Whereas β2-adrenoceptor (β2-AR) has been reported to reduce GABAergic activity in the prefrontal cortex (PFC), the underlying cellular and molecular mechanisms have not been completely determined. Here, we showed that β2-AR agonist Clenbuterol (Clen) decreased GABAergic transmission onto PFC layer V/VI pyramidal neurons via a presynaptic mechanism without altering postsynaptic GABA receptors. Clen decreased the action potential firing rate but increased the burst afterhyperpolarization (AHP) amplitude in PFC interneurons. Application of L-type Ca2+ channel or charybdotoxin-sensitive Ca2+-activated K+ channel inhibitors blocked Clen-induced decreases in action potential firing rate, spontaneous inhibitory postsynaptic current (sIPSC) frequency and Clen-induced enhancement of AHP amplitude, suggesting that the effects of Clen involves L-type Ca2+ Channels and charybdotoxin-sensitive Ca2+-activated K+ channels. Our results provide a potential cellular mechanism by which Clen controls GABAergic neuronal activity in PFC.

中文翻译：

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L型Ca2 +通道和对毒素敏感的Ca2 +激活的K +通道是减少前额叶皮层中β2-肾上腺素能受体诱导的GABA能活性的必需条件。

尽管据报道β2-肾上腺素能受体（β2-AR）会降低前额叶皮层（PFC）中的GABA能活性，但尚未完全确定其潜在的细胞和分子机制。在这里，我们表明β2-AR激动剂克仑特罗（Clen）通过突触前机制减少了GABA能传递到PFC层V / VI锥体神经元上，而没有改变突触后GABA受体。Clen降低了动作电位的发射速率，但增加了PFC中神经元的超极化（AHP）振幅后的爆发。使用L型Ca2 +通道或对毒素敏感的Ca2 +激活的K +通道抑制剂可阻止Clen诱导的动作电位放电速率降低，自发抑制的突触后电流（sIPSC）频率和Clen诱导的AHP幅度增强，提示Clen的作用涉及L型Ca2 +通道和对charybdotoxin敏感的Ca2 +激活的K +通道。我们的结果提供了一种潜在的细胞机制，克伦通过该机制控制PFC中的GABA能神经元活性。