阿戈美拉汀通过协同发挥褪黑素能和 5-HT2C 受体依赖途径阻断应激诱导的大鼠前额叶/额叶皮质谷氨酸释放增加。
Blockade of stress-induced increase of glutamate release in the rat prefrontal/frontal cortex by agomelatine involves synergy between melatonergic and 5-HT2C receptor-dependent pathways.
机构信息
Center of Neuropharmacology - Department of Pharmacological Sciences and Center of Excellence on Neurodegenerative Diseases, University of Milano, Italy.
出版信息
BMC Neurosci. 2010 Jun 3;11:68. doi: 10.1186/1471-2202-11-68.
BACKGROUND
Agomelatine is a melatonergic receptor agonist and a 5HT2C receptor antagonist that has shown antidepressant efficacy. In order to analyze separately the effect of the two receptorial components, rats were chronically treated with agomelatine, melatonin (endogenous melatonergic agonist), or S32006 (5-HT2C antagonist), and then subjected to acute footshock-stress.
RESULTS
Only chronic agomelatine, but not melatonin or S32006, completely prevented the stress-induced increase of glutamate release in the rat prefrontal/frontal cortex.
CONCLUSIONS
These results suggest a potential synergy between melatonergic and serotonergic pathways in the action of agomelatine.
背景
阿戈美拉汀是一种褪黑素受体激动剂和 5HT2C 受体拮抗剂，具有抗抑郁作用。为了分别分析这两种受体成分的作用，大鼠接受了阿戈美拉汀、褪黑素（内源性褪黑素激动剂）或 S32006（5-HT2C 拮抗剂）的慢性治疗，然后进行急性足底电击应激。
结果
只有慢性阿戈美拉汀，而不是褪黑素或 S32006，完全阻止了应激引起的大鼠前额叶/额叶皮质谷氨酸释放的增加。
结论
这些结果表明，阿戈美拉汀的作用中存在褪黑素和 5-羟色胺能途径之间的潜在协同作用。
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