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DOI: 10.1055/s-0033-1351965
Antidepressant and anxiolytic effects of methanolic root extract of Cnestis ferruginea Vahl ex DC (Connaraceae): Role of monoaminergic and GABAergic systems
The root decoction of Cnestis ferruginea (CF) Vahl DC (Connaraceae) is used in African medicine in the treatment of psychiatric disorders [1]. This study presents the antidepressant and anxiolytic effects of methanolic root extract of CF.
The antidepressant effect was studied using the forced swimming (FST) and tail suspension tests (TST) while the hole-board, elevated plus maze (EPM) and light/dark tests were used to evaluate the anxiolytic effect.
Acute treatment with CF extract reduced (P < 0.001) the duration of immobility in FST and TST with peak effects observed at 100 mg/kg in comparison to control animals. The efficacy of the extract was found to be comparable to that of imipramine and fluoxetine (20 mg/kg; p.o.) in FST and TST respectively.
The pretreatment of mice with metergoline (4 mg/kg, i.p., a 5-HT2 receptor antagonist) and reserpine (2 mg/kg, i.p., biogenic amine depleter) 15 mins before the administration of CF (100 mg/kg; p.o.) prevented (P< 0.05) its antidepressant effect in the FST. However, pretreatment with prazosin (62.5 µg/kg, i.p., α1-adrenoceptor antagonist), yohimbine (1 mg/kg, i.p., α2-adrenoceptor antagonist), sulpiride (50 mg/kg, i.p., D2 receptor antagonist), atropine (1 mg/kg, i.p.) did not prevent this effect.
CF (25, 50 and 100 mg/kg; p.o) reduced (P< 0.05) anxiety by increasing the number of head-dips in hole-board test, the time spent on the open arms in the EPM, and the exploration of light chamber in the light/dark test. Pretreatment with flumazenil (3 mg/kg, i.p., GABA receptor antagonist) or cyproheptadine (4 mg/kg, i.p.) 15 min before CF (100 mg/kg; p.o.) reversed (p < 0.05) the anxiety-like behavior of the extract in EPM.
It is concluded from the results obtained that Cnestis ferruginea produces its antidepressant effect through interaction with 5-HT2 receptor and probably through the release of biogenic monoamines while the anxiolytic effect is produced via GABA receptor.
Reference:
[1] Garon, D., et al., (2007). Toxicon 50: 189 – 195.