Cross A J, Crow T J, Killpack W S, Longden A, Owen F, Riley G J
Psychopharmacology (Berl). 1978 Oct 31;59(2):117-21. doi: 10.1007/BF00427744.
It has been suggested that deterioration of central noradrenergic pathways may be responsible for the production of certain schizophrenic symptoms, and that such a degeneration might be reflected in lowered dopamine-beta-hydroxylase (DBH) activity in the brains of schizophrenics. The present study revealed that in rats lowered DBH activity was a sensitive index of noradrenergic degeneration. In the postmortem brains of 12 controls and 12 schizophrenics, however, no significant difference in DBH activity between controls and schizophrenics was found. DBH activity was relatively unstable postmortem and adversely affected by neuroleptic drugs, and these factors may have contributed to the previous finding of lowered DBH activity in the brains of schizophrenics. The activity of catechol-O-methyl transferase, which has also been previously reported as low in the brains of schizophrenics, was found to be no different in the controls of the present study.
有人提出,中枢去甲肾上腺素能通路的退化可能是某些精神分裂症症状产生的原因,而且这种退化可能反映在精神分裂症患者大脑中多巴胺-β-羟化酶(DBH)活性降低。本研究表明,在大鼠中,DBH活性降低是去甲肾上腺素能退化的一个敏感指标。然而,在12名对照者和12名精神分裂症患者的死后大脑中,未发现对照者和精神分裂症患者之间DBH活性有显著差异。DBH活性在死后相对不稳定,且受抗精神病药物的不利影响,这些因素可能导致了先前在精神分裂症患者大脑中发现的DBH活性降低。儿茶酚-O-甲基转移酶的活性在本研究的对照者中也未发现差异,该酶活性先前也被报道在精神分裂症患者大脑中较低。