Inward rectifier K+ channel and T-type Ca2+ channel contribute to enhancement of GABAergic transmission induced by beta(1)-adrenoceptor in the prefrontal cortex
Inward rectifier K+ channel and T-type Ca2+ channel contribute to enhancement of GABAergic transmission induced by beta(1)-adrenoceptor in the prefrontal cortex
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内向整流 K 通道和 T 型 Ca2 通道有助于增强前额皮质 β(1)-肾上腺素受体诱导的 GABA 能传递
DOI：
10.1016/j.expneurol.2016.11.007
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发表时间：
2017
影响因子：
5.3
通讯作者：
Tang Hua
中科院分区：
文献类型：
--
作者：
Luo Fei;Zheng Jian;Sun Xuan;Tang Hua
前额叶皮层（PFC）的功能对去甲肾上腺素（NE）敏感。内源性NE通过激活PFC内不同亚型的肾上腺素能受体（α1、α2、β 1或β2受体）影响突触传递。我们最近的研究表明，β1-肾上腺素能受体（β1-AR）激活调节PFC的多巴胺能传递，而β1-AR在GABA能传递中的作用尚不清楚。本实验观察了β1-AR激动剂多巴酚丁胺（Dobu）对幼年大鼠PFC锥体神经元GABA能传递的影响。Dobu增加了微型IPSC（mIPSC）的频率和振幅。多巴增强mIPSC频率需要通过T型电压门控性Ca ~（2+）通道的Ca ~（2+）内流。Dobu通过调节T-型Ca ~（2+）通道增加GABA释放概率和释放囊泡数量。Dobu使GABA能快峰（FS）中间神经元去极化，但对中间神经元动作电位（AP）放电频率无影响。多巴引起的FS中间神经元去极化需要内向整流钾通道（Kir）。我们的研究结果表明，Dobu通过抑制Kir增加GABA的释放，这进一步使FS中间神经元去极化，导致Ca 2+通过T型Ca 2+通道内流。
The functions of prefrontal cortex (PFC) are sensitive to norepinephrine (NE). Endogenously released NE influences synaptic transmission through activation of different subtypes of adrenergic receptors in PFC including α1, α2, β1or β2-adrenoceptor. Our recent study has revealed that β1-adrenoceptor (β1-AR) activation modulates glutamatergic transmission in the PFC, whereas the roles of β1-AR in GABAergic transmission are elusive. In the current study, we probed the effects of the β1-AR agonist dobutamine (Dobu) on GABAergic transmission onto pyramidal neurons in the PFC of juvenile rats. Dobu increased both the frequency and amplitude of miniature IPSCs (mIPSCs). Ca2 +influx through T-type voltage-gated Ca2 +channel was required for Dobu-enhanced mIPSC frequency. We also found that Dobu facilitated GABA release probability and the number of releasable vesicles through regulating T-type Ca2 +channel. Dobu depolarized GABAergic fast-spiking (FS) interneurons with no effects on the firing rate of action potentials (APs) of interneurons. Dobu-induced depolarization of FS interneurons required inward rectifier K+channel (Kir). Our results suggest that Dobu increase GABA release via inhibition of Kir, which further depolarizes FS interneurons resulting in Ca2 +influx via T-type Ca2 +channel.