Neuro-immuno-endocrinological aspects of pathophysiology of affective disorders

本研究旨在从神经-免疫-内分泌学的角度阐明情感性障碍的病理生理，并发现以下几点事实。在情感性障碍患者中，使用xe - ct检查发现皮质血流量降低。在大鼠额叶皮层，抗抑郁药物抑制多巴胺的摄取。习得性无助可能是抑郁症的一个很好的模型。三甲基锡改变大鼠hpa -轴功能和行为。应激对致死大鼠神经元可塑性和内分泌反应的影响。白细胞介素-1介导应激诱导大鼠下丘脑单胺释放。对癌症患者的精神疾病发病率进行了调查，证实20- 40%的癌症患者存在精神问题。一种新型抗抑郁药物罗利普兰促进了Gs蛋白- ca MP的产生。在原代培养的神经细胞中，一些抗抑郁药物和情绪稳定剂抑制去极化诱导的细胞内钙离子增加，一些激动剂等。抗抑郁药物调节微管相关蛋白II的磷酸化和去磷酸化。这些结果和情感性障碍生物学研究的历史观点被收集、编辑并发表在《情感性障碍的神经免疫内分泌学-脑世纪的新方向》一书中。

This study was undertaken to clarify the pathophysiology of affective disorders in view of neuro-immuno-endocrinology and found several facts as below mentioned.1.Blood flow rate of cortex was reduced in the patients with affective disorders using Xe-CT.2.In rat frontal cortex, antidpressants inhibited dopamine uptake.3.Learned helplessness may be a good model for depression.4.Trimethyltin altered the function of HPA-axis and behavior in rats.5.Stress to fatal rats changed the plasticity of neurons and endocirne response in rats.6.Interleukin-1 mediated the restraint stress-induced monoamine release in hypothalamus of rats.7.Psychiatric morbidity in cancer patients was investigated and it proved that 20-40 % of the cancer patients suffer from psychiatric problems.8.A novel antidepressant drug rolipram facilitated the function of Gs protein-cA MP production.9.Several antidepressant drugs and mood stabilizers inhibited intracellular chlcium increase induced by depolarization, some agonists and so on, in primary cultured neuronal cells.10.Antidepressant drugs modulated the phosphorylation and dephosphorylation of microtubule associated protein II.These results and the historical view of the biological investigations on affective disorders were collected, edited and published in a booknamed Neuro-Immuno-Endocrinology of Affective Disorders-New Direction to the Century of the Brain-.