Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enkephalin and other brain peptides previously have been shown to be active in the dopa potentiation test which may be considered an animal model of mental depression. A recently described model of passive immobility during swimming, also sensitive to tricyclic antidepressants, was therefore used to study a large number of naturally occurring peptides and some of their analogues. It was found that several enkephalins with no opiate activity after peripheral injection reduced the immobility and thus increased the activity of swimming rats. alpha-MSH, but not its 4--10 core or a 4--9 analogue, also caused significantly more swimming than did the diluent control. As we have previously found in several animal and clinical studies, a smaller dose of MIF-I was more effective than larger doses. The results confirm our concept of the CNS actions of brain peptides and support the suggestion that some of them, like the enkephalins, might be useful after peripheral administration in mental depression or other CNS disorders.
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PMID:Enkephalin and other peptides reduce passiveness. 73 38

Experiments on cats revealed an emotiotropic action of melanostatin on the original spectrum of emotional reactivity, similar to the effects of L-DOPA and amantadin. The drug does not possess an antidepressant action proper but activates the aggressive-defensive behaviour in experimental reserpine depression and reduces the provocation-induced aggressive behaviour in experimental haloperidol depression. In reserpinized mice, it antagonizes reserpine hypothermia, increases muscle tone and eliminates ptosis. It decreases haloperidol-induced catalepsia. Melanostatin increases the brain level of dopamine and its metabolite, homovanilic acid.
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PMID:[Psychopharmacologic spectrum of melanostatin]. 610 96

Peptides regulate neuroendocrine and limbic system functioning in animals. Both systems show major disturbances in the affective disorders. Only thyrotropin releasing hormone (TRH), luteinizing hormone releasing hormone (LHRH), melanocyte stimulating hormone inhibiting factor (MIF-I), and 1-desamino-8-D-arginine vasopressin (DDAVP) have been administered to affectively ill patients. The thyroid stimulating hormone (TSH) response to TRH is blunted (less than or equal to 5 microU/ml) in some patients during depression and mania and in alcoholics. The blunted response may be an important tool in the diagnosis of depression and mania. Together with other demonstrated endocrine abnormalities, the blunted TSH response suggests a profound alteration in the physiological relationship between the central nervous system and the anterior pituitary in affective illness. Behaviorally, TRH, LHRH, DDAVP, and MIF-I have general activating effects in human that have not yet been demonstrated to be restricted to or specific to affective illness. The interpretation of peptide challenges, however, in the study of affective illness is obfuscated by the small number of patients used and the multiple sites that peptides at pharmacological doses may affect.
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PMID:Peptide challenges in affective illness. 611 86

Chronic administration of 1-prolyl-l-leucyl-glycinamide (MIF-I) to mice slightly reduced morphine's antinociceptive activity in the hot-plate test and modified the biphasic motor activity response to morphine. MIF-I antagonized the initial depression of activity and potentiated the increased motor activity phase. Chronic treatment of rats with MIF-I prevented morphine's antinociceptive activity in the tail flick tests. MIF-I partly antagonized the inhibition by morphine of the coaxially stimulated guinea-pig ileum preparation. The inhibition of the ileum produced by ethylketocyclazocine was weakly antagonized by MIF-I. In contrast, MIF-I had no effect on the inhibition of the stimulated mouse vas deferens produced by Leu-enkephalin. The findings show that MIF-I weakly and selectively inhibits mu-type opiate receptors which suggests that MIF-I could be an endogenous inhibitor of opiate receptors.
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PMID:Opiate receptor antagonism by L-prolyl-L-leucyl-glycinamide, MIF-I. 611 39

A double-blind 28 day study was conducted to compare the anti-depressant efficacy of MIF-I with that of imipramine. Twenty patients hospitalized with major depressive illness participated. Clinical responses were measured by using the Hamilton Depression Rating Scale, the Global Severity of Illness Scale, the Zung Self-Rating Depression Scale as well as the 100 mm line self-rating for depression. The results indicate that MIF-I was at least as effective as imipramine in this study, and that its anti-depressive effect was a rapid and often dramatic one.
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PMID:Rapid clinical effectiveness of MIF-I in the treatment of major depressive illness. 613 56