Abstract

The consumption of Silkworm, Anaphe venata has been reported to be associated with a high incidence of seasonal ataxia in some parts of Nigeria. Injection of some doses of Aqueous Anaphe venata extract (AAV) by intraperitoneal route into mice has been reported to cause some behavioral changes associated with ataxia. We administered some doses of the extract (50–300 mg/kg) to mice orally in view of finding its effects on their fecal pellet output and elucidating the mechanism of action of the extract in the intestine of the mice. The extract caused a significant increase in fecal pellet weight and intestinal transit which was not dose-dependent. Doses of 200 and 300 mg/kg of the extract caused more significant reversal of loperamide-induced constipation than castor oil. Chlorpheniramine nifedipine and promethazine (1 mg/kg) blocked the increased fecal pellet output induced by the extract, while atropine and hexamethonium (1 mg/kg) did not block this effect of the extract. We concluded that AAV increased fecal pellet output of mice by increasing the peristaltic waves in their intestine via stimulation of H 1 receptors and opening of L-type calcium channels and not through the cholinergic receptors. Keywords: H 1 receptors, L-type calcium channels, intestinal transit, peristalsis

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