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)

Treatment of common marmosets with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 1-4 mg/kg for up to 4 days) caused a profound parkinsonian state. Ten days from the start of MPTP treatment, all animals showed marked motor impairment, consisting of bradykinesia and akinesia, limb rigidity, postural abnormalities, loss of vocalisation and blink reflex, and, on occasions, postural tremor. Measurement of caudate-putamen monoamine content at this time showed a profound loss in 3,4-dihydroxyphenylethylamine, homovanillic acid, and 3,4-dihydroxyphenylacetic acid concentrations. Measurement of neuropeptide concentrations in the caudate-putamen, internal and external segments of the globus pallidus, nucleus accumbens, substantia nigra, frontal cortex, and hippocampus showed met-enkephalin, leu-enkephalin, and cholecystokinin (CCK-8) concentrations to be unaffected by MPTP treatment. There was a small decrease in the substance P content of frontal cortex, but otherwise the content of this neuropeptide was unaltered. Parkinsonism in the marmoset, induced by MPTP treatment 10 days earlier, does not alter neuropeptide concentrations in the manner observed in Parkinson's disease.
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PMID:Lack of change in basal ganglia neuropeptide content following subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment of the common marmoset. 242 37

Intraventricularly-administered beta-endorphin (beta-END) suppresses receptive and proceptive behaviors of the ovariectomized, estrogen-progesterone-primed rat. This rat model was used in a four-way choice paradigm to investigate the behavioral specificity and motivational aspects of sexual suppression by beta-END. The experimental females showed a preference to associate with a sexually active 'stud' male over the other incentive animals as shown by significantly more approaches to and nose pokes into the stud male compartment. beta-END did not alter that choice preference. Rather, there was a decrease in overall social interaction after beta-END treatment, as shown by decreased total nose pokes. This overall decrease in social motivation, which was blocked by subcutaneous naloxone injection, was not specific to the stud male. It was not a result of akinesia, since total movement among the inner alleys was significantly higher after beta-END treatment, an effect also reversed by naloxone. These data suggest that intraventricular beta-END may act to suppress sociosexual motivation as a whole rather than sexual activity specifically.
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PMID:Effect of beta-endorphin on sociosexual proclivity in a choice paradigm. 293 66

In this report we present a series of experiments which have led us to support the notion of the presence of an ACTH receptor in the CNS. A short intense heat-stress (hot-plate) applied to the paws of rats will temporarily reduce activity. During the course of experimentation we were able to eliminate a number of logical mediators. Neither adrenalectomy, adrenal-medullectomy, naloxone administration, nor alpha-MSH-(1-12) were able to affect the observed akinesia. Hypophysectomy, however, was able to abolish or mask the behavior and the reduction in activity could be reinstated by the administration of ACTH-(4-10) to hypophysectomised rats. These data support the notion that a short intense stressor can release ACTH and that this ACTH can be responsible for mediating the short term reduction in activity. In addition, the fact that ACTH-(4-10) has only minimal steroidogenic properties and was able to reinstate the behavior led us to speculate that these effects were of central origin. Furthermore, since naloxone was not capable of altering the behavior, the suggestion is that ACTH in this paradigm acted at a receptor site apart from the naloxone sensitive receptor. This site may in fact be an ACTH specific receptor.
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PMID:Behavioral support for an ACTH receptor in the CNS. 299 24

Open field behavior was observed in conjunction with mating behavior to discern whether the effect of intraventricular (ICV) beta-endorphin (beta-END) on sexual behavior may be secondary to akinesia. Three groups of ovariectomized, estrogen-progesterone-primed rats each received counterbalanced treatments of saline ICV, 2 micrograms beta-END ICV, or 2 micrograms beta-END ICV in combination with a selective opioid receptor antagonist. Receptive behavior (lordosis) and proceptive behaviors (presentation and ear wiggling) were consistently suppressed by beta-END, while ambulation was unaffected. Rearing and grooming were generally decreased, although this effect was statistically significant in only one experiment. Pretreatment with the mu-1 antagonist naloxazone (50 mg/kg intravenously) reversed the effects of beta-END on all behaviors tested. The delta receptor antagonist ICI-154,129 (12.5 and 50 micrograms ICV) only partially reversed the sexual effects of beta-END but completely reversed the open field effects. It is concluded that the suppressive effect of beta-END on sexual behavior, while not behaviorally specific, is not secondary to opioid-induced akinesia.
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PMID:Behavioral specificity of beta-endorphin suppression of sexual behavior: differential receptor antagonism. 301 64