Effect of chronic treatment with agomelatine or venlafaxine on depolarization-evoked glutamate and GABA release and on SNARE complex accumulation in hippocampal synaptosomes. A) 15 mM KCl-evoked glutamate and GABA release and 0.5 mM ionomycin-evoked glutamate release from hippocampal synaptosomes of rats chronically treated with vehicle (CNT), agomelatine (AGO) or venlafaxine (VFX). B) Representative Western Blot of SNARE complexes in hippocampal synaptosomes visualized with a monoclonal antibody for syntaxin-1. The two SNARE complexes at approximately 100 and 80 kDa and syntaxin-1 monomer are indicated by arrows. Each single SNARE complex was normalized on monomeric syntaxin-1 in the same lane. C) Quantitation of syntaxin-1 in CNT and rats chronically treated with VFX or AGO. D) Quantitation of normalized 100 kDa SNARE complex in CNT rats and rats chronically treated with VFX or AGO. E) Quantitation of normalized 80 kDa SNARE complex in CNT rats, and rats chronically treated with VFX or AGO. All data are expressed as mean ± SEM. * p<0.05, ** p<0.01 vs. CNT rats, Newman-Keuls post-hoc tests following one-way ANOVA (n = 6–10 rats/group in duplicate).
Milanese et al. BMC Neuroscience 2013 14:75 doi:10.1186/1471-2202-14-75