Disease relevance of MIF-I

• All drugs tested alone (except MIF-I) caused significant hypothermia [1].
• These results suggest that the reported beneficial effect of MIF-I in Parkinson's disease is unlikely to be due to an interaction with dopamine systems in the brain [2].
• Concomitant administration of alpha-MSH and MIF-I antagonized both the IOP increase and miosis induced by alpha-MSH [3].
• MSH and MIF-I in animal models of tardive dyskinesia [4].

Psychiatry related information on MIF-I

• Five of 8 patients with unipolar or bipolar endogenous depressions taking prolyl-leucyl-glycinamide (MIF-I), 75 mg/day, showed substantial improvement within a few days of beginning treatment compared with similar improvement in only 1 of 10 receiving 750 mg/day of MIF-I and only 1 of 5 patients taking placebo [5].
• MIF-I antagonized the initial depression of activity and potentiated the increased motor activity phase [6].

High impact information on MIF-I

• These include beta-endorphin, bombesin, MIF-I, alpha-MSH, neurotensin, TRH, and DSIP [7].
• The effects of morphine on body temperature provide some notable comparisons with beta-endorphin, as do the similarities between the effects of naloxone and MIF-I [7].
• Several analogues of L-prolyl-L-leucylglycinamide (PLG) were synthesized wherein the prolyl residue was replaced with other heterocyclic amino acid residues [8].
• 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 [9].
• Also concomitant evaluation of the effect of MIF-I on the secretion of anterior pituitary hormones which are under dopaminergic control i.e., growth hormone and prolactin, did not reveal any potentiation of the L-dopa-induced stimulus [10].

Chemical compound and disease context of MIF-I

• Pretreatment with CPZ, MIF-I, and alpha-MSH potentiated d-amphetamine-induced hypothermia in intact rats [1].
• Chlorpromazine hypothermia in the mouse was antagonised by 1-dopa but not by MIF-I; similar findings were obtained in reserpine-pretreated mice [2].
• The tripeptide, prolyl-leucyl glycine amide, a melanocyte-stimulating hormone inhibitory factor (MIF-I), which has been reported to be effective in improving symptoms of Parkinson's disease, has been compared with drugs known to activate dopamine receptors in rat and mouse brain [2].

Biological context of MIF-I

• MIF-I significantly habituated novelty-induced defecation and increased brain DA and NE levels over 5 days of drug X novelty treatment [11].
• The effects of MIF-I, beta-endorphin and alpha-MSH on d-amphetamine induced paradoxical behavioral thermoregulation: possible involvement of the dopaminergic system [12].
• Effects of MIF-I and sex differences on tonic immobility duration in the lizard, Anolis carolinensis [13].
• Unlike naloxone, MIF-I did not seem to reduce food intake in VMH-lesioned rats [14].
• Inhibition by MIF-I of alpha-MSH induced increase of intraocular pressure and miosis in rabbits [3].

Anatomical context of MIF-I

• The inhibition of the ileum produced by ethylketocyclazocine was weakly antagonized by MIF-I [6].
• The hypothalamic peptide Pro-Leu-Gly-NH2 (MIF-I) also has direct effects on the central nervous system that may include alleviation of the symptoms of Parkinson's disease [15].
• MIF-I was found to block the analgesic effects of enkephalins and also morphine in the tail-flick test but not in the vas deferens assay [14].
• Also, neither tyrosine hydroxylase nor dopa decarboxylase activity was altered in the striatum and substantia nigra of rats treated with MIF-I (20 mg/kg IP X 3, 24 hr intervals) [16].

Associations of MIF-I with other chemical compounds

• Development of a radioimmunoassay for Pro-Leu-Gly-NH2 (PLG or MIF-I): evidence that PLG is not present in rat brain [17].
• The daily pretreatment of rats with oxytocin (OXY) or MIF-I prior to ethanol (Et-OH) administration markedly altered the alcohol tolerance when tested on the fifth day of treatment [18].
• The results suggest that both MIF-I and Alaptide improved an animal's capacity to store information received through olfactory cues [19].

Gene context of MIF-I

• The effects of beta-endorphin, MIF-I, and alpha-MSH on d-amphetamine- a CPZ-induced hypothermias in rats kept at 4 degrees C were tested in three experimental groups: (a) intact; (b) rats with lesions of the olfactory tubercle; and (c) rats in which the link between the DA mesolimbic pathway and the striatum was disconnected [1].
• The results indicate that OXY and MIF-I can influence the processes of development of tolerance to some central depressive effects of Et-OH in rats [18].
• Partially purified LKs contained 2 MIF peaks, namely: MIF-I in LKs-II fraction and MIF-II in LKs-IV fraction [20].
• It also focuses on recent and new therapeutic approaches: Levodopa in combindation with a Dopa-decarboxylase inhibitor or MAO-B inhibitor, dopamine agonists and an active tripeptide: L-prolyl-L-leucylglycine amide (MIF-I) [21].

Analytical, diagnostic and therapeutic context of MIF-I

• Recently it has been suggested that MIF-I can act as an opiate antagonist for analgesia [22].
• Toxoplasma growth inhibitory factor (Toxo-GIF) in LKs, with a m.w. of 30,000 to 40,000 was found to be contained in LKs-II or MIF-I fraction after Sephadex G-100 gel filtration [23].

References