@article{oai:niigata-u.repo.nii.ac.jp:00022766,
 author = {富樫, 俊二},
 issue = {10},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Oct},
 note = {Several lines of evidence link the dopaminergic neurotransmitter system to schizophrenia. The antipsychotic action of neuroleptic drugs is correlated well with the bloekade of D_2 dopamine receptors. Amphetamines, which elevate synaptic dopamine levels, can induce psychotic states resembling schizophrenia. Increased numbers of D_2 dopamine receptors have been reported in vitro radioreceptor assay in postmortem studies and in vivo PET studies of the brains of schizophrenic patients. But, in some studies, these increases were attributed to prior neuroleptic treatment of the patient, while in other PET study increases were not found in schizophrenic patients. Hence, interpsetation of the elevation in dopamine receptor of schizophrenia has remained controversial. Animal studies have shown that all effective antidepressant treatment act to decrease NE-stimulated c-AMP accumulation in the brain. This finding was followed by reports showing that treatment with antidepressant drugs for several days reduced the density of both beta-adrenergic receptor and serotonin_2 receptor in rat cerebral cortex. The chronological parallel between such phenomenon and the clinical efficacy of these drugs suggests that the changes of the function of beta-receptor and serotonin_2 receptor may underlie in the pathogenesis of affective disorders. In this review, I summarized the recent investigations concerning the monoamine receptors and functional psychcosis.},
 pages = {813--817},
 title = {5) モノアミンレセプターと機能精神病(シンポジウム レセプターとその臨床, 第443回新潟医学会)},
 volume = {103},
 year = {1989}
}