Calmodulin-induced feeding in the cat: attenuation by calcium chelator EGTA

Cannulas for intracerebroventricular injection of calmodulin (CaM), Ca2+, and other substances were implanted stereotaxically in the cat. Postoperatively, measures of food intake were taken on each day during a 1.0-h interval until feeding had stabilized. Then the Ca2+-binding protein, CaM, was infused intracerebroventricularly into the fasted cat 15 min before the 1.0-h feeding session. CaM (0.15-0.60 nM) significantly enhanced the animal's normal feeding response, which was accompanied by a slight decline in body temperature. Infusion of 6.25-50.0 mM excess Ca2+ reduced body temperature in a concentration-dependent manner with food intake augmented by 6.25-25.0 mM Ca2+. Chelation of Ca2+ in the brain with 0.5-2.5 mM ethyleneglycol-bis(beta-aminoethyl ether)-N,N'-tetra-acetic acid (EGTA) similarly infused intracerebroventricularly into the cat simultaneously suppressed feeding and elevated core temperature. Threshold doses of EGTA selectively attenuated CaM-induced eating but not feeding elicited by the catecholamine neurotransmitter, norepinephrine. Overall these results suggest that CaM, by complexing with cellular Ca2+, could serve as an intermediary factor in governing steady-state activity of neurons in the brain. In turn, this essential cation may mediate specific regulatory processes within the diencephalon that underlie the postulated "setpoint" mechanism for the control of feeding.