AJP - Regulatory, Integrative and Comparative Physiology, Vol 243, Issue 1 159-R163, Copyright © 1982 by American Physiological Society
Peptidergic regulation of stress-induced eating
J. E. Morley, A. S. Levine, S. S. Murray, J. Kneip and M. Grace
By use of the model of stress-induced (mild tail pinch) eating we have
examined the interrelationships of peptides and monoamines responsible for
regulating this behavior. We have shown that the synthetic opiate analog,
D-Ala2-Met-enkephalinamide (1 microgram), when administered
intracerebroventricularly (icv) reverses the suppressive effects of the
serotonin agonist, quipazine (40 micrograms icv), the beta-agonist,
isoproterenol (40 micrograms icv), and the alpha-antagonist, phentolamine
(150 micrograms icv), and partially reversed the effects of atropine (2.5
mg/kg sc) and the dopamine antagonist haloperidol (0.5 mg/kg sc). The
opiate antagonist naloxone (10 mg/kg sc) suppressed tail-pinch-induced
eating, and this effect could not be reversed by the GABA-agonist muscimol
(500 ng icv) nor norepinephrine (20 micrograms icv). The putative satiety
hormones cholecystokinin-octapeptide (5 micrograms/kg sc) and bombesin (5
micrograms/kg sc) suppressed stress-induced eating. The suppressive effect
of these substances was reversed by a number of known appetite stimulants
viz., D-Ala2-Met-enkephalinamide, diazepam, muscimol, and propanolol.
Norepinephrine reversed the suppressive effect of bombesin but not that of
cholecystokinin. Based on these results we present a hypothetical model to
partially explain the peptidergic-monoamine regulation of stress-induced
eating.
