Newman M, Zohar J, Kalian M, Belmaker R H
Brain Res. 1984 Jan 16;291(1):188-92. doi: 10.1016/0006-8993(84)90670-x.
The influence of chronic dietary lithium administration and electroconvulsive therapy on adenosine A1 and A2 receptors in rat brain were determined. A2 receptor activity was measured by accumulation of cyclic AMP in a cerebral cortical slice preparation after in vitro addition of 2-chloro-adenosine, and was unchanged in animals which received chronic Li but reduced following chronic ECT. A similar reduction was found in the response to noradrenaline and a combination of the two agents. A1 receptors were measured by binding of [3H]cyclohexyladenosine. Both Kd and Bmax values were unchanged after chronic Li or a single ECS, but chronic ECT led to a 70% increase in Bmax. It is proposed that this effect may mediate the reduced locomotor activity seen after chronic ECT in rats, and that it may also be related to the increase in seizure thresholds seen during a course of ECS treatment in humans.
测定了长期给予膳食锂及电惊厥治疗对大鼠脑内腺苷A1和A2受体的影响。通过在体外添加2-氯腺苷后,在大脑皮层切片标本中积累环磷酸腺苷来测量A2受体活性,接受慢性锂处理的动物中该活性未改变,但在慢性电惊厥治疗后降低。对去甲肾上腺素及两种药物联合使用的反应中也发现了类似的降低。通过[3H]环己基腺苷结合来测量A1受体。慢性锂处理或单次电休克刺激后,解离常数(Kd)和最大结合容量(Bmax)值均未改变,但慢性电惊厥治疗导致Bmax增加70%。有人提出,这种效应可能介导了大鼠慢性电惊厥治疗后出现的运动活性降低,并且它可能还与人类在电休克治疗过程中癫痫阈值的升高有关。