Electroconvulsive shock increases alpha 1b- but not alpha 1a-adrenoceptor binding sites in rat cerebral cortex.
Electroconvulsive shock increases alpha 1b- but not alpha 1a-adrenoceptor binding sites in rat cerebral cortex.
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电休克会增加大鼠大脑皮层中 α1b- 肾上腺素受体的结合位点，但不会增加 α1a- 肾上腺素受体的结合位点。
DOI：
10.1111/j.1471-4159.1991.tb06350.x
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发表时间：
1991
影响因子：
4.7
通讯作者：
Kellar,KJ
中科院分区：
文献类型：
--
作者：
Blendy,JA;Perry,DC;Pabreza,LA;Kellar,KJ
重复给予电休克（ECS）可增加[3 H]哌唑嗪与大鼠大脑皮层α1-肾上腺素受体的结合。相比之下，已报告皮质中的[3 H] WB 4101结合在ECS后保持不变。[3 H]哌唑嗪标记两种α1-肾上腺素受体亚型，称为α 1a和α1b，而[3 H] WB 4101优先标记α 1a亚型。本研究的目的是确定ECS是否增加大鼠大脑皮层中的一种或两种α1-肾上腺素受体亚型。我们发现，大鼠每日一次给予ECS治疗10-12天，使皮质中的[3 H]哌唑嗪结合增加约25%，但未显著改变[3 H] WB 4101与α1a-肾上腺素受体的结合。通过选择性α 1a拮抗剂5-甲基乌拉地尔与[3 H]哌唑嗪的竞争分析测量α 1a和α 1b受体，并测量与烷基化α 1b结合位点的二乙基可乐定预孵育的匀浆中的[3 H]哌唑嗪结合，也表明ECS指示的α1-肾上腺素受体增加仅限于α 1b亚型。与其对[3 H]哌唑嗪结合的影响相反，ECS没有增加磷酸肌醇水解，如通过去甲肾上腺素或苯肾上腺素刺激的大鼠大脑皮层切片中[3 H]肌醇1-磷酸蓄积所测量的。ECS未能增加苯肾上腺素（苯肾上腺素是该反应的部分激动剂）刺激的[3 H]肌醇1-磷酸蓄积，表明备用受体不能解释ECS对α1-肾上腺素受体介导的磷酸肌醇水解作用的明显缺失。
: Repeated administration of electroconvulsive shock (ECS) increases [3H]prazosin binding to α1‐adrenoceptors in rat cerebral cortex. In contrast, [3H]WB4101 binding in cortex has been reported to be unchanged after ECS. [3H]Prazosin labels two α1‐adrenoceptor subtypes, termed α1aand α1b, whereas [3HJWB4101 labels the α1asubtype preferentially. The purpose of this study was to determine whether ECS increases one or both α1‐adrenoceptor subtypes in rat cerebral cortex. We found that treatment of rats with ECS once daily for 10–12 days increased [3H]prazosin binding in cortex by about 25% but did not significantly alter [3H]WB4101 binding to α1a‐adrenoceptors. Measurement of α1aand α1breceptors by competition analysis of the selective α1aantagonist 5‐methylurapidil against [3H]prazosin and measurement of [3H]prazosin binding in homogenates preincubated with chlorethylclonidine, which alkylates α1bbinding sites, also indicated that the ECS‐indiced increase in α1‐adrenoceptors is confined to the α1bsubtype. In contrast to its effect on [3H]prazosin binding, ECS did not increase phosphoinositide hydrolysis as measured by [3H]inositol 1‐phosphate accumulation in slices of rat cerebral cortex stimulated by either norepinephrine or phenylephrine. The failure of ECS to increase [3H]inositol 1‐phosphate accumulation stimulated by phenylephrine, which is a partial agonist for this response, suggests that spare receptors do not account for the apparent absence of effect of ECS on α1‐adrenoceptor‐mediated phosphoinositide hydrolysis.