Abstract
Introduction: Hausa people of north-western Nigeria were reported to utilize the plant Adansonia digitata for the management of depressive illnesses in an ethnobotanical survey. Thus, this study aimed to establish the mechanism(s) via which methanol stem bark extract of A. digitata (MEAD) exhibits antidepressant activity in mice.
Methods: Antidepressant activity of MEAD was evaluated using tail suspension test (TST) at doses of 250, 500 and 1000 mg/kg. For the mechanistic studies, mice were pre-treated with sulpiride (50 mg/kg), prazosin (1 mg/kg), yohimbine (1 mg/kg), metergoline (1 mg/kg), cyproheptadine (3 mg/kg), L-arginine (50 mg/kg), N omega-nitro-L-arginine (L-NNA; 50 mg/kg), atropine (1 mg/kg) and naloxone (2 mg/kg) 15 minutes prior to MEAD (1000 mg/kg) administration, then antidepressant activity was assessed using TST one hour later. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc test.
Results: The extract (at doses of 250, 500 and 1000 mg/kg) significantly (P < 0.05) and dose-dependently decreased the duration of immobility in the TST. Sulpiride (D2 receptor antagonist), prazosin and yohimbine (α1 and α2 receptor antagonists, respectively), metergoline and cyproheptadine (5-HT1 and 5-HT2 receptor antagonists, respectively) significantly (P < 0.05) reversed the antidepressant effect of MEAD. On the other hand, L-NNA (NOS inhibitor) augmented the antidepressant effect of MEAD while L-arginine (nitric oxide substrate) had no effect on MEAD. However, atropine (muscarinic receptor antagonist) significantly (P < 0.01) augmented the antidepressant effect of MEAD.
Conclusion: The antidepressant activity of methanol stem bark extract of A. digitata was established to be via the monoaminergic, nitric oxide and cholinergic pathways.