res Bull. 16(5):603-37. PMID 3742247
- ^ a b Woolf NJ, Butcher LL. (1989). Cholinergic systems in the rat brain: IV. Descending projections of the pontomesencephalic tegmentum. Brain Res Bull. 23(6):519-40. PMID 2611694
- ^ a b c Eggermann E, Feldmeyer D. (2009). Cholinergic filtering in the recurrent excitatory microcircuit of cortical layer 4. Proc Natl Acad Sci U S A. 106:11753–11758 PMID 19564614 doi:10.1073/pnas.0810062106
- ^ Katzung, B.G. (2003). Basic and Clinical Pharmacology (9th ed.). McGraw-Hill Medical. ISBN 0-07-141092-9
- ^ Nałecz, Ka; Miecz, D; Berezowski, V; Cecchelli, R (Oct 2004). "Carnitine: transport and physiological functions in the brain". Molecular aspects of medicine 25 (5-6): 551–67. doi:. ISSN 0098-2997. PMID 15363641.
- Brenner, G. M. and Stevens, C. W. (2006). Pharmacology (2nd ed.). Philadelphia, PA: W.B. Saunders Company (Elsevier). ISBN 1-4160-2984-2
- Canadian Pharmacists Association (2000). Compendium of Pharmaceuticals and Specialties (25th ed.). Toronto, ON: Webcom. ISBN 0-919115-76-4
- Carlson, NR (2001). Physiology of Behavior (7th ed.). Needham Heights, MA: Allyn and Bacon. ISBN 0-205-30840-6
- Gershon, Michael D. (1998). The Second Brain. New York, NY: HarperCollins. ISBN 0-06-018252-0
- Siegal A & Sapru HN (2006) Essential Neuroscience. Revised 1st ed. Philadelphia: Lippincott, Williams & Wilkins. Ch. 15, pp. 255-267.
- Hasselmo, ME. "Neuromodulation and cortical function: Modeling the physiological basis of behavior." Behavioral Brain Research. 1995 Feb; 67(1):1-27. PMID 7748496
- Yu, AJ & Dayan, P. "Uncertainty, neuromodulation, and attention." Neuron. 2005 May 19; 46(4):681-92. PMID 15944135
External links
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| Translations: Acetylcholine |
Dansk (Danish)
n. - acetylklorin
Nederlands (Dutch)
acetylcholine (bepaalde neurotransmitter)
Français (French)
n. - acétylcholine
Deutsch (German)
n. - (chem.) Acetylcholin
Ελληνική (Greek)
n. - ακετυλχολίνη
Italiano (Italian)
acetilcolina
Português (Portuguese)
n. - acetilcolina (f) (Quím.)
Español (Spanish)
n. - compuesto que transmite impulsos de fibras nerviosas
Svenska (Swedish)
n. - acetylkolin
中文（简体）(Chinese (Simplified))
醋胆素
中文（繁體）(Chinese (Traditional))
n. - 醋膽素
עברית (Hebrew)
n. - אצטילכולין (תרופה)
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Mentioned in
- cholinergic
- Acetylcholinesterase (in medicine)
- esteratic site
- Anticolinergic drugs (in medicine)
- Anti-cholinergic drug (in medicine)
- Cholinergic drug (in medicine)
- esterophilic site
- cholinesterase
- junctional receptor (physiology)
- neurohumor (neuroscience)
- cholinolytic
- How does acetylcholine interact with muscle cells? (anatomy)
- anticholinesterase
- gallamine
