Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of intracameral (i.c.) administration of MIF-I on the ocular response to alpha-MSH were tested in rabbits. In confirmation of previous studies, i.c. alpha-MSH significantly increased intraocular pressure (IOP) and reduced pupillary diameter (PD). Concomitant administration of alpha-MSH and MIF-I antagonized both the IOP increase and miosis induced by alpha-MSH. Aqueous humor (AH) dynamics studies revealed that alpha-MSH increases IOP, possibly, by decreasing AH outflow. The decreased AH outflow induced by alpha-MSH was antagonized by concurrent administration of MIF-I and alpha-MSH. MIF-I did not affect IOP or PD when administered alone. These results add more support for a role of alpha-MSH in ocular function, and suggest that the ocular response to alpha-MSH may be subject to inhibitory control by MIF-I.
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PMID:Inhibition by MIF-I of alpha-MSH induced increase of intraocular pressure and miosis in rabbits. 290 21

Recently it has been suggested that MIF-I can act as an opiate antagonist for analgesia. Therefore, rats kept at 4 degrees C were pretreated with MIF-I in an attempt to extend the observation to a nonanalgesic opiate effect by determining any blockade of the thermal response to beta-endorphin and morphine. MIF-I, at an ip dose of 1.0 mg/kg, was found to block the thermal responses to beta-endorphin injected ip at doses of 0.1 and 1.0 mg/kg. A lower dose (0.1 mg/kg, ip) of MIF-I, or naloxone (10 mg/kg), was also able to block the thermal effects of 30 and 60 mg/kg doses of morphine. However, an ip dose of 1.0 mg/kg MIF-I potentiated the hypothermic effects of morphine but, like naloxone, reduced the magnitude of the decrease in the level of motor activity induced by beta-endorphin or by morphine. The results of this study demonstrate a nonanalgesic situation in which MIF-I can act as an antagonist of opiate effects after peripheral injection.
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PMID:Antagonistic actions of MIF-I on the hypothermia and hypomotility induced by beta-endorphin or morphine. 610 37

Several peptides are now known to affect thermoregulation. These include beta-endorphin, bombesin, MIF-I, alpha-MSH, neurotensin, TRH, and DSIP. Some of these have been found to interact with the thermal effects of d-amphetamine, a drug with well established actions on thermoregulation. 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. In general, it seems that two of the major variables which interact and modify the thermal effects of peptides are ambient temperature and route of administration.
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PMID:Peptides and thermoregulation. 611 Jan 98

Administration of several doses of MIF-I or alpha-MSH did not modify colonic temperature or the level of motor activity of rats in ambient temperatures of 4 degree or 20 degrees C. However, the thermoregulatory but not motor effects of the interaction between MIF-I or alpha-MSH with d-amphetamine were dependent upon ambient temperature. At 4 degree C, 1.0 mg/kg of both peptides enhanced the d-amphetamine-induced hypothermia, but at 20 degrees C both peptides blocked the hyperthermic effects of d-amphetamine. The hypothermic effect of chlorpromazine (CPZ) at 4 degree C and 20 degrees C was blocked by 1.0 mg/kg MIF-I but not by 1.0 mg/kg alpha-MSH. No linear dose response relationships between various doses of MIF-I or alpha-MSH and thermal responses were found. Administration of melanin or the use of hypophysectomized rats did not alter the significant interactions observed after peripheral injections.
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PMID:Interaction of MIF-I or alpha-MSH with D-amphetamine or chlorpromazine on thermoregulation and motor activity of rats maintained at different ambient temperatures. 611 34

The pituitary-hypothalamo-pineal complex involving MSH, MIF-I and melatonin has been strongly emphasized in the adaptive mechanism of the animal. A series of experiments was conducted to investigate the effects of alpha-MSH, MIF-I and melatonin on novelty-induced defecation, step-down activity, plasma 11-OHCS levels and whole brain DA and NE concentrations over days of novelty X drug treatment. alpha-MSH consistently enhanced and sustained novelty-induced defecation, increased plasma 11-OHCS levels in the resting intact rats and in the novelty exposed hypophysectomized (hypox) rats, and decreased brain DA and NE levels in intact, hypox and sham-hypox rats. MSH did not increase plasma 11-OHCS in intact and sham-hypox rats during exposure to novelty. MIF-I significantly habituated novelty-induced defecation and increased brain DA and NE levels over 5 days of drug X novelty treatment. Melatonin, on the other hand, inhibited novelty-induced defecation, decreased plasma 11-OHCS and increased brain DA level over 5 days of melatonin X novelty treatment. MSH, MIF-I or melatonin did not show any significant effect on the step-down activity of the rats. The results suggest the possibility that central CAs may be implicated in the behavioral changes observed after alpha-MSH, MIF-I and melatonin administration and in the interaction of the pituitary-hypothalamo-pineal complex involving MSH, MIF-I and melatonin.
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PMID:alpha-MSH, MIF-I and melatonin: effects on novelty-induced defecation, plasma 11-OHCS and central catecholamines in rats. 611 65

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. All drugs tested alone (except MIF-I) caused significant hypothermia. Pretreatment with CPZ, MIF-I, and alpha-MSH potentiated d-amphetamine-induced hypothermia in intact rats. Pretreatment with alpha-MSH potentiated CPZ-induced hypothermia. beta-Endorphin partially blocked d-amphetamine-induced hypothermia, but did not interact with CPZ, MIF-I, or alpha-MSH. All potentiations were either reduced or disappeared in the incisioned rats. CPZ and alpha-MSH caused hypothermia in olfactory tubercle-lesioned rats. The results indicate that: (a) the DA mesolimbic pathway is involved in the hypothermic response of all drugs tested; (b) an intact feedback loop is required for the potentiation of the hypothermic response of CPZ on d-amphetamine, MIF-I on d-amphetamine, and alpha-MSH on d-amphetamine and CPZ; (c) beta-endorphin acts as a partial blocker of d-amphetamine; MIF-I is a weak potentiator of d-amphetamine, alpha-MSH acts as a negative modulator of the DA system, most probably in the striatum.
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PMID:Modification of d-amphetamine- or chlorpromazine-induced hypothermia by beta-endorphin, MIF-I, and alpha-MSH: mediation by the dopaminergic system. 612 51

In two experiments the effects of the pituitary peptide alpha-MSH, the hypothalamic tripeptide MIF-I (P-L-G-NH2) and the pineal hormone melatonin were investigated on the attenuation of morphine analgesia measured by a tail flick test. In Experiment 1, alpha-MSH had minimal effect on morphine analgesia, whereas, MIF-I and melatonin clearly delayed the onset of morphine analgesia, and melatonin also shortened the duration of analgesia. Experiment 2 was designed to investigate the possible synergistic effect of MIF-I and melatonin. The combined treatment of MIF-I and melatonin significantly delayed the onset of morphine analgesia, and melatonin alone shortened the duration of analgesia. The relationships among the pituitary, hypothalamus and the pineal for the modulation of pain and response to morphine were discussed.
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PMID:Attenuation of morphine analgesia by alpha-MSH, MIF-I, melatonin and naloxone in the rat. 612 66

1. Melanostatin, a thirty-six amino acid peptide recently isolated from the frog brain due to its ability to inhibit alpha-melanocyte-stimulating hormone (alpha-MSH) release, is the amphibian counterpart of mammalian neuropeptide Y (NPY). The effect of synthetic melanostatin on the bioelectrical activity of cultured frog melanotrophs was studied in 124 cells by using the whole-cell patch-clamp technique. 2. In current-clamp experiments, melanostatin (1 microM) provoked a reversible hyperpolarization and a suppression of spontaneous action potentials. In some cells the hyperpolarizing response was absent, but an arrest of spike firing still occurred. 3. Melanostatin-induced hyperpolarization was associated with a decrease in membrane resistance. In voltage-clamp experiments, melanostatin induced an outward current at a constant command potential. This hyperpolarizing outward current appeared to be carried by potassium ions. 4. Cell dialysis with the non-hydrolysable GTP analogue guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S) sustained the outward current produced by melanostatin. Dopamine (1 microM), which generates a similar hyperpolarizing outward current in frog melanotrophs, was not capable of increasing the current provoked by melanostatin and sustained by GTP gamma S. 5. Melanostatin also modulated voltage-operated currents. The amplitude of voltage-activated potassium current was increased by 30%. 6. Melanostatin reduced the fast sodium current. This inhibitory effect was rather persistent compared to the other modulated currents. 7. Melanostatin markedly scaled down high voltage-activated N- and L-like calcium currents. The activation kinetics of these two calcium currents were not altered by the peptide. 8. Pretreatment of melanotrophs with pertussis toxin (1 microgram ml-1) blocked melanostatin-induced inhibition of N- and L-like calcium currents. 9. It is concluded that the NPY-related peptide melanostatin generates a very complex pattern of electrical responses in frog melanotrophs, including hyperpolarization and modulation of voltage-activated currents underlying action potentials. G proteins appear to mediate at least part of these effects.
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PMID:Melanostatin (NPY) inhibited electrical activity in frog melanotrophs through modulation of K+, Na+ and Ca2+ currents. 791 31

Iron deficiency (ID) induces in rats marked reduction of brain iron and dopamine D2 receptor. The resultant effects are a wide variety of changes in dopamine-mediated behaviors including thermo-regulation, motor activity, stereotyped behavior and diminished learning. Another behavioral change resulting from ID rats is an increase in the pain threshold, which is dependent on the duration and severity of ID. The results showed that peripheral administration of enkaphalines (0.1-3.0 mg/kg I.P.) potentiates ID-induced analgesia and causes a higher pain threshold, a phenomenon not observed in control rats.This effect may be associated with the known functional alteration in blood brain barrier resulting from ID. The opiate antagonists, naloxone (2 mg/kg and MIF-I (1 mg/kg), blocked the opiate-induced pain threshold potentiation in ID. Furthermore, the levels of dynorphin B and met-enkephalin are significantly increased in dopamine opiate-rich brain areas (caudate nucleus, substantia nigra, nucleus accumbens and globus pallidus) during ID. These phenomena can be reversed by placing rats on iron plus (control) diet for 24 days. It is concluded that a decrease in brain dopamine neurotransmission is associated with an increased functional level of the opiate system and that this mechanism mediates not only the analgesic effect but may also be associated with learning deficit observed in ID rats.
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PMID:The Involvement of Enkephalin System in Analgesia Induced by Brain Iron Deficiency. 2741 34


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