MODULATION OF EXTRACELLULAR GAMMA-AMINOBUTYRIC-ACID IN THE VENTRAL PALLIDUM USING INVIVO MICRODIALYSIS
MODULATION OF EXTRACELLULAR GAMMA-AMINOBUTYRIC-ACID IN THE VENTRAL PALLIDUM USING INVIVO MICRODIALYSIS
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DOI：
10.1111/j.1471-4159.1992.tb10979.x
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发表时间：
1992-06-01
影响因子：
4.7
通讯作者：
KALIVAS, PW
中科院分区：
文献类型：
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作者：
BOURDELAIS, AJ;KALIVAS, PW
颅内微透析用于研究腹侧苍白球中细胞外γ-氨基丁酸（GABA）的起源。测定了膜去极化剂、离子通道阻滞剂和受体激动剂引起的基础 GABA 水平的变化。在不含 Ca2+ 的灌注缓冲液中，高 Mg2+ 对 Ca2+ 通量的拮抗作用使 GABA 水平降低了 30%。通过添加河豚毒素抑制电压依赖性 Na+ 通道也显着降低基础细胞外 GABA 浓度高达 45%，而用维拉帕米阻断 Ca2+ 和 Na+ 通道则使细胞外 GABA 浓度降低多达 30%。添加 GABA(A) 激动剂蝇蕈醇或 GABA(B) 激动剂巴氯芬可使细胞外 GABA 减少 40%。高 K+ 和添加藜芦碱以增加 Na+ 流入可刺激 GABA 释放。高 K+ 诱导的释放主要是 Ca2+ 依赖性的，而藜芦定的作用在细胞外 Ca2+ 不存在的情况下增强。高钾离子和藜芦定诱导的细胞外 GABA 升高均被巴氯芬抑制，而只有藜芦定诱导的释放被蝇蕈醇拮抗。这些结果表明，腹侧苍白球中至少 50% 的基础细胞外 GABA 源自 Ca2+ 或 Na+ 依赖性机制。他们还表明，可以在体内显示通过逆转摄取载体而依赖 Na+ 的 GABA 释放。
Intracranial microdialysis was used to investigate the origin of extracellular gamma-aminobutyric acid (GABA) in the ventral pallidum. Changes in basal GABA levels in response to membrane depolarizers, ion-channel blockers, and receptor agonists were determined. Antagonism of Ca2+ fluxes with high Mg2+ in a Ca2+-free perfusion buffer decreased GABA levels by up to 30%. Inhibition of voltage-dependent Na+ channels by the addition of tetrodotoxin also significantly decreased basal extracellular GABA concentrations by up to 45%, and blockade of Ca2+ and Na+ channels with verapamil reduced extracellular GABA by as much as 30%. The addition of either the GABA(A) agonist, muscimol, or the GABA(B) agonist, baclofen, produced a 40% reduction in extracellular GABA. GABA release was stimulated by high K+ and the addition of veratridine to increase Na+ influx. High K+-induced release was predominately Ca2+-dependent, whereas the effect of veratridine was potentiated in the absence of extracellular Ca2+. Both high K+- and veratridine-induced elevations in extracellular GABA were inhibited by baclofen, whereas only veratridine-induced release was antagonized by muscimol. These results demonstrate that at least 50% of basal extracellular GABA in the ventral pallidum is derived from Ca2+- or Na+-dependent mechanisms. They also suggest that Na+-dependent release of GABA via reversal of the uptake carrier can be shown in vivo.