CALCIUM-CHANNEL BLOCKERS INHIBIT THE ANTIDIPSOGENIC EFFECT OF CENTRALINJECTIONS OF ZINC IN RATS

Previous data from our laboratory have indicated that acute third vent ricle injections of Zn2+ elicit a significant antidipsogenic response in rats in three different situations: dehydration, and central angiot ensinergic or cholinergic stimulation. In the present study we analyze d whether this response depends on voltage-dependent calcium channels. Dehydrated (14 h of water deprivation, overnight) animals received 2- mu l icv injections of zinc acetate (Zn(Ac)(2); 300 pmol/rat) after pr etreatment with the voltage-dependent calcium channel blockers gadolin ium (Gd3+; 0.03, 3.0 and 30 pmol/rat) or verapamil (VER; 0.027, 0.05 a nd 0.11 pmol/rat). Both blockers reversed the antidipsogenic effect of third ventricle injections of Zn2+ in a dose-dependent manner. After 120 min, animals pretreated with saline receiving Zn(Ac)(2) drank 3.10 +/- 0.57 ml/100 g body weight while those pretreated with Gd3+ at the highest dose displayed a water intake of 5.45 +/- 0.41 ml/100 g body weight (P<0.01). Animals pretreated with the vehicle of VER receiving Zn(Ac)(2) drank 3.15 +/- 0.45 ml/100 g while animals pretreated with V ER at the highest dose receiving Zn(Ac)(2) drank 6.16 +/- 0.62 ml/100 g (P<0.01). The antidipsogenic effect of Zn(Ac)(2) seems to be specifi c since the metal (same dose and injection procedures) did not modify food intake in rats after 24 h of food deprivation. It is suggested th at Zn2+ exerts its antidipsogenic effect by activation of mechanism(s) depending on the functional integrity of voltage-dependent calcium ch annels.