Bicarbonate contributes to GABAA receptor-mediated neuronal excitation in surgically resected human hypothalamic hamartomas.

Bicarbonate contributes to GABAA receptor-mediated neuronal excitation in surgically resected human hypothalamic hamartomas.
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DOI:
10.1016/j.eplepsyres.2008.09.008
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发表时间:
2009-01
期刊:
影响因子:
2.2
通讯作者:
Rho, Jong M.
Rho, Jong M.
中科院分区:
医学4区
文献类型:
--
作者:
Kim, Do-Young;Fenoglio, Kristina A.;Kerrigan, John F.;Rho, Jong M.

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使用细胞电生理学和钙成像技术研究碳酸氢盐 (HCO3-) 在 GABAA 受体介导的人下丘脑错构瘤 (HH) 神经元去极化中的作用。在 HCO3 缓冲液中,用蝇蕈醇 (30 μM) 激活 GABAA 受体可引起超过 70% 的大 (18-22 μM) HH 神经元的神经元兴奋。随后灌注不含 HCO3 的 HEPES 缓冲液,部分抑制了蝇蕈醇诱导的兴奋。此外,在无 HCO3 的条件下,53% 的大 HH 神经元表现出蝇蕈醇导致的细胞内钙积累减少。这些结果表明,HCO3-通过大HH神经元亚群上的GABAA受体流出可能有助于膜去极化和随后L型钙通道的激活。
The role of bicarbonate (HCO3-) in GABAA receptor-mediated depolarization of human hypothalamic hamartoma (HH) neurons was investigated using cellular electrophysiological and calcium imaging techniques. Activation of GABAA receptors with muscimol (30 μM) provoked neuronal excitation in over 70% of large (18-22 μM) HH neurons in HCO3- buffer. Subsequent perfusion of HCO3--free HEPES buffer produced partial suppression of muscimol-induced excitation. Additionally, 53% of large HH neurons under HCO3--free conditions exhibited reduced intracellular calcium accumulation by muscimol. These results suggest that HCO3- efflux through GABAA receptors on a subpopulation of large HH neurons may contribute to membrane depolarization and subsequent activation of L-type calcium channels.
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