Palomo Tomas, Archer Trevor, Kostrzewa Richard M, Beninger Richard J
Servicio Psiquiatrico, Hospital Universitario 12 de Octubre, 28041 Madrid, Spain.
Neurotox Res. 2007 Jul;12(1):17-27. doi: 10.1007/BF03033898.
Substance abuse is a frequent comorbid condition with other psychiatric disorders including schizophrenia and depression. These disorders may share a common substrate at the neurotransmitter or neurocircuit level. One candidate is hypofunction of the glutamate system. Several lines of evidence suggest that N-methyl-D-aspartate (NMDA) receptors may hypofunction in schizophrenia. Thus, NMDA receptor antagonists are schizophrenogenic; postmortem and imaging results point to reduced NMDA receptor function in schizophrenic brains; a number of genes that have been linked to schizophrenia code for proteins that influence NMDA function; and there is preliminary evidence that pro-NMDA drugs may be therapeutic in the treatment of schizophrenia. One of the most effective therapeutics for the treatment of substance abuse in schizophrenic people is clozapine, and clozapine may act at the glycine modulatory site to enhance NMDA receptor function. This preliminary line of evidence may link schizophrenia and drug abuse to a common neurochemical base, subnormal NMDA receptor function. People with schizophrenia and drug abusers similarly show deficits in tasks known to be sensitive to ventromedial prefrontal cortical damage, and both groups show decreased activation in the ventral striatum during reward anticipation in functional magnetic resonance imaging studies. These observations implicate common prefrontal cortical-striatal circuits and their modulation by hippocampal projections in schizophrenia and substance abuse. Withdrawal from substance abuse and depression both have been linked to changes in the function of several neurotransmitters including serotonin, dopamine and glutamate. These findings suggest possible common substrates and novel therapeutic approaches. Further studies are needed to fully characterize the neurocircuits and transmitters involved in various psychiatric disorders and their possible common elements in comorbid drug abuse.
物质滥用是一种常见的共病情况,常与包括精神分裂症和抑郁症在内的其他精神障碍并发。这些障碍可能在神经递质或神经回路水平上有共同的基础。一个可能的因素是谷氨酸系统功能低下。有几条证据表明,N-甲基-D-天冬氨酸(NMDA)受体在精神分裂症中可能功能低下。因此,NMDA受体拮抗剂具有致精神分裂症作用;尸检和影像学结果表明精神分裂症患者大脑中的NMDA受体功能降低;一些与精神分裂症相关的基因编码影响NMDA功能的蛋白质;并且有初步证据表明促NMDA药物可能对精神分裂症的治疗有疗效。治疗精神分裂症患者物质滥用最有效的药物之一是氯氮平,氯氮平可能作用于甘氨酸调节位点以增强NMDA受体功能。这一初步证据线索可能将精神分裂症和药物滥用与一个共同的神经化学基础——NMDA受体功能异常联系起来。精神分裂症患者和药物滥用者在已知对腹内侧前额叶皮质损伤敏感的任务中同样表现出缺陷,并且在功能磁共振成像研究中,两组在奖励预期期间腹侧纹状体的激活都减少。这些观察结果表明,在精神分裂症和物质滥用中,存在共同的前额叶皮质-纹状体回路及其受海马投射的调节。物质滥用戒断和抑郁症都与包括血清素、多巴胺和谷氨酸在内的几种神经递质功能变化有关。这些发现提示了可能的共同基础和新的治疗方法。需要进一步研究以全面表征参与各种精神障碍的神经回路和神经递质及其在共病药物滥用中可能的共同元素。