Blocking the BK channel impedes acquisition of trace eyeblink conditioning
Blocking the BK channel impedes acquisition of trace eyeblink conditioning
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DOI：
10.1101/lm.1289809
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发表时间：
2009-02-01
影响因子：
2
通讯作者：
Disterhoft, John F.
中科院分区：
文献类型：
--
作者：
Matthews, Elizabeth A.;Disterhoft, John F.
大钾离子电导（BK）通道介导的动作电位后快速后超极化（AHPs）在眨眼条件反射后减少。用paxilline阻断BK通道增加体外诱发放电频率和体内自发锥体活动。为了研究BK通道阻断后兴奋性增加如何影响学习，大鼠在微量眨眼条件反射前接受双侧海马CA1区灌注帕希林、生理盐水或不灌注。药物组获得任务的速度较慢，但学习并没有完全受损。这表明，非特异性增加兴奋性和基线神经元放电率所造成的体内阻断BK通道可能会破坏正确的处理的输入，从而损害海马依赖性学习。
Big-K+ conductance (BK)-channel mediated fast afterhyperpolarizations (AHPs) following action potentials are reduced after eyeblink conditioning. Blocking BK channels with paxilline increases evoked firing frequency in vitro and spontaneous pyramidal activity in vivo. To examine how increased excitability after BK-channel blockade affects learning, rats received bilateral infusions of paxilline, saline, or nothing into hippocampal CA1 prior to trace eyeblink conditioning. The drug group was slower to acquire the task, but learning was not completely impaired. This suggests that nonspecific increases in excitability and baseline neuronal firing rates caused by in vivo blockade of the BK channel may disrupt correct processing of inputs, thereby impairing hippocampus-dependent learning.