Hyde T M, Crook J M
Clinical Brain Disorders Branch, IRP, NIMH, NIH, Bethesda, MD 20892, USA.
J Chem Neuroanat. 2001 Jul;22(1-2):53-63. doi: 10.1016/s0891-0618(01)00101-6.
Post mortem schizophrenia research has been driven first by the dopamine and then the glutamate hypotheses. These hypotheses posit primary pathology in pathways dependent upon dopamine or glutamate neurotransmission. Although the dopamine and glutamate hypotheses retain considerable theoretical strength, neurobiological findings of altered dopamine or glutamate activity in schizophrenia do not explain all features of this disorder. A more synthetic approach would suggest that focal pathological change in either the prefrontal cortex or mesial temporal lobe leads to neurochemical changes in multiple neurotransmitter systems. Despite the limited experimental evidence for abnormal cholinergic neurotransmission in psychiatric disorders, increased understanding of the role of acetylcholine in the human brain and its relationship to other neurotransmitter systems has led to a rapidly growing interest in the cholinergic system in schizophrenia. This review focuses on the basic anatomy of the mammalian cholinergic system, and its possible involvement in the neurobiology of schizophrenia. Summaries of cholinergic cell groups, projection pathways, and receptor systems, in the primate and human brain, are followed by a brief discussion of the functional correlations between aberrant cholinergic neurotransmission and the signs and symptoms of schizophrenia.
死后精神分裂症研究首先由多巴胺假说驱动，随后是谷氨酸假说。这些假说认为在依赖多巴胺或谷氨酸神经传递的通路中存在原发性病理改变。尽管多巴胺和谷氨酸假说仍具有相当大的理论优势，但精神分裂症中多巴胺或谷氨酸活性改变的神经生物学发现并不能解释该疾病的所有特征。一种更综合的方法表明，前额叶皮质或内侧颞叶的局灶性病理改变会导致多个神经递质系统发生神经化学变化。尽管精神疾病中胆碱能神经传递异常的实验证据有限，但对乙酰胆碱在人脑中的作用及其与其他神经递质系统关系的深入了解，已引发了对精神分裂症中胆碱能系统的兴趣迅速增长。本综述重点关注哺乳动物胆碱能系统的基本解剖结构及其在精神分裂症神经生物学中的可能作用。在总结灵长类动物和人类大脑中的胆碱能细胞群、投射通路和受体系统之后，将简要讨论胆碱能神经传递异常与精神分裂症的体征和症状之间的功能相关性。
