Background. Agomelatine is a melatonergic receptor agonist and a 5HT2C receptor antagonist that has shown ntidepressant 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.

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 / D. Tardito, M. Milanese, T. Bonifacino, L. Musazzi, A. Mallei, E. Mocaer, C. Gabriel, G. Racagni, M. Popoli, G. Bonanno. - In: BMC NEUROSCIENCE. - ISSN 1471-2202. - 11(2010), pp. 68.68.1-68.68.4. [10.1186/1471-2202-11-68]

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

D. Tardito
Primo
;
L. Musazzi;A. Mallei;G. Racagni;M. Popoli
Penultimo
;
2010

Abstract

Background. Agomelatine is a melatonergic receptor agonist and a 5HT2C receptor antagonist that has shown ntidepressant 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.
Settore BIO/14 - Farmacologia
2010
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/145842
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