The possible additional role of the cystic fibrosis transmembrane regulator to motoneuron inhibition produced by glycine effects
作者： F.R. Morales , V. Silveira , A. Damián , R. Higgie , I. Pose
DOI: 10.1016/J.NEUROSCIENCE.2010.12.034
关键词:
摘要: In the present work we study contribution of chloride channel Cystic Fibrosis Transmembrane Regulator (CFTR) in postsynaptic inhibition somatic motoneurons during rapid-eye-movement (REM) sleep atonia. Postsynaptic is partially responsible for atonia that occurs REM sleep. Disfacilitation an additional mechanism lowers motoneuron excitability this state. mediated by release glycine from synaptic terminals on motoneurons, and GABA plays a complementary role to glycine. look brain stem neonatal rats at unrelated actions glycine, or disfacilitation which depends CFTR. We studied presence CFTR immunocytochemistry. electrophysiological experiments utilizing whole cell recordings vitro slices examined consequences blocking channel. The effects application glibenclamide (a blocker) again were studied. Glycine produced hyperpolarization, decrease input resistance, all characteristic changes neurotransmitter. Glibenclamide increase resistance motoneurons' repetitive discharge as well shift equilibrium potential ions indicated displacement reversal glycinergic actions. treated with glibenclamide, but effect was smaller when compared elicited control conditions. fact CFTR-chloride influences suggests may play
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