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神经肽甘丙肽抑制副交感神经元中对ω-芋螺毒素GVIA敏感的钙通道。

Neuropeptide galanin inhibits omega-conotoxin GVIA-sensitive calcium channels in parasympathetic neurons.

作者信息

Merriam L A, Parsons R L

机构信息

Department of Anatomy and Neurobiology, University of Vermont, College of Medicine, Burlington 05405, USA.

出版信息

J Neurophysiol. 1995 Apr;73(4):1374-82. doi: 10.1152/jn.1995.73.4.1374.

Abstract
  1. We determined the effect of the neuropeptide galanin on barium currents (IBa) flowing through voltage-gated calcium channels. We voltage clamped parasympathetic neurons dissociated from mudpuppy cardiac ganglia using both the standard whole cell and the perforated-patch variations of the patch-clamp technique. 2. Galanin produced a concentration-dependent inhibition of IBa. The maximal inhibition was 50-60% and the concentration that produced half-maximal inhibition (IC50) was 0.42 nM. In mud-puppy parasympathetic neurons, omega-conotoxin-GVIA (CTX)-sensitive channels are the predominant type of calcium channels, and only a small portion of IBa is contributed by dihydropyridine-sensitive channels. Galanin preferentially inhibited a portion of the CTX-sensitive current. 3. In currents recorded with the standard whole cell technique, activation of IBa was slowed in the presence of galanin. In contrast, in the majority of neurons studied with the perforated-patch technique, galanin decreased IBa without altering the kinetics of current activation. With both recording methods, the decrease in IBa was greatest with voltage steps to 0 mV and persisted with steps to +50 mV. For control currents, large depolarizing voltage steps (+70 to +120 mV) did not markedly facilitate IBa when either recording technique was used. However, the degree of facilitation in galanin was significantly greater with the standard whole cell recording technique. 4. IBa exhibited inactivation under the conditions of these experiments. Inactivation of IBa recorded during a 900-ms depolarizing voltage step was fitted to a double exponential. Galanin decreased the amplitude of IBa but did not alter the time constants of inactivation.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 我们测定了神经肽甘丙肽对通过电压门控钙通道的钡电流(IBa)的影响。我们使用膜片钳技术的标准全细胞模式和穿孔膜片模式,对从泥螈心脏神经节分离出的副交感神经元进行电压钳制。2. 甘丙肽对IBa产生浓度依赖性抑制。最大抑制率为50 - 60%,产生半数最大抑制的浓度(IC50)为0.42 nM。在泥螈副交感神经元中,ω-芋螺毒素-GVIA(CTX)敏感通道是主要的钙通道类型,只有一小部分IBa由二氢吡啶敏感通道产生。甘丙肽优先抑制一部分CTX敏感电流。3. 在标准全细胞技术记录的电流中,甘丙肽存在时IBa的激活减慢。相反,在大多数用穿孔膜片技术研究的神经元中,甘丙肽降低了IBa,但不改变电流激活的动力学。两种记录方法中,向0 mV的电压阶跃时IBa的降低最大,向+50 mV的阶跃时仍持续。对于对照电流,当使用任何一种记录技术时,大的去极化电压阶跃(+70至+120 mV)都不会明显促进IBa。然而,标准全细胞记录技术下甘丙肽的促进程度明显更大。4. 在这些实验条件下,IBa表现出失活。在900毫秒去极化电压阶跃期间记录的IBa失活拟合为双指数曲线。甘丙肽降低了IBa的幅度,但没有改变失活的时间常数。(摘要截断于250字)

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