Lahti A C, Holcomb H H, Medoff D R, Tamminga C A
Maryland Psychiatric Research Center, University of Maryland, Department of Psychiatry, Baltimore 21228, USA.
Neuroreport. 1995 Apr 19;6(6):869-72. doi: 10.1097/00001756-199504190-00011.
The non-competitive NMDA antagonist ketamine, given to schizophrenic individuals in subanesthetic doses, produced a short-lived, discrete activation of their psychotic symptoms, which had striking similarities to symptoms of their usual psychotic episodes. To further study this psychotomimetic property of ketamine, we administered 0.3 mg kg-1 of the drug to schizophrenic individuals during a [15O] water cerebral blood flow study. Regional cerebral blood flow (rCBF) was measured using H2(15)O and positron emission tomography (PET) before and after ketamine administration to identify regions of flow change, rCBF was increased in anterior cingulate cortex and was reduced in the hippocampus and primary visual cortex (lingual and fusiform gyri). These data encourage further consideration of altered glutamatergic transmission in schizophrenic and PCP-induced psychoses.
非竞争性N-甲基-D-天冬氨酸（NMDA）拮抗剂氯胺酮，以亚麻醉剂量给予精神分裂症患者时，会使其精神症状产生短暂、离散的激活，这与他们通常的精神病发作症状有惊人的相似之处。为了进一步研究氯胺酮的这种拟精神病特性，我们在一项[15O]水脑血流研究中，给精神分裂症患者施用了0.3毫克/千克的该药物。在氯胺酮给药前后，使用H2(15)O和正电子发射断层扫描（PET）测量局部脑血流（rCBF），以确定血流变化区域。前扣带回皮质的rCBF增加，而海马体和初级视觉皮质（舌回和梭状回）的rCBF减少。这些数据促使人们进一步考虑精神分裂症和苯环己哌啶（PCP）所致精神病中谷氨酸能传递的改变。
