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At least 19 recordsLinked to original sources
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

Influence of three short-chain peptides (alpha-MSH, MSH/ACTH 4-10, MIF-I on) dimensional attention.

Male, albino rats were treated with alpha-MSH, MSH/ACTH 4-10, MIF-I or a diluent control solution and then tested on a visual discrimination problem. Immediately after acquistion of the visual task the animals were tested with a spatial extradimensional shift problem. The animals treated with the MSH/ACTH 4-10 and MIF-I acquired the discrimination nonsignificantly faster than animals treated with alpha-MSH or a placebo. A subproblem analysis of the EDS behavior indicated that the peptides significantly improved performance probably by affecting attention.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

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↗
PubMedDate not supplied

Alpha-MSH and MIF-I effects on catecholamine levels and synthesis in various rat brain areas.

Attempts were made to find a biochemical correlate with previously observed behavioral alterations after administration of alpha-melanocyte-stimulating hormone (MSH) and MSH release-inhibiting factor (MIF-I). Brains of intact and hypophysectomized (hypox) rats were analyzed for endogenous catecholamine levels and the disappearance rate of endogenous norepinephrine (NE) after treatment with the tyrosine hydroxylase inhibitor alpha-methyl-para-tyrosine (AMPT). The studies undertaken show the following: (1) After the injection of MSH (100 mug/kg IP daily x 3) and AMPT, samples in different groups of intact and hypox rats were taken at 0, 1, 2, 4 and 6 hrs in 7 different brain areas. In the mid-brain area for the intact group of rats, the rate of disappearance of NE was faster and for the hypox rats it was slower than the rate for control rats not treated with the peptides. NE levels in the same area at time 0 were 11 percent lower than controls in hypox rats and unchanged in unoperated animals. (2) After the injection of MIF-I (20 mg/kg IP daily x 3) in similar experiments as with MSH, a reduced rate (p less than 0.05) of NE disappearance for the first 4 hr and an increased rate (p less than 0.05) of NE disappearance for the last 2 hr of the experiments occurred for both the intact and hypox rats in the mid-brain area where endogenous NE levels were lowered by 11 and 12 percent at 0 min. In no other brain areas were alterations in NE breakdown found in both the intact and hypox rat groups. Behavioral changes have been found previously under similar experimental conditions in both intact and hypox rats. (3) Rates of dopamine disappearance in experiments similar to those described for NE disappearance indicated that in the striatal brain area no change was found in the intact rats after either MSH or MIF-I, whereas a decrease in DA disappearance was found for hypox rats during the six hour experimental period only after MSH. The results indicate that a correlation between behavioral changes, rates of disappearance and endogenous levels of NE in the mid-brain area may occur after MIF-I at the times examined but that a similar correlation for MSH did not appear likely.

Animals↗
PubMed1976

[Cyto-immunologic location of alpha-MSH and ACTH in the lead-hematoxylin (HPb)-stainable pituitary cells, in the eel].

The lead-haematoxylin positive cells of the pars intermedia react with anti-alpha-MSH and anti-1-24ACTH or anti-17-39ATCH; those of the rostal pars distalis are only revealed with antisera anti-1-24ACTH and anti-17-39ACTH. Intensity of cytoimmunological staining, which is modified after various experimental treatments (reserpine, metyrapon, pimozid, cortisol...) and during black or white background adaptaiton, corresponds essentially to that of the PbH staining.

Adrenocorticotropic Hormone↗
PubMed1978

[Antigenic determinants of beta-LPH, beta-MSH, alpha-endorphin, ACTH and alpha-MSH revealed by anti-beta-endorphin in neurons of the human infundibular nucleus].

Comparison of adjacent serial sections of the tubero-infundibular region of Human adult hypothalamus demonstrates that the same perikarya, axons and terminals are stained both with anti-beta-endorphin and anti 17-39 ACTH antisera. The most immunoreactive of these neurons are also revealed with anti alpha-endorphin, anti alpha and beta-MSH, anti-1-24 ACTH and anti beta-LPH. These results suggest that neurons of the infundibular nucleus can store and probably secrete peptide similar to propiocortin or fragment(s) of this molecule.

Adrenocorticotropic Hormone↗
PubMed1978

Melanocyte-stimulating hormone--mimetic action of the phenothiazines.

We have compared the melanophore-stimulating action of four phenothiazines, trifluoperazine, perphenazine, chlorpromazine, and prochlorperazine, with alpha-MSH on the skin of the lizard Anolis carolinensis, using a new rate method of bioassay. The dose-response curves for the phenothiazines were parallel to that of alpha-MSH, and when given together alpha-MSH and chlorpromazine were additive. The phenothiazines may therefore stimulate melanosome dispersion in the lizard skin by the same mechanism as alpha-MSH; a MSH-mimetic action of phenothiazines may similarly explain their pigmentary action in man. The pigmentary potency of the phenothiazines corresponded with their therapeutic potency in man; this is in keeping with a neuro-regulatory role for MSH peptides and suggests a possible therapeutic use for them.

Animals↗
PubMed1977

[Control of pituitary secretion of melanotropin in an anuran amphibian by thyrotropin releasing factor (TRH). Study in vitro].

Intermediate lobes from Rana esculenta pituitary glands were continuously superfused for 7 hrs at 28 degrees C with amphibian culture medium. alpha-MSH release was measured by use of a sensitive double antibody radio-immunoassay system. alpha-MSH secretion was inhibited by low temperatures. A large increase in alpha-MSH release was observed when Thyrotropin Releasing Hormone (TRH) at doses ranging from 10(-9) to 10(-7) molar was added to the superfusion medium. Since large amounts of TRH are to be found in the hypothalamus of amphibians but have no effect over pituitary TSH secretion, the action of TRH over alpha-MSH release may have a physiological significance.

Animals↗
PubMed1976

Hormonal influences of the extinction of conditioned taste aversion.

Conditioned taste aversion for a 5% glucose solution (sugar water) was induced in rats by an i.p. injection of LiCl 30 min after the first presentation of sugar water. Extinction of conditioned taste aversion was measured either in the forced-drinking test or in the preference-drinking test. In the forced-drinking test sugar water was the only fluid presented to the animals during extinction sessions. In the preference-drinking test the animals had the choice of tap water or sugar water. The rate of extinction was much slower in the preference test. The ACTH-analogues, ACTH 4-10 and ACTH 4-10 7d Phe, and alpha-MSH delayed extinction in the preference test but not extinction in the forced-drinking test. ACTH 11-24 was without any effect. MSH-release inhibiting factor (MIF) facilitated extinction in the forced-drinking test but did not alter extinction in the preference test. The peptides did not affect intake of tap water of preference of sugar water over tap water by control rats.

Adrenocorticotropic Hormone↗
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↗
PubMed1976

Neurochemical responses of mice to ACTH and lysine vasopressin.

Subcutaneous administration of ACTH 1-24 to mice increased the incorporation of [3H]lysine into brain and liver proteins, an effect which resembled that due to footshock. Corticosterone administration did not mimic these effects. ACTH 4-10 increased the [3H]lysine incorporation into brain or liver. These results are consistent with ACTH mediating the effects of footshock. However, dexamethasone decreased the brain responses to both footshock and ACTH, but while the liver response to ACTH was blocked, the footshock response was only diminished. This suggests a neural component in the response of the liver and possibly the brain. Intraventricular administration of ACTH 1-24 or ACTH 4-10 (D-phe), but not ACTH 4-10, increased [3H]lysine incorporation into brain protein. These neurochemical responses parallelled a distinctive pattern of behavior characterized by stretching, yawning and excessive grooming. Treatment for 3 days with long-acting preparations of ACTH 4-10, ACTH 4-10 (D-phe) or ACTH 1-24 increased the conversion of [3H]tyrosine into dopamine but not norepinephrine, alpha-MSH, beta-MSH or LVP had no such effect. Similar treatment with ACTH 4-10 or ACTH 1-24 increased striatal tyrosine hydroxylase activity measured in vitro, but did not significantly alter the enzyme activity from other brain regions. We conclude that ACTH peptides can stimulate protein and dopamine metabolism in mouse brain and that LVP has no such effects.

Adrenocorticotropic Hormone↗
PubMed1976

Stimulation of growth hormone release by luteinizing hormone-releasing hormone and melanocyte-stimulating hormone-release inhibiting hormone in the hypophysectomized rat bearing an ectopic pituitary.

Intrajugular administration of LHRH (0-6 and 1-2 mug) in hypophysectomized rats which received renal grafts of anterior pituitary induced a small but significant rise in plasma GH 5 and 10 min post-treatment. LHRH, at the same dose levels, was ineffective in weight-matched intact controls. MIF, at the dose of 1-2 mug, induced a slight GH rise 5 min after treatment in hypophysectomized trasnplanted rats, while it was ineffective in intact controls. Unlike the two hypothalamic peptides, alpha-MSH (0-6 and 1-2 mug) was ineffective as a GH-releaser in both transplanted and intact rats.

Animals↗
PubMed1977

New evidence that demonstrates that L-pro-L-leu-L-gly-NH2 might be the natural MIF.

A wide range of doses was used to study the effect of Pro-Leu-Gly-NH2 (MIF) on the MSH release in rat pituitaries incubated in vitro. The Pro-Leu-Gly-NH2 was added to one half of the gland, and the other was used as control. The MSH released into the medium was measured by a bioassay and the activity of the samples referred to a standard of synthetic alpha-MSH. Pro-Leu-Gly-NH2 in doses of 10 to 30 ng/ml inhibited the MSH release in about 60%. Doses between 10(3) to 10(4) ng/ml induced neither release nor inhibition of the release of MSH. Dose of 10(5) ng/ml clearly induced release of MSH. The results of the additional experiments presented, although they represent no proof, are in line with the contention that Pro-Ley-Gly-NH2 in the natural MIF.

Animals↗