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首页> 美国卫生研究院文献>other >Electrophysiological and Immunohistochemical Evidence for an Increase in GABAergic Inputs and HCN Channels in Purkinje Cells that Survive Developmental Ethanol Exposure
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Electrophysiological and Immunohistochemical Evidence for an Increase in GABAergic Inputs and HCN Channels in Purkinje Cells that Survive Developmental Ethanol Exposure

机译：电生理和免疫组织化学证据以生存的乙醇暴露的浦肯野细胞中GABA能输入和HCN通道的增加。

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Ethanol exposures during the early postnatal period of the rat result in significant death of Purkinje cells (PCs). The magnitude, time-course, and lobular specificity of PC death have been well characterized in several studies. Additionally, significant reduction of climbing fiber inputs to the surviving PCs has been characterized. This study investigates whether further alterations to the cerebellar cortical circuits might occur as a result of developmental ethanol exposures. We first examined the firing pattern of PCs in acute slice preparations on postnatal days 13–15. While the basic firing frequency was not significantly altered, PCs from rat pups treated with ethanol on postnatal days 4–6 showed a significantly increased number of inhibitory postsynaptic potentials (IPSCs) and a larger Ih current. We conducted immunofluorescent studies to identify the probable cause of the increased IPSCs. We found a significant 21 % increase in the number of basket cells per PC and a near doubling of the volume of colocalized basket cell axonal membrane with PC. In addition, we identified a significant (~147 %) increase in HCN1 channel volume co-localized to PC volume. Therefore, the cerebellar cortex that survives targeted postnatal ethanol exposure is dramatically altered in development subsequent to PC death. The cerebellar cortical circuit that results is one that operates under a significant degree of increased resting inhibition. The alterations in the development of cerebellar circuitry following ethanol exposure, and the significant loss of PCs, could result in modifications of the structure and function of other brain regions that receive cerebellar inputs.
机译：大鼠出生后早期的乙醇暴露导致浦肯野细胞（PC）大量死亡。 PC死亡的程度，时程和小叶特异性已在多项研究中得到了很好的表征。另外，已经证明了大大减少了幸存PC的攀爬光纤输入。这项研究调查了发育性乙醇暴露是否会引起小脑皮质回路的进一步改变。我们首先检查了出生后13-15天急性切片制剂中PC的发射模式。虽然基本放电频率没有明显改变，但在出生后第4-6天用乙醇处理的幼鼠的PC表现出抑制性突触后电位（IPSC）数量显着增加和更大的Ih电流。我们进行了免疫荧光研究，以确定IPSCs增加的可能原因。我们发现每台PC的篮状细胞数量显着增加了21％，与PC共同定位的篮状细胞轴突膜的体积几乎增加了一倍。此外，我们发现与计算机体积共存的HCN1通道体积显着增加（〜147％）。因此，在PC死亡后，在有针对性的产后乙醇暴露中存活的小脑皮质在发育中发生了巨大变化。产生的小脑皮质回路是在明显增加的静息抑制下运作的。乙醇暴露后小脑回路发育的改变以及PC的大量丢失，可能会导致其他接受小脑输入的大脑区域的结构和功能发生改变。

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