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Acetylcholine Nicotine. Nicotinic acetylcholine receptors, or nAChRs, are receptor polypeptides that respond to the neurotransmitter acetylcholine. Nicotinic receptors also respond to drugs such as the agonist nicotine. They are found in the central and peripheral nervous system, muscle, and many other tissues of many organisms.
Its physiological effects stem from the stimulation of nicotinic acetylcholine receptors, which are located throughout the central and peripheral nervous systems. [56] The α4β2 nicotinic receptor subtype is the main nicotinic receptor subtype. [57] Nicotine activates brain receptors which produce sedative as well as pleasurable effects. [58]
A nicotinic agonist is a drug that mimics the action of acetylcholine (ACh) at nicotinic acetylcholine receptors (nAChRs). The nAChR is named for its affinity for nicotine. Examples include nicotine (by definition), acetylcholine (the endogenous agonist of nAChRs), choline, epibatidine, lobeline, varenicline and cytisine. [1]
For instance, genetic markers for a specific type of nicotinic receptor (the α5-α3-β4 nicotine receptors) have been linked to increased risk for dependence. [ 19 ] [ 37 ] The most well-known hereditary influence related to nicotine dependence is a mutation at rs16969968 in the nicotinic acetylcholine receptor CHRNA5 , resulting in an amino ...
A 2015 review noted that stimulation of the α4β2 nicotinic receptor is responsible for certain improvements in attentional performance; [62] among the nicotinic receptor subtypes, nicotine has the highest binding affinity at the α4β2 receptor (k i =1 nM), which is also the biological target that mediates nicotine's addictive properties. [63]
Nicotine found in cigarette smoke binds to nicotinic acetylcholine receptors. [1] This binding leads to an increase in calcium levels which in turn can activate the cAMP response element-binding protein (CREB) transcription factor.
The alpha-3 beta-2 nicotinic receptor, also known as the α3β2 receptor, is a type of nicotinic acetylcholine receptor, consisting of α3 and β2 subunits. It occurs alongside the more common α3β4 nicotinic receptor in autonomic ganglia , and as an facilitatory presynaptic autoreceptor at the neuromuscular junction (NMJ).
Nicotinic receptors are the primary mediator of the effects of nicotine. In myasthenia gravis, the receptor at the neuromuscular junction is targeted by antibodies, leading to muscle weakness. Muscarinic acetylcholine receptors can be blocked by the drugs atropine and scopolamine.
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