The sweet taste inhibitor methyl 4,6-dichloro-4,6-dideoxy-α-d-galactopyranoside inhibits sucrose stimulation of the chorda tympani nerve and of the adenylate cyclase in anterior lingual membranes of rats

The effects of the sweet taste inhibitor methyl 4,6-dichloro-4,6-dideoxy-α-D-galactopyranoside (MAD-diCl-Gal) and a few disaccharides, on the electrophysiological responses of the chorda tympani nerve and on adenylate cyclase in membranes prepared from the anterior tongue epithelium, were studied in rats. MAD-diCl-Gal inhibited the sucrose stimulation of whole chords tympani responses, and this inhibition was reversible. In addition, MAD-diCl-Gal inhibited the sucrose stimulation of adenylate cyclase activity in lingual (gustatory) membranes in a dose-dependent manner. High concentrations of MAD-diCl-Gal abolished the sucrose induced adenylate cyclase activity. The disaccharides sucrose, maltose, trehalose and melibiose stimulated both chords tympani nerve responses and adenylate cyclase activity. These stimulations were dose dependent. Sucrose was the most potent stimulator of the chorda tympani nerve. Other disaccharides resulted in lower responses than sucrose. Sucrose was also a more effective stimulus than maltose for adenylate cyclase activity. In contrast to electrophysiological data, trehalose and melibiose stimulated the adenylate cyclase activity to the same extent as sucrose. The results of this study support the suggestion of cAMP involvement in the cellular transduction of sweet taste in the rat.