Axonal GABAA receptors increase cerebellar granule cell excitability and synaptic activity.
Axonal GABAA receptors increase cerebellar granule cell excitability and synaptic activity.
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DOI：
10.1523/jneurosci.4506-10.2011
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发表时间：
2011-01-12
期刊：
影响因子：
--
通讯作者：
Jahr CE
中科院分区：
文献类型：
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作者：
Pugh JR;Jahr CE
我们在这里报告，小脑颗粒细胞轴突上的GABAA受体的激活调节下游递质的释放和上游的轴突和索马的兴奋性。轴突GABAA受体使轴突兴奋，增加轴突的兴奋性并引起轴突静脉曲张处的钙内流。GABA介导的阈下去极化在轴突电张力传播到索马促进顺向动作电位启动。当氯离子浓度不受干扰时，GABA离子电渗使平行纤维的兴奋性增加，表明GABAA受体介导的反应通常是去极化的。从分子层中间神经元释放GABA激活平行纤维GABAA受体，这反过来又增加了平行纤维和分子层中间神经元之间突触的释放概率。这些结果描述了一种正反馈机制，即从颗粒细胞到浦肯野细胞和分子层中间神经元的传输将在感觉刺激诱发的颗粒细胞锋电位爆发期间得到加强。
We report here that activation of GABAA receptors on cerebellar granule cell axons modulates both downstream transmitter release and upstream excitability of the axon and soma. Axonal GABAA receptors depolarize the axon, increasing excitability of the axon and causing calcium influx at axonal varicosities. GABA-mediated subthreshold depolarizations in the axon spread electrotonically to the soma promoting orthodromic action potential initiation. When chloride concentrations are unperturbed, GABA iontophoresis elicits spikes and increases excitability of parallel fibers, indicating that GABAA receptor-mediated responses are normally depolarizing. GABA release from molecular layer interneurons activates parallel fiber GABAA receptors, and this, in turn, increases release probability at synapses between parallel fibers and molecular layer interneurons. These results describe a positive feedback mechanism whereby transmission from granule cells to Purkinje cells and molecular layer interneurons will be strengthened during granule cell spike bursts evoked by sensory stimulation.