Naghdi Nasser, Asadollahi Ali
Department of Physiology and Pharmacology, Pasteur Institute of Iran, Pasteur Ave., Tehran 13164, Iran.
Behav Brain Res. 2004 Aug 12;153(1):1-6. doi: 10.1016/j.bbr.2003.10.027.
In addition to their well-known genomic effects via intracellular receptors, androgens rapidly alter neuronal excitability through a nongenomic pathway. The nongenomic effect of testosterone, as the main androgen, apart from its traditional effects, was assessed in one of the fundamental centers of learning and memory, the hippocampus, on long-term memory (LTM) in passive avoidance conditioning. Different doses of testosterone enanthate (T) or testosterone-BSA (T-BSA) bilaterally were injected into the CA1 region of the hippocampus 15 min before shock delivery (1 mA during 5 s) in a two-compartment passive avoidance apparatus. After 24 h, animals were tested for passive avoidance retrieval. Bilateral injection of 20 microg T or 55 microg T-BSA into the CA1 significantly decreases step-through latency. Therefore, it seems that testosterone can impair LTM in passive avoidance conditioning both via intracellular receptors and through nongenomic pathway.
除了通过细胞内受体产生众所周知的基因组效应外,雄激素还通过非基因组途径迅速改变神经元兴奋性。作为主要雄激素的睾酮,除了其传统作用外,其非基因组效应在学习和记忆的一个基本中枢——海马体中,针对被动回避条件反射中的长期记忆(LTM)进行了评估。在双室被动回避装置中,于电击(5秒内1毫安)前15分钟,将不同剂量的庚酸睾酮(T)或睾酮-牛血清白蛋白(T-BSA)双侧注射到海马体的CA1区域。24小时后,对动物进行被动回避恢复测试。向CA1双侧注射20微克T或55微克T-BSA可显著缩短穿通潜伏期。因此,似乎睾酮可通过细胞内受体和非基因组途径损害被动回避条件反射中的长期记忆。