Lodge Daniel J, Grace Anthony A
Department of Pharmacology & Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, MC 7764, San Antonio, TX 78229, USA.
Int J Dev Neurosci. 2011 May;29(3):207-13. doi: 10.1016/j.ijdevneu.2010.08.002. Epub 2010 Aug 19.
Psychological stress is a contributing factor for a wide variety of neuropsychiatric diseases including substance use disorders, anxiety, depression and schizophrenia. However, it has not been conclusively determined how stress augments the symptoms of these diseases. Here we review evidence that the ventral hippocampus may be a site of convergence whereby a number of seemingly discrete risk factors, including stress, may interact to precipitate psychosis in schizophrenia. Specifically, aberrant hippocampal activity has been demonstrated to underlie both the elevated dopamine neuron activity and associated behavioral hyperactivity to dopamine agonists in a verified animal model of schizophrenia. In addition, stress, psychostimulant drug use, prenatal infection and select genetic polymorphisms all appear to augment ventral hippocampal function that may therefore exaggerate or precipitate psychotic symptoms. Such information is critical for our understanding into the pathology of psychiatric disease with the ultimate aim being the development of more effective therapeutics.
心理压力是包括物质使用障碍、焦虑、抑郁和精神分裂症在内的多种神经精神疾病的一个促成因素。然而，压力如何加剧这些疾病的症状尚未得到最终确定。在此，我们综述了相关证据，即腹侧海马体可能是一个汇聚点，许多看似不相关的风险因素，包括压力，可能在此相互作用，从而在精神分裂症中引发精神病症状。具体而言，在一个经过验证的精神分裂症动物模型中，异常的海马体活动已被证明是多巴胺神经元活动升高以及对多巴胺激动剂相关行为多动的基础。此外，压力、使用精神兴奋剂药物、产前感染和特定的基因多态性似乎都增强了腹侧海马体的功能，因此可能会夸大或引发精神病症状。这些信息对于我们理解精神疾病的病理至关重要，最终目标是开发更有效的治疗方法。
