EN
Benzodiazepines (BZ) have long been known to impair memory as a result of their action at γ-aminobutyric acid (GABA)A receptors. But it is not clear what stages of memory (acquisition, consolidation or retrieval) are affected by BZ. Flunitrazepam (FNZ) – one of the BZ drug – has highly ability to cause amnesia and it is known as a daterape drug. Recent evidence suggests that agmatine (AGM), the metabolite of L-arginine, exists in the mammalian brain and can modulate behavior function, including learning and memory. The mechanism of AGM action has not been completely explained. Many studies showed that AGM regulates the L-arginine:nitric oxide(NO):cGMP pathway because AGM is a metabolite of L-arginine and AGM can inhibit neuronal NO synthase. Our previous research has indicated that modulators of L-arginine:NO:cGMP affected BZ-induced memory impairment. The aim of this study was to assess the role of AGM in the amnesic effects of FNZ in the modified elevated plus-maze task (mEPM) in mice. Our experiments showed that FNZ (0.05 and 0.1 mg/kg, sc) disrupted acquisition and consolidation of memory in mice. The amnesic properties of FNZ were prevented by AGM (20 mg/kg, ip – the acquisition stage) and (5, 10 and 20 mg/ kg, ip – the consolidation stage). The above results suggest that AGM may be involved in the amnesic effects of FNZ.