Characterization of Rebound Depolarization in Neurons of the Rat Medial Geniculate Body In Vitro  

作　　者：Xin-Xing Wang Yan Jin Hui Sun Chunlei Ma Jinsheng Zhang Ming Wang Lin Chen 

机构地区：[1]CAS Key Laboratory of Brain Function and Diseases, School of Life Sciences, University of Science and Technology of China [2]Auditory Research Laboratory, School of Life Sciences,University of Science and Technology of China [3]Department of Physiology, Binzhou Medical University [4]Department of Otolaryngology - Head and Neck Surgery,Wayne State University School of Medicine

出　　处：《Neuroscience Bulletin》2016年第1期16-26,共11页神经科学通报（英文版）

基　　金：supported by the National Basic Research Development Program of China(2011CB504506 and2012CB932502);the National Natural Science Foundation of China(81570915,81371503 and 31170965);the Open Fund from CAS Key Laboratory of Brain Function and Diseases,China(2012-3)

摘　　要：Rebound depolarization （RD） is a response to the offset from hyperpolarization of the neuronal mem- brane potential and is an important mechanism for the synaptic processing of inhibitory signals. In the present study, we characterized RD in neurons of the rat medial geniculate body （MGB）, a nucleus of the auditory thala- mus, using whole-cell patch-clamp and brain slices. RD was proportional in strength to the duration and magnitude of the hyperpolarization; was effectively blocked by Ni2＋ or Mibefradil; and was depressed when the resting membrane potential was hyperpolarized by blocking hyperpolarization-activated cyclic nucleotide-gated （HCN） channels with ZD7288 or by activating G-protein-gated inwardly-rectifying K＋ （GIRK） channels with baclofen. Our results demonstrated that RD in MGB neurons, which is carried by T-type Ca2＋ channels, is critically regulated by HCN channels and likely by GIRK channels.Rebound depolarization （RD） is a response to the offset from hyperpolarization of the neuronal mem- brane potential and is an important mechanism for the synaptic processing of inhibitory signals. In the present study, we characterized RD in neurons of the rat medial geniculate body （MGB）, a nucleus of the auditory thala- mus, using whole-cell patch-clamp and brain slices. RD was proportional in strength to the duration and magnitude of the hyperpolarization; was effectively blocked by Ni2＋ or Mibefradil; and was depressed when the resting membrane potential was hyperpolarized by blocking hyperpolarization-activated cyclic nucleotide-gated （HCN） channels with ZD7288 or by activating G-protein-gated inwardly-rectifying K＋ （GIRK） channels with baclofen. Our results demonstrated that RD in MGB neurons, which is carried by T-type Ca2＋ channels, is critically regulated by HCN channels and likely by GIRK channels.

关 键 词：Medial geniculate body Brain sliceRebound depolarizationchannel GIRK channel-type calcium channel - HCNResting membrane potential 

分 类 号：R338[医药卫生—人体生理学]