A single administration of Neurotropin reduced the elongated immobility time in the forced swimming test of rats exposed to repeated cold stress

行为绝望测验 丙咪嗪 海马体 抗抑郁药 医学 神经营养因子 内科学 脑源性神经营养因子 内分泌学 扁桃形结构 前额叶皮质 麻醉 心理学 精神科 病理 替代医学 受体 认知
作者
Teruaki Nasu,Asako Kubo,Luis F. Queme,Kazue Mizumura
出处
期刊:Behavioural Pharmacology [Lippincott Williams & Wilkins]
卷期号:30 (7): 547-554 被引量:12
标识
DOI:10.1097/fbp.0000000000000488
摘要

Many people suffer from a major depressive disorder, and chronic pain conditions are often associated with depressive symptoms. Neurotropin, an extract from the inflamed skin of rabbits inoculated with vaccinia virus, has been used for pain relief. Decrease of brain-derived neurotrophic factor (BDNF) in the brain is one of the proposed mechanisms for the major depressive disorders, and Neurotropin has been reported to restore the decreased BDNF in the hippocampus. In this experiment, we examined whether Neurotropin had an antidepressant-like effect in a model of fibromyalgia and whether BDNF in the brain was altered after repeated cold stress (RCS) and Neurotropin treatment. Rats were exposed to RCS because these animals have been used as a model for fibromyalgia syndrome. Depression-like behavior was evaluated using elongation of immobility time in a forced swimming test. Change in expression of BDNF in the brain was also examined by western blot analysis of several brain areas. Depression-like behavior in the forced swimming test was significantly increased 10–14 days after RCS, and this increase was reversed by a single injection of an antidepressant, imipramine, but not by PBS. Increased depression-like behavior was also dose-dependently suppressed by a single administration of Neurotropin (50–200 NU/kg, subcutaneously). BDNF expression was not changed in the brain areas examined (hippocampus, amygdala, prefrontal cortex, and striatum) either after RCS or by Neurotropin injected after RCS. These results suggest that RCS induced a depression-like state in rats, and Neurotropin reversed this state. However, we did not observe a BDNF-related mechanism for these effects.

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