Peptidergic regulation of stress-induced eating

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.