Velbinger K, De Vry J, Jentzsch K, Eckert A, Henn F, Müller W E
Central Institute of Mental Health, Department of Psychopharmacology and Psychiatry, Mannheim, Germany.
Pharmacopsychiatry. 2000 Jul;33(4):132-7. doi: 10.1055/s-2000-11220.
Previous reports have demonstrated reduced elevations of free intracellular calcium concentration in blood cells of depressed patients after various stimuli. Therefore, a disturbance of intracellular calcium (Ca2+) homeostasis has been postulated to be involved in the pathophysiology of mood disorders. It was the aim of the present study to investigate whether Ca2+ signaling was affected in spleen T-lymphocytes of rats submitted to a learned helplessness paradigm, an animal model of depression with a high level of construct, face and predictive validity. In addition, we tested for effects of acute stress on the Ca2+ signaling in helpless rats, as compared to non-stressed rats. It was found that mitogen-induced Ca2+ signaling only tended to be reduced in helpless rats. However, when helpless rats were submitted to acute immobilization stress, Ca2+ signaling appeared to be significantly blunted, whereas the same stressor did not affect Ca2+ signaling in the non-helpless control rats. These acute stress-induced differences in Ca2+ signaling were not paralleled by a differential increase in plasma corticosterone. It is hypothesized that blunted Ca2+ signaling, as assessed in spleen T-lymphocytes of helpless rats, may be a correlate of the increased vulnerability of helpless rats to acute stressors.
先前的报告表明，抑郁症患者的血细胞在受到各种刺激后，细胞内游离钙浓度的升高幅度降低。因此，有人推测细胞内钙（Ca2+）稳态紊乱与情绪障碍的病理生理学有关。本研究的目的是调查在经历习得性无助范式的大鼠的脾脏T淋巴细胞中，Ca2+信号是否受到影响。习得性无助范式是一种抑郁症动物模型，具有较高的构想效度、表面效度和预测效度。此外，与未受应激的大鼠相比，我们测试了急性应激对无助大鼠Ca2+信号的影响。结果发现，有丝分裂原诱导的Ca2+信号在无助大鼠中仅呈降低趋势。然而，当无助大鼠遭受急性固定应激时，Ca2+信号明显减弱，而相同的应激源对未无助的对照大鼠的Ca2+信号没有影响。这些急性应激诱导的Ca2+信号差异与血浆皮质酮的差异增加并不平行。据推测，在无助大鼠的脾脏T淋巴细胞中评估的Ca2+信号减弱可能与无助大鼠对急性应激源的易感性增加有关。
