Effect of lipid-derived second messengers on electrophysiological taste responses in the gerbil

Integrated chorda tympani (CT) recordings were made to salty, sour, sweet, bitter, and glutamate tastants before and after a 4-min application of modulators of lipid-derived second messenger systems. The modulators included two membrane-permeable analogues of DAG, 1-oleoyl-2-acetyl glycerol (OAG) and dioctanoyl glycerol (DiC8); thapsigargin, which releases Ca++ from intracellular stores; ionomycin, a calcium ionophore; lanthanum chloride, an inorganic calcium channel blocker; nifedipine, a dihydropyridine calcium channel blocker; quinacrine diHCl, a phospholipase A2 antagonist; melittin, a phospholipase A2 agonist; and indomethacin, which decreases the release of prostaglandins by inhibiting the enzyme cyclo-oxygenase. The main findings were: OAG (125 microM) and DiC8 (100 microM) blocked the responses of several bitter compounds while enhancing the taste response to several sweeteners. Lanthanum chloride blocked all responses, which may be due to the fact that it blocks tight junctions. Quinacrine (1 mM) suppressed several bitter responses while enhancing the response to several sweeteners. The enhancement of sweet taste responses by DAG analogues suggests that there is cross-talk between the adenylate cyclase system and one (or more) pathways involving lipid-derived second messengers in taste cells.