AJP - Regulatory, Integrative and Comparative Physiology, Vol 246, Issue 3 375-R379, Copyright © 1984 by American Physiological Society
Calmodulin-induced feeding in the cat: attenuation by calcium chelator EGTA
R. D. Myers and T. F. Lee
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.
