Anti-depressant-like effect of vitexin in BALB/c mice and evidence for the involvement of monoaminergic mechanisms

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The present study was designed to investigate the putative effect of vitexin, a flavone C–glucoside present in some drugs, medicinal plants and nutraceuticals, on the central nervous system. Vitexin (10–30mg/kg) did not show significant alterations in the behaviour of mice tested in hole-board, plus-maze or activity cage tests. However, immobility time of the mice significantly reduced by vitexin administrations in both the tail-suspension and modified forced swimming tests. The anti-immobility effect of vitexin in the tail-suspension test was reversed with α-methyl-para-tyrosine methyl ester (AMPT, an inhibitor of catecholamine synthesis, 100mg/kg, i.p.), yohimbine (an α2-adrenoceptor antagonist, 1mg/kg, i.p.), NAN 190 (a 5-HT1A antagonist, 0.5mg/kg, i.p.), SCH 23390 (a dopamine D1 antagonist, 0.05mg/kg, s.c.) and sulpiride (a dopamine D2/D3 antagonist, 50mg/kg, i.p.). The same effect was not reversed, however, by p-chlorophenylalanine methyl ester (PCPA; an inhibitor of serotonin synthesis 100mg/kg, i.p., administered for 4 consecutive days), ketanserin (a 5-HT2A/2C antagonist, 1–4mg/kg, i.p.), ondansetron (a 5-HT3 antagonist, 0.1–0.4mg/kg, i.p.), prazosin (an α1-adrenoceptor antagonist, 1–4mg/kg, i.p.), or propranolol (a non-selective β-adrenoceptor antagonist, 5–20mg/kg, i.p.). These results suggest that the anti-depressant-like effect of vitexin is mediated through an increase in catecholamine levels in the synaptic cleft as well as through interactions with the serotonergic 5-HT1A, noradrenergic α2, and dopaminergic D1, D2, and D3 receptors. To our knowledge, this is the first study to show findings that indicate an anti-depressant-like effect of vitexin and its underlying mechanisms.