Hudson C J, Young L T, Li P P, Warsh J J
Department of Psychiatry, University of Toronto, Clarke Institute of Psychiatry, Canada.
Synapse. 1993 Mar;13(3):278-93. doi: 10.1002/syn.890130311.
Until recently, research on the neurochemical basis of affective disorders (AD) and schizophrenia (SCZ) focused on detecting postulated disturbances in presynaptic neurotransmitter release and metabolism, or postsynaptic receptor function. New insights into the molecular mechanisms involved in the propagation of neurotransmitter signals across biological membranes and in the regulation of neuronal responses have allowed the development of novel hypotheses, which may explain the altered postsynaptic neuroreceptor responsivity thought to be integral to the pathophysiology of these disorders. In this review we evaluate evidence from both basic science and clinical research implicating disturbances in postreceptor signal transduction in the pathophysiology and pharmacotherapy of AD and SCZ. Specific findings regarding potential postreceptor sites of pathophysiology are highlighted in each of these disorders, together with the growing body of data on the possible postreceptor loci of psychotropic drug action, especially lithium and antidepressants.
直到最近,对情感障碍(AD)和精神分裂症(SCZ)神经化学基础的研究一直集中在检测突触前神经递质释放和代谢或突触后受体功能中假定的紊乱情况。对神经递质信号跨生物膜传播以及神经元反应调节所涉及分子机制的新见解,催生了新的假说,这些假说或许可以解释被认为是这些疾病病理生理学不可或缺的突触后神经受体反应性改变。在本综述中,我们评估了基础科学和临床研究的证据,这些证据表明受体后信号转导紊乱与AD和SCZ的病理生理学及药物治疗有关。在这些疾病中,分别强调了关于病理生理学潜在受体后位点的具体发现,以及关于精神药物(尤其是锂盐和抗抑郁药)可能的受体后作用位点的越来越多的数据。