大鼠蓝斑神经元中增加钾离子电导的α2-肾上腺素能受体的特性研究

Characterization of alpha 2-adrenoceptors which increase potassium conductance in rat locus coeruleus neurones.

作者信息

Williams J T, Henderson G, North R A

出版信息

Neuroscience. 1985 Jan;14(1):95-101. doi: 10.1016/0306-4522(85)90166-6.

Abstract

Intracellular recordings were made from locus coeruleus neurones in a slice of rat pons superfused in vitro. A single-electrode voltage-clamp amplifier was used to measure membrane currents. Superfusion of the slice with clonidine (3-100 nM) or noradrenaline (100 nM-100 microM), or brief application of noradrenaline from a pipette by a pressure pulse, caused dose-dependent membrane hyperpolarizations. Phenylephrine (10 microM) and isoprenaline (10 microM) were ineffective. The hyperpolarizations were accompanied by a decrease in neurone input resistance. The hyperpolarization evoked by pressure ejection of noradrenaline could be reversed by membrane polarization to -110 mV. Clonidine and noradrenaline caused a membrane current which was linearly related to membrane potential between -50 and -120 mV, being outward at resting levels and reversing at -110 mV. The concentration-response curves for clonidine and noradrenaline were shifted rightwards in a parallel manner by alpha 2-adrenoceptor antagonists. The antagonist KeS estimated from the degree of shift were: RX 781094 9 nM, yohimbine 14 nM, phentolamine 20 nM and piperoxane 49 nM. These experiments indicate that in locus coeruleus neurones an increase in potassium conductance results from activation of alpha 2-adrenoceptors similar to those characterized on peripheral neurones.

摘要

在体外灌流的大鼠脑桥切片中，对蓝斑神经元进行细胞内记录。使用单电极电压钳放大器测量膜电流。用可乐定（3 - 100 nM）或去甲肾上腺素（100 nM - 100 μM）灌流切片，或通过压力脉冲从移液管短暂施加去甲肾上腺素，会引起剂量依赖性的膜超极化。苯肾上腺素（10 μM）和异丙肾上腺素（10 μM）无效。超极化伴随着神经元输入电阻的降低。去甲肾上腺素压力喷射诱发的超极化可通过将膜极化至 -110 mV 来逆转。可乐定和去甲肾上腺素引起的膜电流在 -50 至 -120 mV 之间与膜电位呈线性关系，在静息水平时为外向电流，在 -110 mV 时反转。α2 - 肾上腺素能拮抗剂使可乐定和去甲肾上腺素的浓度 - 反应曲线平行右移。根据右移程度估算的拮抗剂 KeS 分别为：RX 781094 9 nM、育亨宾 14 nM、酚妥拉明 20 nM 和哌罗克生 49 nM。这些实验表明，在蓝斑神经元中，钾电导的增加是由类似于外周神经元中所表征的α2 - 肾上腺素能受体激活所致。