Leumorphin is a 29-amino-acid peptide derived from preproenkephalin B. Intracerebroventricular (i.c.v.) injection of leumorphin through an implanted cannula into the lateral ventricle of rats dose-dependently inhibited water intake induced by water deprivation, angiotensin II (AII) and carbachol. This effect was partially reversed by intraperitoneal injection of naloxone, an opiate antagonist. Naloxone alone rather attenuated water intake. The antidipsogenic effect of leumorphin was very potent: 0.6 pmol of the peptide significantly inhibited AII-induced drinking. Dynorphin 1–17 was almost as potent as leumorphin in inhibiting drinking, whereas α-neo-endorphin and leucine-enkephalin (Leu-enkephalin) were far less effective. Leumorphin given i.c.v. dose-dependently enhanced eating and this effect was abolished by naloxone. Dynorphin was as potent as leumorphin in inducing feeding, whereas α-neo-endorphin and Leu-enkephalin had no significant activity when 6 nmol was used. General activity measured by an Automex was enhanced by i.c.v. injection of leumorphin but required larger amounts of the peptide than did drinking behavior. The very potent and specific effects of leumorphin and dynorphin on drinking behavior suggest that the antidipsogenic activity of these peptides is of physiological significance like their effect on feeding.

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