首页> 外文期刊>Journal of the autonomic nervous system >Gamma-aminobutyric acid-induced responses in acutely dissociated neurons from the rat sacral dorsal commissural nucleus.
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Gamma-aminobutyric acid-induced responses in acutely dissociated neurons from the rat sacral dorsal commissural nucleus.

机译:γ-氨基丁酸诱导的大鼠from背连合神经元急性解离神经元的反应。

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The electrophysiological and pharmacological properties of GABA-activated Cl- currents (IGABA) were investigated in enzymatically dissociated rat sacral dorsal commissural nucleus (SDCN) neurons using the nystatin perforated patch recording configuration under voltage-clamp conditions. Exogenous application of GABA to SDCN neurons induced Cl- currents which increased in a concentration-dependent manner. Bicuculline (BIC) and strychnine (STR) antagonized the IGABA in a concentration-dependent manner. Zn2+ suppressed the IGABA with an IC50 of 2.8 X 10(-5) M. Muscimol mimicked the IGABA, while baclofen evoked no response. Pentobarbital (PB) and 5beta-pregnan-3alpha-ol-20-one (pregnanolone, PGN) also induced GABAA-mimic Cl- currents. Diazepam (DZP), PB and PGN all enhanced the IGABA by increasing the apparent affinity of the GABAA receptors to GABA. Moreover, spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) were observed in mechanically dissociated SDCN neurons attached with synaptic boutons, so called 'synaptic bouton preparation'. These results indicate that SDCN neurons express GABAA receptors with relatively low sensitivity to Zn2+ inhibition, and that GABA may have a functional role as an inhibitory transmitter in the SDCN regulating nociceptive, analgesic, and autonomic functions.
机译:在电压钳制条件下,使用制霉菌素穿孔的斑块记录配置,研究了酶解离的大鼠背连合神经核(SDCN)神经元中GABA激活的Cl电流(IGABA)的电生理和药理特性。 GABA在SDCN神经元上的外源应用导致Cl电流以浓度依赖的方式增加。 Bicuculline(BIC)和士的宁(STR)以浓度依赖性方式拮抗IGABA。 Zn2 +抑制IGABA,IC50为2.8 X 10(-5)M。Muscimol模仿IGABA,而巴氯芬则未引起反应。戊巴比妥(PB)和5beta-pregnan-3alpha-ol-20-one(孕烯醇酮,PGN)也诱导了GABAA模拟的Cl电流。地西p(DZP),PB和PGN都通过增加GABAA受体对GABA的表观亲和力来增强IGABA。此外,在与突触钮扣相连的机械分离的SDCN神经元中观察到自发的GABA能抑制突触后电流(IPSC),即所谓的“突触钮扣制备”。这些结果表明,SDCN神经元表达对Zn2 +抑制的敏感性相对较低的GABAA受体,并且GABA可能在SDCN中起抑制伤害性递质的作用,调节伤害性,镇痛性和自主神经功能。

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