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渗透压调节大鼠海马中间神经元而非CA1锥体神经元上的钾离子通道功能。

Osmolarity modulates K+ channel function on rat hippocampal interneurons but not CA1 pyramidal neurons.

作者信息

Baraban S C, Bellingham M C, Berger A J, Schwartzkroin P A

机构信息

Department of Neurological Surgery, University of Washington, Seattle 98195, USA.

出版信息

J Physiol. 1997 Feb 1;498 ( Pt 3)(Pt 3):679-89. doi: 10.1113/jphysiol.1997.sp021892.

DOI:10.1113/jphysiol.1997.sp021892
PMID:9051579
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1159184/
Abstract
  1. Whole-cell and single-channel recording methods were used in conjunction with infrared video microscopy techniques to examine the properties of voltage-activated potassium channels in hippocampal neurons during the application of hyposmolar solutions to hippocampal slices from rats. 2. Hyposmolar external solutions (osmolarity reduced by 10% to 267 mosmol l-1) produced a significant potentiation of voltage-activated K+ current on lacunosum/moleculare (L/M) hippocampal interneurons, but not on CA1 and subiculum pyramidal neurons. Hyperpolarization-activated (IH) and leak currents were not altered during the application of hyposmolar solutions in all cell types. 3. Mean channel open time and the probability of channel opening were dramatically increased under hyposmolar recording conditions for outside-out patches from L/M interneurons; no changes were observed for patches from CA1 pyramidal neurons. Mean current amplitude and the threshold for channel activation were not affected by hyposmotic challenge. 4. Hyposmolar external solutions produced a significant reduction in the firing frequency of L/M interneurons recorded in current-clamp mode. Hyposmolar solutions had no effect on resting membrane potential, action potential amplitude or duration, and spike after-hyperpolarization amplitude. 5. These results indicate that selective modulation of interneuron ion channel activity may be a critical mechanism by which osmolarity can regulate excitability in the central nervous system.
摘要
  1. 全细胞和单通道记录方法与红外视频显微镜技术结合使用,以研究在向大鼠海马切片施加低渗溶液期间海马神经元中电压激活钾通道的特性。2. 低渗外部溶液(渗透压降低10%至267 mosmol l-1)使海马腔隙/分子层(L/M)中间神经元上的电压激活K+电流显著增强,但对CA1和海马下托锥体神经元没有影响。在所有细胞类型中,低渗溶液施加期间超极化激活电流(IH)和漏电流未发生改变。3. 在低渗记录条件下,L/M中间神经元外向型膜片的平均通道开放时间和通道开放概率显著增加;CA1锥体神经元的膜片未观察到变化。平均电流幅度和通道激活阈值不受低渗刺激的影响。4. 低渗外部溶液使电流钳模式下记录的L/M中间神经元的放电频率显著降低。低渗溶液对静息膜电位、动作电位幅度或持续时间以及动作电位后超极化幅度没有影响。5. 这些结果表明,中间神经元离子通道活性的选择性调节可能是渗透压调节中枢神经系统兴奋性的关键机制。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1525/1159184/558552910d60/jphysiol00288-0119-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1525/1159184/558552910d60/jphysiol00288-0119-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1525/1159184/558552910d60/jphysiol00288-0119-a.jpg

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