Mann J J, Mahler J C, Wilner P J, Halper J P, Brown R P, Johnson K S, Kocsis J H, Chen J S
Department of Psychiatry, Cornell University Medical College, New York, NY.
Arch Gen Psychiatry. 1990 May;47(5):461-4. doi: 10.1001/archpsyc.1990.01810170061009.
Electroconvulsive therapy has been reported to desensitize brain beta-adrenergic receptors in rodents, but this effect has not been studied in man. We examined the effect of a course of electroconvulsive therapy on lymphocyte beta-adrenergic responsivity in 19 inpatients with melancholia. Before treatment, beta-adrenergic cyclic adenosine monophosphate response to isoproterenol was significantly blunted in the patients compared with controls. Following a course of electroconvulsive therapy, beta-adrenergic responsivity increased such that patients no longer differed from controls. Thus, blunted lymphocyte beta-adrenergic responsivity is a state-dependent effect of melancholia that can be corrected by a therapeutic course of electroconvulsive therapy. The effect of electroconvulsive therapy on this beta-adrenergic system is in the opposite direction to that reported for rodent forebrain, where electroconvulsive therapy causes desensitization, and may reflect differences between peripheral and central effects, species differences, or disease effects.
据报道，电休克疗法可使啮齿动物大脑中的β-肾上腺素能受体脱敏，但尚未在人类中研究过这种效应。我们研究了一个疗程的电休克疗法对19例忧郁症住院患者淋巴细胞β-肾上腺素能反应性的影响。治疗前，与对照组相比，患者对异丙肾上腺素的β-肾上腺素能环磷酸腺苷反应明显减弱。经过一个疗程的电休克治疗后，β-肾上腺素能反应性增加，患者与对照组不再有差异。因此，淋巴细胞β-肾上腺素能反应性减弱是忧郁症的一种状态依赖性效应，可通过电休克疗法的治疗疗程得到纠正。电休克疗法对该β-肾上腺素能系统的影响与啮齿动物前脑的报道相反，在啮齿动物前脑中，电休克疗法会导致脱敏，这可能反映了外周和中枢效应、物种差异或疾病效应之间的差异。
