While high threshold voltage‐dependent Ca²⁺ channels (VDCCs) of the N and P/Q families are crucial for evoked neurotransmitter release in the mammalian CNS, it remains unclear to what extent L‐type Ca²⁺ channels (LTCCs), which have been mainly considered as acting at postsynaptic sites, participate in the control of transmitter release. Here, we investigate the possible role of LTCCs in regulating GABA release by cerebellar molecular layer interneurons (MLIs) from rats. We found that BayK8644 (BayK) markedly increases mIPSC frequency in MLIs and Purkinje cells (PCs), suggesting that LTCCs are expressed presynaptically. Furthermore, we observed (1) a potentiation of evoked IPSCs in the presence of BayK, (2) an inhibition of evoked IPSCs in the presence of the LTCC‐specific inhibitor Compound 8 (Cp8), and (3) a strong reduction of mIPSC frequency by Cp8. BayK effects are reduced by dantrolene, suggesting that ryanodine receptors act in synergy with LTCCs. Finally, BayK enhances presynaptic AP‐evoked Ca²⁺ transients and increases the frequency of spontaneous axonal Ca²⁺ transients observed in TTX. Taken together, our data demonstrate that LTCCs are of primary importance in regulating GABA release by MLIs.

中文翻译：

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突触前L型电压依赖性钙通道在小脑分子层间神经元GABA释放中的生理参与。

N和P / Q家族的高阈值电压依赖性Ca ²⁺通道（VDCCs）对于哺乳动物CNS中诱发的神经递质释放至关重要，但目前尚不清楚L型Ca ²⁺在多大程度上通道（LTCC）主要被认为在突触后部位发挥作用，它们参与了对发射器释放的控制。在这里，我们研究了LTCCs在调节大鼠小脑分子层间神经元（MLIs）释放GABA中的作用。我们发现，BayK8644（BayK）显着增加了MLI和Purkinje细胞（PC）中的mIPSC频率，表明LTCCs是突触表达的。此外，我们观察到（1）在BayK存在下诱发的IPSCs增强，（2）在LTCC特异性抑制剂化合物8（Cp8）存在下对诱发的IPSCs的抑制，以及（3）mIPSC的强烈降低频率由Cp8决定。丹特罗降低了BayK的作用，表明ryanodine受体与LTCC协同作用。最后，BayK增强了突触前AP诱发的Ca ²⁺瞬变，并增加了在TTX中观察到的自发性轴突Ca ²⁺瞬变的频率。综上所述，我们的数据表明，LTCC在调节MLI释放GABA方面具有最重要的作用。