Kafka M S, van Kammen D P
Arch Gen Psychiatry. 1983 Mar;40(3):264-70. doi: 10.1001/archpsyc.1983.01790030034004.
alpha-Adrenergic receptor function was assessed in platelets from drug-free schizophrenic patients and control subjects. The number of alpha-receptors was similar in platelet membranes from schizophrenic patients and control subjects. In intact platelets from schizophrenic male, but not female, patients, prostaglandin E1 (PGE1)-stimulated cyclic adenosine monophosphate (cAMP) level was less than in control subjects. This defect may be due, at least in part, to decreased adenylate cyclase activity. In platelet lysates from schizophrenic patients, but not from normal control subjects, adenylate cyclase activity was diminished and PGE1-stimulated adenylate cyclase activity could be restored partially by the addition of guanosine triphosphate. Treatment with neuroleptic drugs or lithium carbonate did not change alpha-receptor number or cAMP production in platelets from schizophrenic patients, but high doses of propranolol hydrochloride increased cAMP production without affecting the number of alpha-receptors. If the production of cAMP in neurons is similar to that in platelets, diminished cAMP production may be associated with a vulnerability to schizophrenia.
对未服用药物的精神分裂症患者和对照受试者的血小板中的α-肾上腺素能受体功能进行了评估。精神分裂症患者和对照受试者血小板膜中的α-受体数量相似。在精神分裂症男性患者而非女性患者的完整血小板中,前列腺素E1(PGE1)刺激的环磷酸腺苷(cAMP)水平低于对照受试者。这种缺陷可能至少部分归因于腺苷酸环化酶活性降低。在精神分裂症患者的血小板裂解物中,腺苷酸环化酶活性降低,而正常对照受试者的血小板裂解物中则未出现这种情况,并且通过添加三磷酸鸟苷可部分恢复PGE1刺激的腺苷酸环化酶活性。使用抗精神病药物或碳酸锂治疗不会改变精神分裂症患者血小板中的α-受体数量或cAMP生成,但高剂量的盐酸普萘洛尔可增加cAMP生成,而不影响α-受体数量。如果神经元中cAMP的生成与血小板中的相似,那么cAMP生成减少可能与精神分裂症易感性有关。