ArticleProceedings of the National Academy of Sciences of the United States of America1995
Effects of serotonergic agents on neuronal nicotinic acetylcholine receptors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 62 citations in OpenAlex.
- Antagonistic effect of dopamine structural analogues on human GABAρ1 receptor.Scientific reports · 2017Article
- Structural basis of ligand recognition in 5-HT3 receptors.EMBO reports · 2013Article
- Dopamine and serotonin modulate human GABAρ1 receptors expressed in Xenopus laevis oocytes.ACS chemical neuroscience · 2012Article
- Quercetin Inhibits α3β4 Nicotinic Acetylcholine Receptor-Mediated Ion Currents Expressed in Xenopus Oocytes.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
- Mammalian nicotinic acetylcholine receptors: from structure to function.Physiological reviews · 2009Review
- Chronologically overlapping occurrences of nicotine-induced anxiety- and depression-related behavioral symptoms: effects of anxiolytic and cannabinoid drugs.BMC neuroscience · 2007Article
- Excitatory effect of ATP on rat area postrema neurons.Purinergic signalling · 2006Article
- Combined actions of zinc and fluoxetine on nicotinic acetylcholine receptors.The pharmacogenomics journal · 2004Article
- Antagonism of nicotinic acetylcholine receptors by inhibitors of monoamine uptake.Molecular psychiatry · 2001Article
- Modulation of nicotinic acetylcholine receptors by strychnine.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Neuronal nicotinic threonine-for-leucine 247 alpha7 mutant receptors show different gating kinetics when activated by acetylcholine or by the noncompetitive agonist 5-hydroxytryptamine.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Blockage of muscle and neuronal nicotinic acetylcholine receptors by fluoxetine (Prozac).Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Threonine-for-leucine mutation within domain M2 of the neuronal alpha(7) nicotinic receptor converts 5-hydroxytryptamine from antagonist to agonist.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Serotonergic modulation of the mudpuppy (Necturus maculatus) locomotor pattern in vitro.Experimental brain research · 1996Article
- Serotonergic modulation of muscle acetylcholine receptors of different subunit composition.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Inherited and experimentally induced changes in gating kinetics of muscle nicotinic acetylcholine receptor.Journal of molecular neuroscience : MNReview
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2 authors at 1 institution in 1 country.
Funding
Abstract
In Xenopus oocytes expressing neuronal nicotinic acetylcholine receptors (nAcChoRs), made up of alpha 2 and beta 4 subunits, acetylcholine (AcCho) elicited ionic membrane currents (AcCho currents) that were modulated by serotonergic agents. Both agonists and antagonists specific for various serotonin (5-hydroxytryptamine, 5HT) receptor subtypes interacted directly with alpha 2 beta 4 nAcChoRs: 5HT, (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin, methysergide, spiperone, and ketanserin reversibly reduced the amplitude of AcCho currents and accelerated their decay. The AcCho-current time course decayed with two exponential functions. In the presence of 5HT, the fast time constant of current decay (tau f) was not greatly modified, but the slow time constant (tau s) was reduced. With AcCho and 5HT both at 100 microM, tau s was reduced from 140 s to 85 s. The order of potency for inhibition of AcCho current amplitudes was (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin > methysergide > spiperone > ketanserin > 5HT. The inhibition was voltage-dependent but the magnitude of the voltage dependence for the different blockers did not correspond to their blocking potency: e.g., the block with spiperone was stronger than with 5HT, but it was less voltage-dependent. Our results suggest that serotonergic agents block neuronal nAcChoRs in a noncompetitive manner, similar to the block of muscle nAcChoR by curare and other substances. These results show that neuronal nAcChoR channels that have been activated by their specific neurotransmitter may be modulated by nonspecific neurotransmitters and their antagonists. These effects may help to better understand brain functions as well as the mode of action of the many serotonergic agents that are used in medical practice.
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