Please use this identifier to cite or link to this item: https://ah.lib.nccu.edu.tw/handle/140.119/77943
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dc.contributor心智、大腦與學習研究中心
dc.creatorClarkson, Andrew N.;Talbot, Caroline L.;Wang, Pei-Yu;MacLaughlin, David T.;Donahoe, Patricia K.;McLennan, Ian S.
dc.date2011-10
dc.date.accessioned2015-08-24T03:25:27Z-
dc.date.available2015-08-24T03:25:27Z-
dc.date.issued2015-08-24T03:25:27Z-
dc.identifier.urihttp://nccur.lib.nccu.edu.tw/handle/140.119/77943-
dc.description.abstractMüllerian Inhibiting Substance (MIS, Anti-Müllerian hormone) is a gonadal hormone that contributes to the subtle sex-biases in the nervous system. Mature neurons of both sexes also produce MIS, suggesting that MIS may be a paracrine regulator of adult neural networks. We report here that murine hypoglossal motor neurons produce MIS and its receptors, MISRII and bone morphogenetic protein receptor 1A (BMPR1A, ALK3), but differentially transport them, with only MIS being detectable in axons. The production of MIS and its receptors were rapidly down regulated after axonal damage, which is a characteristic of genes involved in mature neuronal function. MIS is a survival factor for embryonic spinal motor neurons, but the rate of cell loss after hypoglossal nerve avulsion was normal in Mis−/− mice and was not attenuated by intraventricular administration of MIS. These observations suggest that MIS may be involved in anterograde rather than autocrine or retrograde regulation of neurons.
dc.format.extent424536 bytes-
dc.format.mimetypeapplication/pdf-
dc.relationExperimental Neurology, 231(2), 304-308
dc.subjectAxonal transport;Avulsion;MISRII;ALK3
dc.titleMüllerian inhibiting substance is anterogradely transported and does not attenuate avulsion-induced death of hypoglossal motor neurons
dc.typearticleen
dc.identifier.doi10.1016/j.expneurol.2010.12.019
dc.doi.urihttp://dx.doi.org/10.1016/j.expneurol.2010.12.019
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextopen-
item.openairetypearticle-
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