{"title":"烟碱乙酰胆碱受体在耳蜗毛细胞传出抑制中的作用。","authors":"Gi Jung Im","doi":"10.7874/kja.2012.16.3.108","DOIUrl":null,"url":null,"abstract":"<p><p>The α9α10 nicotinic acetylcholine receptors (nAChRs) mediates efferent inhibition of hair cell function within the auditory sensory organ. Gating of the nAChRs leads to activation of calcium-dependent potassium channels to hyperpolarize the hair cell. In efferent system, main calcium providers to SK channel are nAChR and synaptic cistern, which contribution to efferent inhibition is different between avian and mammalian species. Calcium permeation is more effective in nAChRs of mammalian cochlea than avian cochlea, and mammalian calcium permeability of nAChRs is about 3 times more than avian hair cell. Thus, mammalian nAChRs is a main component of efferent inhibition in cochlear hair cell system. </p>","PeriodicalId":90252,"journal":{"name":"Korean journal of audiology","volume":"16 3","pages":"108-13"},"PeriodicalIF":0.0000,"publicationDate":"2012-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/31/fe/kja-16-108.PMC3936662.pdf","citationCount":"4","resultStr":"{\"title\":\"Role of nicotinic acetylcholine receptor on efferent inhibition in cochlear hair cell.\",\"authors\":\"Gi Jung Im\",\"doi\":\"10.7874/kja.2012.16.3.108\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The α9α10 nicotinic acetylcholine receptors (nAChRs) mediates efferent inhibition of hair cell function within the auditory sensory organ. Gating of the nAChRs leads to activation of calcium-dependent potassium channels to hyperpolarize the hair cell. In efferent system, main calcium providers to SK channel are nAChR and synaptic cistern, which contribution to efferent inhibition is different between avian and mammalian species. Calcium permeation is more effective in nAChRs of mammalian cochlea than avian cochlea, and mammalian calcium permeability of nAChRs is about 3 times more than avian hair cell. Thus, mammalian nAChRs is a main component of efferent inhibition in cochlear hair cell system. </p>\",\"PeriodicalId\":90252,\"journal\":{\"name\":\"Korean journal of audiology\",\"volume\":\"16 3\",\"pages\":\"108-13\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2012-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/31/fe/kja-16-108.PMC3936662.pdf\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Korean journal of audiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.7874/kja.2012.16.3.108\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2012/12/18 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Korean journal of audiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.7874/kja.2012.16.3.108","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2012/12/18 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Role of nicotinic acetylcholine receptor on efferent inhibition in cochlear hair cell.
The α9α10 nicotinic acetylcholine receptors (nAChRs) mediates efferent inhibition of hair cell function within the auditory sensory organ. Gating of the nAChRs leads to activation of calcium-dependent potassium channels to hyperpolarize the hair cell. In efferent system, main calcium providers to SK channel are nAChR and synaptic cistern, which contribution to efferent inhibition is different between avian and mammalian species. Calcium permeation is more effective in nAChRs of mammalian cochlea than avian cochlea, and mammalian calcium permeability of nAChRs is about 3 times more than avian hair cell. Thus, mammalian nAChRs is a main component of efferent inhibition in cochlear hair cell system.