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向雌性大鼠注射雌二醇对反复给予地昔帕明或电惊厥休克诱导的α2和β肾上腺素能受体功能变化的影响。

The influence of injection of oestradiol to female rats on changes in alpha 2- and beta-adrenoceptor function induced by repeated administration of desipramine or electroconvulsive shock.

作者信息

Heal D J, Bristow L J, De Souza R J, Bloomfield J G, Hurst E M, Elliott J M

机构信息

MRC Unit, Radcliffe Infirmary, Oxford, U.K.

出版信息

Neuropharmacology. 1988 Nov;27(11):1151-9. doi: 10.1016/0028-3908(88)90011-1.

DOI:10.1016/0028-3908(88)90011-1
PMID:2849729
Abstract

Repeated daily administration to female rats of either an electroconvulsive shock (110 V, 1 sec) or desipramine (DMI; 5 mg/kg x 2) caused a progressive decrease in presynaptic alpha 2-adrenoceptor function assessed by the hypoactivity (sedation) response to clonidine (0.5 mg/kg). This reduction was maximal after approximately seven electroshocks or 8-12 days of injection of DMI. Daily administration of oestradiol (100 micrograms s.c.), starting one day prior to the commencement of administration of DMI or treatment with electroshock, markedly accelerated the onset of decreased hypoactivity responses to clonidine, but did not alter the maximum reduction induced by repeated injection of DMI or administration of electroshock. Injection of oestradiol alone had no effect on the responses to clonidine. Administration of DMI for 14 days decreased the number of both alpha 2- and beta-adrenoceptors in the cortex. Cortical beta-, but not alpha 2-adrenoceptors, were also decreased after 4 days of injection of DMI. Two and ten electroshocks moderately increased and decreased cortical alpha 2-adrenoceptors, respectively. beta-Adrenoceptors were also decreased by ten electroshocks, but two were without effect. Simultaneous administration of oestradiol had little influence on the changes in the binding of alpha 2- or beta-adrenoceptors induced by repeated administration of DMI or treatment with electroshock. Oestradiol increased the numbers of cortical alpha 2- and beta-adrenoceptors 3 and 15 days after injection, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

每天对雌性大鼠重复给予电惊厥休克(110伏,1秒)或去甲丙咪嗪(DMI;5毫克/千克×2),会导致通过可乐定(0.5毫克/千克)引起的活动减退(镇静)反应评估的突触前α2 - 肾上腺素能受体功能逐渐下降。这种下降在大约七次电击或注射DMI 8 - 12天后达到最大程度。从开始注射DMI或电击治疗前一天开始,每天皮下注射雌二醇(100微克),显著加速了对可乐定活动减退反应降低的起始,但并未改变重复注射DMI或电击治疗所诱导的最大降低程度。单独注射雌二醇对可乐定反应无影响。注射DMI 14天会使皮质中α2 - 和β - 肾上腺素能受体的数量均减少。注射DMI 4天后,皮质β - 肾上腺素能受体减少,但α2 - 肾上腺素能受体未减少。两次和十次电击分别适度增加和减少了皮质α2 - 肾上腺素能受体。十次电击也使β - 肾上腺素能受体减少,但两次电击无影响。同时给予雌二醇对重复注射DMI或电击治疗所诱导的α2 - 或β - 肾上腺素能受体结合变化影响很小。注射后3天和15天,雌二醇分别增加了皮质α2 - 和β - 肾上腺素能受体的数量。(摘要截短至250字)

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