In the eyeblink conditioning paradigm, cerebellar Purkinje cells learn to respond to the conditional stimulus with an adaptively timed pause in its spontaneous firing. Evidence suggests that the pause is elicited by glutamate released from parallel fibers and acting on metabotropic receptors (mGluR7) which initiates a delayed-onset suppression of firing. We suggested that G protein activation of hyperpolarizing K_ir3 channels (or ‘GIRK’, G protein-coupled inwardly-rectifying K⁺ channels) could be part of such a mechanism. Application of the K_ir3 antagonist Tertiapin-LQ locally in the superficial layers of the cerebellar cortex in decerebrate ferrets suppressed normal performance of Purkinje cell pause responses to the conditional stimulus. Importantly, there was no detectable effect on spontaneous firing. These findings suggest that intact functioning of K_ir3 channels in the cerebellar cortex is required for normal conditioned Purkinje cell responses.

在眨眼条件反射范式中，小脑浦肯野细胞学会对条件刺激做出反应，并在其自发放电中进行适时的暂停。有证据表明，暂停是由平行纤维释放的谷氨酸盐引起的，并作用于代谢型受体 (mGluR7)，从而启动延迟发作的射击抑制。我们建议 G 蛋白激活超极化 K _ir 3 通道（或“GIRK”，G 蛋白偶联的内向整流 K ⁺通道）可能是这种机制的一部分。K _{ir 的}应用3 拮抗剂 Tertiapine-LQ 在去脑雪貂的小脑皮层浅层局部抑制了浦肯野细胞对条件刺激的暂停反应的正常表现。重要的是，对自发射击没有可检测到的影响。这些发现表明小脑皮层中 K _ir 3 通道的完整功能是正常条件浦肯野细胞反应所必需的。