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IH current generates the afterhyperpolarisation following activation of subthreshold cortical synaptic inputs to striatal cholinergic interneurons

机译：IH电流在纹状胆碱能中间神经元的阈下皮层突触输入激活后产生超极化后。

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摘要

Pauses in the tonic firing of striatal cholinergic interneurons emerge during reward-related learning and are triggered by neutral cues which develop behavioural significance. In a previous in vivo study we have proposed that these pauses in firing may be due to intrinsically generated afterhyperpolarisations (AHPs) evoked by excitatory synaptic inputs, including those below the threshold for action potential firing. The aim of this study was to investigate the mechanism of the AHPs using a brain slice preparation which preserved both cerebral hemispheres. Augmenting cortically evoked postsynaptic potentials (PSPs) by repetitive stimulation of cortical afferents evoked AHPs that were unaffected by blocking either GABAA receptors with bicuculline, or GABAB receptors with saclofen or CGP55845. Apamin (a blocker of small conductance Ca2+-activated K+ channels) had minimal effects, while chelation of intracellular Ca2+ with BAPTA reduced the AHP by about 30%. In contrast, blocking hyperpolarisation and cyclic nucleotide activated (HCN) cation current (IH) with ZD7288 or Cs+ diminished the size of the AHPs by 60% and reduced the proportion of episodes that contained this hyperpolarisation. The reversal potential (−20 mV) and voltage dependence of the AHPs were consistent with the hypothesis that a transient deactivation of IH caused most of the AHP at hyperpolarised potentials, while the slow AHP-type Ca2+-activated K+ channels increasingly contributed at more depolarised membrane potentials. Subthreshold somatic current injections yielded similar AHPs with a median duration of ∼700 ms that were not affected by firing of a single action potential. These results indicate that transient deactivation of HCN channels evokes pauses in tonic firing of cholinergic interneurons, an event likely to be elicited by augmentation of afferent synaptic inputs during learning.
机译：在奖励相关的学习过程中，纹状体胆碱能中间神经元补药放电出现暂停​​，并由中立提示触发，从而产生行为学意义。在先前的一项体内研究中，我们已经提出，射击中的这些暂停可能是由于兴奋性突触输入（包括低于动作电位射击阈值的那些）引起的内在产生的超极化（AHP）。这项研究的目的是研究使用保留两个大脑半球的脑片制剂制备AHP的机制。通过反复刺激皮层传入的诱发AHP增强皮质诱发的突触后电位（PSPs），而AHP则不会受到双小分子阻断GABAA受体或沙氯芬或CGP55845阻断GABAB受体的影响。 Apamin（小电导Ca2 +激活的K +通道的阻滞剂）作用最小，而细胞内Ca2 +与BAPTA的螯合使AHP降低了约30％。相反，用ZD7288或Cs +阻止超极化和环状核苷酸激活（HCN）阳离子电流（IH）可使AHP的大小减小60％，并减少了包含这种超极化的发作的比例。 AHP的反向电势（−20 mV）和电压依赖性与以下假设相符：IH的瞬时失活导致大多数AHP处于超极化电势，而缓慢的AHP型Ca2 +激活的K +通道越来越多地导致更多的去极化膜电位。亚阈值的体电流注入产生相似的AHP，中位持续时间约为700毫秒，不受单个动作电位触发的影响。这些结果表明，HCN通道的瞬时失活会引起胆碱能中间神经元补药性放电的暂停，这一事件很可能是由于学习过程中传入突触输入的增加而引起的。

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