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Alpha-MSH and MIF-2 effects on serotonin levels and accumulation in various rat brain areas.

Levels as well as accumulation of serotonin (5-HT) were measured in various brain regions of the rat after administration of alpha-melanocyte-stimulating hormone (MSH) and Pro-Leu-Gly-NH2 (MIF-I). The method used in determining the serotonin measured both 5-OH-tryptamine (5-HT) and 5-methoxytryptamine (5-MT). No statistically significant changes in levels or accumulation of serotonin after pargyline injection were found when unoperated control rats were treated with either MSH or MIF-I. Similar treatment of hypophysectomized rats indicated that both peptides significantly (p less than 0.05) lowered serotonin accumulation only in the area of the frontal cortex; a similar but smaller, not statistically significant, decrease was seen in the hypothalamus and hippocampus of the hypophysectomized rat. Since only hypophysectomized rats were affected, no correlation between the behavioral effects of these peptides (which has been found to occur in both unoperated and hypophysectomized rats) and the biochemical changes could be made.

Animals↗
PubMed1976

MIF, TRH, and simian social and motor behavior.

MSH-release-inhibiting factor (MIF) and thyrotropin-releasing hormone (TRH) both have been reported to modify mood and activity in man. These two hypothalamic peptides were given intramuscularly across a 1000-fold dose range to 5 juvenile male M. nemestrina monkeys living in a social group. Motor activity was recorded automatically, and an observer counted various social behaviors. MIF increased motor activity for up to 11 hr. It decreased quiet foraging behavior, but did not change behaviors of social interaction. TRH did not stimulate motor behavior; high doses strongly suppressed it and produced apparent somatic distress. TRH increased behaviors of quiet rest and association and decreased environment exploration and low-intensity dominance behaviors. The lowest dose of TRH increased social play. Two monkeys showed repetitive, stereotyped behaviors even in baseline observations, and certain doses of TRH and MIF may have increased the frequency of these behaviors.

Animals↗
PubMed1976

A comparison between a melanocyte-stimulating hormone inhibitory factor (MIF-I) and substances known to activate central dopamine receptors.

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. Unlike apomorphine, amphetamine and amantadine it was incapable of producing sterotyped behaviour in the rat and unlike 1-dopa it was also ineffective in rats pretreated with the monoamineoxidase inhibitor mebanazine. Neither did it potentiate apomorphine nor amphetamine in this test. MIF-I did not antagonise chlorpromazine-induced loss of locomotor activity in mice, an effect which was antagonised by apomorphine, amphetamine and amantadine. Chlorpromazine hypothermia in the mouse was antagonised by 1-dopa but not by MIF-I; similar findings were obtained in reserpine-pretreated mice. 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.

Amantadine↗
PubMed1976

Possible association of increased rat behavioral effects and increased striatal dopamine and norepinephrine levels during the DOPA-potentiation test.

Previous reports have indicated that alpha-MSH release inhibiting hormone (MIF-1) increased the behavior occurring as a result of the dihydroxyphenylalanine (DOPA) potentiation test [3,7]. This study was undertaken to see whether dopamine (DA) or norepinephrine (NE) levels likewise increased in the test animals. The DOPA potentiation test was performed as follows: 2-4 hr before behavior measurement, 40 mg/kg of the monoamine oxidase inhibitor pargyline HCl was given orally. Two hr later this was followed by the intraperitoneal (IP) injection of MIF-1 at doses of 0.1, 0.3 or 1.0 mg/kg. Behavioral measurement was begun after the IP injection of 200 mg/kg of dl-DOPA 1-2 hr after the MIF-1. The parameters included social interaction, aggressiveness, fighting, ataxia, jumping, defecation, urination and salivation. The animals were beheaded while the behavior was still increased and the striatal area removed, placed in aluminum foil, and kept at -50 degrees C until assayed. In general, especially among the younger animals, a significant correlation (p=0.05 to p=0.01) was found between the increased behavioral responses to MIF-I and the rise in DA. Because of a few exceptions to this correlation the possibility is suggested that MIF-I might also affect behavior by acting directly on the postsynaptic membrane thus bypassing any change in NE or DA which is known to increase cycli AMP in the striatum.

Animals↗
PubMed1977

Formaldehyde-induced fluorescence in the telencephalon and diencephalon of the eel (Anguilla anguilla l.). A fluorescence-microscopic and microspectrofluorometric investigation with special reference to the innervation of the pituitary.

In the telencephalon and diencephalon of the eel (Anguilla anguilla L.) formaldehyde-induced fluorescence was studied microscopically and microfluorometrically with special emphasis on the innervation of the pituitary. In the telencephalon fluorescent fibers contained predominantly noradrenaline fluorophores. Fluorescent nuclei could not be established. In the diencephalon fluorescent perikarya were found in: (1) the paraventricular organ (PVO), possessing either dopamine or, to a lesser extent, serotonin fluorophores; (2) the PVO-accompanying group, exhibiting spectral data resembling those of noradrenaline fluorophores; (3) the nucleus hypothalami anterior (NHA), a small paired group of catecholamine-containing cells posterior to the commissura transversa.--The nucleus lobi inferioris exhibited a high density of delicate, most probably dopamine-containing terminals, while fibers surrounding this nucleus contained noradrenaline fluorophores. A high density of fluorescent terminals containing dopamine and/or noradrenaline was found in the habenular complex. Fluorescent terminals in the pituitary contained fluorophores resembling either dopamine or noradrenaline. Fluorescent tracts entered the pituitary from different directions. A rostral, unpaired tract enters the neurointermediate lobe, as also verified experimentally. The rostral pars distalis receives two paired tracts, one from a rostral and one from a dorsal direction. The proximal pars distalis also receives two paired tracts, one from a dorsal and one from a posterior direction.

Anguilla↗
PubMed1977

Comparison of thyrotropin-releasing hormone with melanocyte-stimulating-hormone-release-inhibiting factor as pentobarbital antagonists in monkeys.

Thyrotropin-releasing hormone (TRH), 0.1 mg/kg, i.m., significantly counteracted pentobarbital narcosis in six monkeys, but melanocyte-stimulating-hormone-release-inhibiting factor (MIF), 0.1 mg/kg i.m., did not. Earlier dose-response studies in unanesthetized monkeys had shown that this dose of MIF stimulated motor activity; this dose of TRH had shown no stimulant effect, but a higher dose depressed activity. Thus, an MIF dose that stimulates unanesthetized monkeys does not reverse pentobarbital narcosis; a TRH dose that by itself is neither stimulant nor depressant does partially reverse pentobarbital narcosis.

Animals↗
PubMed1977

On the optimal dosage of Pro-Leu-Gly-NH2 (MIF) in neuropharmacological tests and clinical use.

Pro-Leu-Gly-NH2 (MIF) inhibits the tremor induced by oxotremorine. Objective measurement of this tremor permits the drawing of a dose-effect curve. The inhibitory effect of the peptide increases linearly with increasing doses until an optimum is reached (between 30 and 40 mg/kg i.p.). At still higher doses the peptide is inactive. The same phenomenon is observed with analogues of MIF. This finding may have important bearings on the interpretation of clinical and experimental data obtained with MIF.

Animals↗
PubMed1976

Investigations on alpha-MSH and MIF-1 effects on cyclic AMP levels in rat brain.

It has been suggested that the peptides alpha-metanocyte stimulating hormone (alpha-MSH) and MSH-release inhibitory factor (MIF-1) may alter adenosine-3', 5'-cyclic monophosphate (cAMP) metabolism [13,26]. Normal and hypophysectomized (hypoxed) rats were administered saline (controls IP daily X 3), alpha-MSH (80 mug/kg IP daily X 3) or MIF-1 (1 or 10 mg/kg IP daily X 3) and sacrificed 30 min after the third injection in a focused microwave oven (1.5 KW; 2-3 sec). Various brain areas were then assayed for cAMP levels after each treatment. The occipital cortex area was the only area to show consistent changes in both normal and hypoxed rats after alpha-MSH treatment. These findings were replicated for the occipital cortex in a second group of normal and hypoxed rats which were similarly treated. The results suggest a correlation between the rise in cAMP found and reported changes in visual acuity and attention in rats and human after treatment with alpha-MSH [8,14, 23].

Animals↗
PubMed1976

Effects of L-prolyl-L-leucyl-glycine amide (MIF-I) on dopaminergic neurons.

In an attempt to determine the mechanism of action of L-proly-L-leucyl-glycine amide (MIF-I) in the treatment of Parkinson's disease, various parameters of dopaminergic neuronal function were studied in rats. It was found that the active uptake of 3H-dopamine (3H-DA) by synaptosome-rich homogenates of the striatum of rats treated with MIF-I (1 mg/kg IP X 3, 24 hr intervals) was unaltered 1 hr after final treatment with MIF-I. 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). Thus, vital functional processes associated with dopaminergic neurons apparently are not altered by MIF-I under the conditions studied. These findings illustrate the importance of concurrent DOPA administration in observing an effect of MIF-I on dopaminergic neuronal function.

Animals↗
PubMed1976

Peptides readily penetrate the blood-brain barrier: uptake of peptides by synaptosomes is passive.

The intracarotid artery quick injection technique of Oldendorf was utilized to determine the Brain Uptake Index (BUI) of radio-labeled peptides in comparison with 3H2O or 14C-antipyrine as counterlabels. The normalized BUI values for 3H-MIF-I, 3H-alpha-MSH and 14C-AVP were 13.7, 9.6 and 13.0 respectively at 15 sec after injection consistent with their having readily penetrated the blood-brain barrier. The BUI values were similar, though somewhat increased, at 10 min postinjection consistent with their ready exit across the blood-brain barrier. At 15 sec after injection 0.5+/-0.1%/g brain of the originally injected peptide label was recovered; and 0.1+/-0.2%/g brain was recovered after 10 min. The label was distributed uniformly in the major brain regions at both times. However, the percentage of the originally injected label/g of pineal and pituitary gland tissue was 10-20 X increased as compared with the major brain regions as would be expected by their location outside the blood-brain barrier. The in vitro uptake of the radio-labeled peptides by synaptosomes prepared from the whole brain and the major brain regions was passive; it was not temperature dependent, nor was it Na+ dependent. However, the binding of the three peptides by the synaptosomes varied considerably: AVP greater than MSH greater MIF: 50 greater than 5 greater 1. The penetratin of the blood-brain barrier by the three peptides is consistent with their having CNS effects.

Animals↗
PubMed1978

Study of the structural requirements for dopa potentiation and oxotremorine antagonism by L-prolyl-L-leucylglycinamide.

A number of analogs of the tripeptide L-prolyly-L-leucylglycinamide (1) were synthesized and evaluated in the Dopa potentiation and oxotremorine antagonism tests. The replacement of the glycinamide residue with either the glycine methylamide, glycine, aminoacetonitrile, amino-2-propanone, semicarbazide, or beta-alaninamide residues resulted in a loss of activity in both tests. A 1:1 mixture of L-prolyl-L-leucyl-(-)-thiazolidine-2-carboxamide (8) and L-prolyl-L-leucyl-(+)-thiazolidine-2-carboxamide (9) showed marked activity in the Dopa potentiation test but was unable to antagonize the tremors induced by oxotremorine. L-Prolyl-L-leucyl-L-prolinamide (11), on the other hand, was active in the oxotremorine antagonism test but inactive in the Dopa potentiation test. The replacement of the pyrrolidine ring of 1 with either a thiazolidine or cyclopentane ring system caused a loss of activity. The cyclopentanecarboxylic acid analogue 13, however, was found to have moderate activity in the serotonin potentiation test.

Aggression↗
PubMed1977

Synthetic MIF analogues. Part II: Dopa potentiation and fluphenazine antagonism.

A comparison is described between the activity of the melanocyte-stimulating hormone release inhibiting factor (MIF) and those of five synthetic tripeptide analogues of MIF. The comparison was based upon the ability of the compounds to potentiate the behavioral effects of L-dopa in mide and to antagonize fluphenazine-induced catalepsy in rats. Three of the tripeptides potentiated L-dopa in a manner similar to that of MIF. All of the synthetic analogues antagonized fluphenazine after a single dose although their potency and their duration of action differed. MIF was active in the latter test only following chronic administration. The possible mechanism of action and the potential clinical applicability of the tripeptides are briefly discussed.

Animals↗
PubMed1976

Double-blind evaluation of oral L-prolyl-Lleucyl-glycine amide in Parkinson's disease.

A 4-month double-blind study comparing the effect of increasing oral doses (up to 1.0 g daily) of synthetic L-proyl-L-leucyl-glycine amide (PLG) and placebo in 20 parkinsonian patients showed no significant improvement in objective scores of functional disability. However, important trends and some significant results were observed with the lower doses of PLG. These essentially negative results may be attributed to poor intestinal absorption of the compound, a short biologic half-life in the blood, or administration of oral doses that were much higher than required, or a combination of factors. In further studies with this peptide, which are encouraged, the intravenous route should be used until the question of intestinal absorption is resolved.

Adult↗
PubMed1975

[Infusion therapy with mif (melanocyte inhibiting factor) in Parkinson's disease (author's transl)].

On the basis of reports in the literature and of our own clinical experience it appears that melanocyte inhibiting factor (MIF) is a very promising therapeutic agent in the management of Parkinson's disease. Besides theoretical considerations relating to biochemical and pathophysiological spheres, the question of the current dosage for clinical usage seems to be of the utmost importance. We are of the opinion that the currently-employed dosage of 400 mg daily is still too low. Hence, the present investigation will be continued with a view to establishing the optimum dosage for maximal therapeutic effect.

Aged↗