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Acetylcholine (ACh) is an excitatory, small-molecule neurotransmitter involved in synaptic transmission at neuromuscular junctions controlling the vagus nerve and cardiac muscle fibers, as well as in the skeletal and visceral motor systems and various sites within the central nervous system. [3]
Similarly, acetylcholine released from parasympathetic neurons may interact with M 2 and M 4 receptors to inhibit further release of acetylcholine. An atypical example is given by the β-adrenergic autoreceptor in the sympathetic peripheral nervous system, which acts to increase transmitter release. [1]
Acetylcholine receptor; Acetylcholinesterase inhibitor; Ann Silver; Atrax yorkmainorum; Choline acetyltransferase; Cholinergic; Cholinergic blocking drug; Cholinesterase; Cholinesterase inhibitor; History of psychiatry; Muscarine; Muscarinic acetylcholine receptor; Neuronal acetylcholine receptor subunit alpha-5; Nicotinic acetylcholine ...
Acetylcholine is a choline molecule that has been acetylated at the oxygen atom. Because of the charged ammonium group, acetylcholine does not penetrate lipid membranes. . Because of this, when the molecule is introduced externally, it remains in the extracellular space and at present it is considered that the molecule does not pass through the blood–brain
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The parasympathetic nervous system, which uses acetylcholine almost exclusively to send its messages, is said to be almost entirely cholinergic. Neuromuscular junctions, preganglionic neurons of the sympathetic nervous system , the basal forebrain , and brain stem complexes are also cholinergic, as are the receptor for the merocrine sweat glands.
Whittaker's work demonstrating acetylcholine in vesicle fractions from guinea-pig brain was first published in abstract form in 1960 and then in more detail in 1963 and 1964, [36] [37] and the paper of the de Robertis group demonstrating an enrichment of bound acetylcholine in synaptic vesicle fractions from rat brain appeared in 1963. [38]
Acetylcholine is known to promote wakefulness in the basal forebrain. Stimulating the basal forebrain gives rise to acetylcholine release, which induces wakefulness and REM sleep, whereas inhibition of acetylcholine release in the basal forebrain by adenosine causes slow wave sleep.