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慢性文拉法辛、奥氮平和尼古丁对海马和皮质脑源性神经营养因子(BDNF)浓度的影响。

Influences of chronic venlafaxine, olanzapine and nicotine on the hippocampal and cortical concentrations of brain-derived neurotrophic factor (BDNF).

机构信息

Department of Pharmacoeconomics and Social Pharmacy, University of Medical Sciences, Dabrowskiego 79, PL 60-529, Poland.

出版信息

Pharmacol Rep. 2009 Nov-Dec;61(6):1017-23. doi: 10.1016/s1734-1140(09)70163-x.

Abstract

Brain-derived neurotrophic factor (BDNF) is a key neurotrophic factor in the brain. It plays an important role in the etiopathogenesis and pharmacotherapy of mental disorders, such as depression or schizophrenia. In recent years, studies have shown that cognitive processes, which are impaired in the course of mental disorders, significantly change BDNF levels in the brain. Administered to rats at a dose of 20 mg/kg (b.d. for 5 weeks), venlafaxine (VEN) increases BDNF levels in the hippocampus and cortex, compared to controls. Administered at a dose of 0.5 mg/kg (b.d. for 5 weeks), olanzapine (OLA) significantly increases BDNF levels in both the cortex and the hippocampus. Similarly, nicotine (NIC) administered at a dose of 0.2 mg/kg (b.d. for 5 weeks) increases BDNF concentrations in both the hippocampus and the cortex. Combined administration of NIC with VEN or OLA does not increase BDNF levels in the hippocampus or the cortex. Based on our study, it can be claimed that BDNF mediates behavioral responses only to drugs used individually and participates in the antidepressant and procognitive effects of the study compounds. BDNF also initiates plastic changes and modulation of synaptic activity in rat brains.

摘要

脑源性神经营养因子(BDNF)是大脑中的一种关键神经营养因子。它在精神障碍(如抑郁症或精神分裂症)的病因和药物治疗中起着重要作用。近年来的研究表明,在精神障碍过程中受损的认知过程会显著改变大脑中的 BDNF 水平。给予大鼠 20mg/kg 剂量(连续 5 周每天两次)的文拉法辛(VEN)会增加海马体和皮质中的 BDNF 水平,与对照组相比。给予 0.5mg/kg 剂量(连续 5 周每天两次)的奥氮平(OLA)会显著增加皮质和海马体中的 BDNF 水平。同样,给予 0.2mg/kg 剂量(连续 5 周每天两次)的尼古丁(NIC)会增加海马体和皮质中的 BDNF 浓度。NIC 与 VEN 或 OLA 联合给药不会增加海马体或皮质中的 BDNF 水平。基于我们的研究,可以声称 BDNF 仅介导对单独使用的药物的行为反应,并参与研究化合物的抗抑郁和认知促进作用。BDNF 还会启动大鼠大脑中突触活动的可塑性变化和调节。

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