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糖尿病中的中枢单胺功能障碍:心理治疗意义:伏安法电分析

Central monoamine dysfunction in diabetes: psychotherapeutic implications: electroanalysis by voltammetry.

作者信息

Broderick P A, Jacoby J H

机构信息

Department of Pharmacology, City University of New York Medical School, NY.

出版信息

Acta Physiol Pharmacol Latinoam. 1989;39(3):211-25.

PMID:2534495
Abstract

The effects of chemically, i.e., streptozotocin-induced diabetes or induced hyperglycemia on dopamine and serotonin release in striatum were examined in vivo in rats by employing voltammetry. In the acutely diabetic state, an increased (67%) striatal dopamine release was seen, whereas in the chronically diabetic state, striatal dopamine release was increased, but not to the same extent (19%). The acutely diabetic rat, in which electrochemical signals for serotonin were studied 3 days after the single intraperitoneal injection of STZ, responded with a significant increased release of serotonin (62%). Chronically diabetic rats showed a reversal of serotonin release to basal values. When L-tryptophan was injected in nondiabetic rats, the results showed a decrease (45%) in striatal dopamine release. Injection of L-tryptophan into nondiabetic rats produced a significant increase (25%) over control values in the striatal release of serotonin. The maximum increase was most evident 90 min after injection and the increase remained elevated an additional 90 min. Long term diabetic animals showed a significant decrease (73%) in striatal dopamine release after L-tryptophan. Long term diabetes produced a significant inhibition of serotonin release over control values to 70% below baseline levels. The effects of hyperglycemia on non-diabetic rats were a decreased (52%) striatal dopamine release and an increased (304%) striatal serotonin release. These changes imply that the untreated diabetic state is associated with progressive impairment of neurotransmitter release. These data can be interpreted as implying that mood changes may be related to impaired neurotransmitter availability in the diabetic state.

摘要

采用伏安法在大鼠体内研究了化学诱导的糖尿病或高血糖对纹状体中多巴胺和血清素释放的影响。在急性糖尿病状态下,纹状体多巴胺释放增加(67%),而在慢性糖尿病状态下,纹状体多巴胺释放也增加,但程度不同(19%)。在单次腹腔注射链脲佐菌素3天后研究血清素电化学信号的急性糖尿病大鼠,其血清素释放显著增加(62%)。慢性糖尿病大鼠的血清素释放恢复到基础值。当向非糖尿病大鼠注射L-色氨酸时,结果显示纹状体多巴胺释放减少(45%)。向非糖尿病大鼠注射L-色氨酸后,纹状体血清素释放比对照值显著增加(25%)。注射后90分钟增加最为明显,并且在接下来的90分钟内仍保持升高。长期糖尿病动物在注射L-色氨酸后纹状体多巴胺释放显著减少(73%)。长期糖尿病导致血清素释放比对照值显著抑制,降至基线水平以下70%。高血糖对非糖尿病大鼠的影响是纹状体多巴胺释放减少(52%)和纹状体血清素释放增加(304%)。这些变化表明未经治疗的糖尿病状态与神经递质释放的进行性损害有关。这些数据可以解释为暗示情绪变化可能与糖尿病状态下神经递质可用性受损有关。

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