EFFECT OF LIPID-DERIVED 2ND-MESSENGERS ON ELECTROPHYSIOLOGICAL TASTE RESPONSES IN THE GERBIL

Integrated chorda tympani (CT) recordings were made to salty, sour, sw eet, bitter, and glutamate tastants before and after a 4-min applicati on of modulators of lipid-derived second messenger systems. The modula tors included two membrane-permeable analogues of DAG, 1-oleoyl-2-acet yl glycerol (OAG) and dioctanoyl glycerol (DiC8); thapsigargin, which releases Ca++ from intracellular stores; ionomycin, a calcium ionophor e; lanthanum chloride, an inorganic calcium channel blocker; nifedipin e, a dihydropyridine calcium channel blocker; quinacrine diHCl, a phos pholipase A(2) antagonist; melittin, a phospholipase A(2) agonist; and indomethacin, which decreases the release of prostaglandins by inhibi ting the enzyme cyclo-oxygenase. The main findings were: OAG (125 mu M ) and DiC8 (100 mu M) blocked the responses of several bitter compound s while enhancing the taste response to several sweeteners. Lanthanum chloride blocked all responses, which may be due to the fact that it b locks tight junctions. Quinacrine (1 mM) suppressed several bitter res ponses while enhancing the response to several sweeteners. The enhance ment of sweet taste responses by DAG analogues suggests that there is cross-talk between the adenylate cyclase system and one (or more) path ways involving lipid-derived second messengers in taste cells.