Role of serotonergic and dopaminergic neurotransmission in the antidepressant effects of malt extract

The benefit of malt extract in clonidine-induced depression was previously reported. The present study aimed to explore its mechanism of action. Animals were classified into normal and depressed rats. Induction of depression was done by i.p. injection of clonidine (0.8 mg/kg) daily for 7 days. Depressed rats were sub-classified into 6 groups treated for one week as follows: Group I received 1% tween 80 p.o. (control group); the remaining groups received malt extract (1250 mg/kg; p.o) alone or preceded (30 min) by i.p. injection of spiperone (0.03 mg/kg), sulpiride (7.5 mg/kg), phentolamine (5 mg/kg) or propranolol (7.5 mg/kg), respectively. Forced swimming test (FST) was carried out 24 h thereafter. Brains were isolated for estimation of serotonin, dopamine and norepinephrine contents as well as inflammatory and oxidative stress biomarkers. Clonidine increased total immobility time and decreased struggling time in FST parallel to alterations in brain neurotransmitters, inflammatory and oxidative stress markers. Treatment with malt extract reversed clonidine-induced behavioral and neurochemical changes. Such effects were partly antagonized in groups pre-treated with spiperone or sulpiride. Serotoninergic and dopaminergic transmission are involved in the antidepressant effects of malt extract in addition to its antioxidant and anti-inflammatory effects.