- 作者: Ellas K. Nanitsos; Khoa T. D. Nguyen; Frantisek St'astny; Vladimir J. Balcar
- 作者服務機構: 1 Anatomy and Histology, Institute for Biomedical Research and School of Medical Sciences, The University of Sydney, Anderson Stuart Building F 13, Sydney, NSW 2006, Australia; ; 2 Laboratory of Biochemistry and Brain Pathophysiology, Prague Psychiatric Center, Charles University, 3rd Faculty of Medicine, Prague, Czech Republic
- 中文摘要: --
- 英文摘要: Hypothetical model based on deficient glutamatergic neurotransmission caused by hyperactive glutamate transport in astrocytes surrounding excitatory synapses in the prefrontal cortex is examined in relation to the aetiology of schizophrenia. The model is consistent with actions of neuroleptics, such as clozapine, in animal experiments and it is strongly supported by recent findings of increased expression of glutamate transporter GLT in prefrontal cortex of patients with schizophrenia. It is proposed that mechanisms regulating glutamate transport be investigated as potential targets for novel classes of neuroactive compounds with neuroleptic characteristics. Development of new efficient techniques designed specifically for the purpose of studying rapid activity-dependent translocation of glutamate transporters and associated molecules such as Na + , K +-ATPase is essential and should be encouraged.
- 中文關鍵字: --
- 英文關鍵字: clozapine, EAAT, GLAST, GLT, glutamatergic synapses, Na+ ,K+-ATPase, neuroleptics, prefrontal cortex, psychosis, synaptic excitation