Prolyl-leucyl-glycinamide Research Articles

Effects of desglycinamide( 9)-lysine( 8)-vasopressin and prolyl-leucyl-glycinamide on oral ethanol intake in the rat

Rats given ethanol in their drinking water at a concentration that permitted adequate fluid intake gradually accepted higher concentrations and consumed larger amounts of ethanol. These increases were augmented when daily subcutaneous injections of 1 μg of desglycinamide 9-lysine 8-vasopressin (DGLVP) or 10 μg of prolyl-leucyl-glycinamide (PLG) were given concomitantly. Nonsignificant changes in ethanol consumption were seen with injections of 1 μg PLG, or 0.42 or 42 μg of lysine 8-vasopressin (LVP). In a second experiment 4 μg DGLVP given every second day as a long-acting zinc phophate complex, commencing after the increases in ethanol intake had taken place, failed to produce any change in ethanol consumption subsequently. In both Experiments 1 and 2, the rats were switched from forced ethanol intake to achoice between ethanol and tap water. On these tests there was only marginal evidence of peptide-produced changes in ethanol intake.

Antagonism of morphine-induced catalepsy by L-prolyl-L-leucyl-glycinamide

In vew of the recently demonstrated extra-endocrine central actions of hypothalamic releasing hormones, we have investigated the effects of prolyl-leucyl-glycinamide (PLG) and thyrotropin releasing hormone (TRH) on morphine-induced catalepsy. Although acute administration of PLG (10 mg kg − s.c.) slightly attenuated the cataleptic response, chronic PLG treatment (10 mg kg − s.c. for 10 days) virtually abolished morphine-induced catalepsy. TRH, administered subcutaneously, exhibited little or no anti-cataleptic activity. These results are discussed in relation to the possible central site of narcotic-induced catalepsy and the therapeutic potential of PLG in Parkinson's disease.

Prolyl-leucyl-glycinamide (PLG); regional effects on α-MPT-induced catecholamine disappearance in rat brain

Prolyl-leucyl-glycinamide (PLG); regional effects on α-MPT-induced catecholamine disappearance in rat brain

The Modulation of Memory Processes by Vasotocin, the Evolutionarily Oldest Neurosecretory Principle

Publisher Summary This chapter presents the experiments to show that effects on consolidation, retrieval, and amnesia (repression) are present in various parts of the oldest neurohypophysial principle, vasotocin. The different behavioral effects of the neurohypophysial hormones and their fragments suggest that they act as precursor molecules for neuropeptides that modulate memory processes. If this were true, one would expect that specific enzymes that generate the linear and the ring portion of these molecules would be present in the brain. It has been found that a membrane-bound hypothalamic exopeptidase is able to generate MIF—prolyl-leucyl-glycinamide (PLG)—from oxytocin that inhibits the release of melanocyte-stimulating hormone (MSH). Such enzymes have not been detected for vasopressin. There are enzymes in the brain that inactivate vasopressin by hydrolysis of peptide bonds in the acyclic position of the molecule, but no enzymes have been identified so far that remove the proline residue to yield pressinamide. The ancestral molecule of the neurohypophysial hormones vasopressin and oxytocin, which generated these hormones during evolution, is arginine 8 -vasotocin (AVT). This peptide is found in the neurohypophysis of all non-mammalian vertebrates and in the pineal gland of mammals.

DOPA potentiation in ablated animals and brain levels of biogenic amines in intact animals after prolyl-leucylglycinamide.

Prolyl-leucylglycinamide (PLG) wasfound to augment the behavioral effects of DOPA and pargyline in mice and rats when administered orally. Behavioral studies in the DOPA test with repeated doses of PLG over 5 days did not reveal either cumulative or tolerance effects. Ablation of the pituitary, adrenals, ovaries, testes, pineal, spleen, thyroid, parathyroid, one kidney, or thymus did not disrupt this behavioral potentiation of DOPA by PLG. Furthermore, a neurochemical study in mice and rats did not show any significant increase in the content of dopamine, norepinephrine, or serotonin in the mouse brain. These studies suggest that PLG may have direct stimulatory effects on the mouse brain which do not require the presence of a number of somatic organs.