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 stu...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.展开更多
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)
文摘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.
