RETROGRADE SIGNALING AT GABA(A)-RECEPTOR SYNAPSES IN THE MAMMALIAN CNS
RETROGRADE SIGNALING AT GABA(A)-RECEPTOR SYNAPSES IN THE MAMMALIAN CNS
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DOI：
10.1016/0166-2236(95)93923-l
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发表时间：
1995-08-01
影响因子：
15.9
通讯作者：
PITLER, TA
中科院分区：
文献类型：
--
作者：
ALGER, BE;PITLER, TA
最近的研究强调了从靶细胞以逆行方向传播到与靶细胞突触并影响其输出的信号的作用。虽然大多数研究的重点是兴奋性突触的长期变化，但海马和小脑中GABA（A）受体介导的抑制作用的短暂减少涉及逆行传递的证据已经开始积累。突触后主细胞的短暂去极化导致细胞内Ca 2+浓度增加，GABA（A）受体介导的反应减少1-2分钟。未检测到突触后GABA（A）受体反应性的伴随减少。相反，从神经元-中间神经元末梢释放的GABA似乎减少。这种“去极化诱导的抑制抑制”的特性可能适合于独特的生理作用。
Recent studies have emphasized the role of signals that travel from a target cell, in a retrograde direction, to cells that synapse on the target and influence their output. While the focus of most research on this topic has been on long-lasting alterations at excitatory synapses, evidence that implicates retrograde transmission in the transient reduction of GABA(A)-receptor-mediated inhibition in hippocampus and cerebellum has begun to accumulate. Brief depolarizations of the postsynaptic principal cells lead to increases in the intracellular concentration of Ca2+, and a reduction in GABA(A)-receptor-mediated responses for 1-2 min. No concomitant reduction in postsynaptic GABA(A)-receptor responsiveness has been detected. Rather, release of GABA from inhibitory-interneuron terminals appears to be reduced. The properties of this 'depolarization-induced suppression of inhibition' might be appropriate for unique physiological roles.