Summary
In this study, we show that female African malaria mosquitoes Anopheles gambiae (Giles) starved for 3-5 hours start to engorge on sucrose at concentrations between 50 to 75 mM. Half of the feeding response (ED50) is reached at 111 mM and the maximum response (0.4 mg) occurs from 146 mM (5% m/v). Two receptor cells in a trichoid sensillum of the labellum, called the 'sucrose' and the 'water' neurones, are activated by sucrose and water, respectively. The electrophysiological response of the sucrose receptor cell starts well below the level of sugar necessary to induce feeding. An. gambiae is most sensitive to small increments in sucrose concentration up to 10 mM with a response plateau at a maximum frequency of 53 spikes per 2 s from 50 mM, the concentration at which female An. gambiae start to engorge on sucrose. Fructose has a mild phagostimulatory effect on An. gambiae, whereas no significant differences in meal sizes between water and glucose were found. However, when 146 mM fructose plus glucose are mixed, the same engorgement as on 146 mM sucrose is observed. Likewise, even though the sucrose receptor cell is not activated by either fructose or glucose alone, equimolar solutions of fructose plus glucose activate the neurone. We conclude that there is a behavioural and a neurophysiological synergism between fructose and glucose, the two hexose sugars of sucrose. We show that bitter tasting products for humans have a deterrent effect on feeding in An. gambiae. When 1 mM quinidine, quinine or denatonium benzoate is added to 146 mM sucrose, feeding is almost totally inhibited. The effect of berberine is lower and no significant inhibition on engorgement occurs for caffeine. The deterrent effect depends on concentration for both quinine and quinidine. Capillary feeding experiments show that contact chemosensilla on the mouthparts are sufficient for the detection of sucrose and bitter products. The feeding assay findings with deterrents correlate with the neurophysiological responses of the sucrose and the water labellar neurones which are both inhibited by the bitter compounds denatonium benzoate, quinine and berberine between 0.01 and 1 mM, but not by the same concentrations of caffeine which has no effect on feeding. In conclusion, sucrose which stimulates feeding activates the labellar sucrose neurone whereas feeding deterrents inhibit both the sucrose and the water neurones. This study provides an initial understanding of the physiological mechanisms involved in sugar feeding in An. gambiae and shows how some bitter products interfere with it.
