Casebolt T L, Li X H, Jope R S
Department of Psychiatry, University of Alabama, Birmingham.
J Neural Transm Gen Sect. 1990;82(3):197-204. doi: 10.1007/BF01272762.
Administration to rats of dietary lithium for 30 days was followed by evaluation of alpha-1 adrenergic receptor binding and of adrenergic-stimulated cyclic AMP (cAMP) accumulation in rat cerebral cortex. Chronic lithium treatment did not alter the binding characteristics of [3H]prazosin or the proportion of alpha-1 adrenergic receptor subtypes distinguished by chlorethyl-clonidine (CEC) pretreatment in rat cerebral cortical membranes. Accumulation of cAMP in cortical slices incubated with adrenergic agonists was unaffected in lithium-treated rats. These results demonstrate that chronic lithium treatment-induced reduction of norepinephrine (NE)-stimulated phosphoinositide (PI) hydrolysis (Casebolt and Jope, 1987) is not due to changes in the alpha-1 adrenergic receptor and is more sensitive to in vivo lithium treatment than is adrenergic-stimulated cAMP accumulation.
给大鼠喂食锂30天,随后评估大鼠大脑皮层中α-1肾上腺素能受体结合以及肾上腺素刺激的环磷酸腺苷(cAMP)积累情况。慢性锂治疗并未改变[3H]哌唑嗪的结合特性,也未改变经氯乙基可乐定(CEC)预处理区分的大鼠大脑皮层膜中α-1肾上腺素能受体亚型的比例。在与肾上腺素能激动剂一起孵育的皮层切片中,cAMP的积累在锂治疗的大鼠中未受影响。这些结果表明,慢性锂治疗导致去甲肾上腺素(NE)刺激的磷酸肌醇(PI)水解减少(Casebolt和Jope,1987)并非由于α-1肾上腺素能受体的变化,并且与肾上腺素刺激的cAMP积累相比,对体内锂治疗更敏感。