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dc.contributor.author | Iha, Higor A. | en |
dc.contributor.author | Kunisawa, Naofumi | en |
dc.contributor.author | Shimizu, Saki | en |
dc.contributor.author | Tokudome, Kentaro | en |
dc.contributor.author | Mukai, Takahiro | en |
dc.contributor.author | Kinboshi, Masato | en |
dc.contributor.author | Ikeda, Akio | en |
dc.contributor.author | Ito, Hidefumi | en |
dc.contributor.author | Serikawa, Tadao | en |
dc.contributor.author | Ohno, Yukihiro | en |
dc.contributor.alternative | 池田, 昭夫 | ja |
dc.date.accessioned | 2017-08-03T05:05:03Z | - |
dc.date.available | 2017-08-03T05:05:03Z | - |
dc.date.issued | 2017-02-09 | - |
dc.identifier.issn | 1663-9812 | - |
dc.identifier.uri | http://hdl.handle.net/2433/226653 | - |
dc.description.abstract | Nicotinic acetylcholine (nACh) receptors are implicated in the pathogenesis of epileptic disorders; however, the mechanisms of nACh receptors in seizure generation remain unknown. Here, we performed behavioral and immunohistochemical studies in mice and rats to clarify the mechanisms underlying nicotine-induced seizures. Treatment of animals with nicotine (1–4 mg/kg, i.p.) produced motor excitement in a dose-dependent manner and elicited convulsive seizures at 3 and 4 mg/kg. The nicotine-induced seizures were abolished by a subtype non-selective nACh antagonist, mecamylamine (MEC). An α7 nACh antagonist, methyllycaconitine, also significantly inhibited nicotine-induced seizures whereas an α4β2 nACh antagonist, dihydro-β-erythroidine, affected only weakly. Topographical analysis of Fos protein expression, a biological marker of neural excitation, revealed that a convulsive dose (4 mg/kg) of nicotine region-specifically activated neurons in the piriform cortex, amygdala, medial habenula, paratenial thalamus, anterior hypothalamus and solitary nucleus among 48 brain regions examined, and this was also suppressed by MEC. In addition, electric lesioning of the amygdala, but not the piriform cortex, medial habenula and thalamus, specifically inhibited nicotine-induced seizures. Furthermore, microinjection of nicotine (100 and 300 μg/side) into the amygdala elicited convulsive seizures in a dose-related manner. The present results suggest that nicotine elicits convulsive seizures by activating amygdalar neurons mainly via α7 nACh receptors. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Frontiers Media SA | en |
dc.rights | © 2017 Iha, Kunisawa, Shimizu, Tokudome, Mukai, Kinboshi, Ikeda, Ito, Serikawa and Ohno. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. | en |
dc.subject | nicotine | en |
dc.subject | convulsive seizures | en |
dc.subject | nicotinic acetylcholine receptors | en |
dc.subject | amygdala | en |
dc.subject | Fos expression | en |
dc.title | Nicotine Elicits Convulsive Seizures by Activating Amygdalar Neurons | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | Frontiers in Pharmacology | en |
dc.identifier.volume | 8 | - |
dc.relation.doi | 10.3389/fphar.2017.00057 | - |
dc.textversion | publisher | - |
dc.identifier.artnum | 57 | - |
dc.identifier.pmid | 28232801 | - |
dcterms.accessRights | open access | - |
出現コレクション: | 学術雑誌掲載論文等 |
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