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 on prolactin secretion of three peptide-derivatives of beta-endorphin which show neuroleptic-like activities in rats were studied. Intravenous administration of gamma-endorphin (beta-endorphin (beta E) 1-17) enhanced plasma prolactin levels. Gamma-Endorphin did not affect the prolactin secretion by hemipituitary glands incubated in vitro and by cultured pituitary cells, but it reversed, in a dose-dependent way, the dopamine-induced inhibition of prolactin release. This effect of gamma-endorphin could be prevented by co-incubation with the opiate-antagonist naloxone. In vivo studies with non-opiate-like fragments of gamma-endorphin, des-Tyr1-gamma-endorphin (DT gamma E, beta E 2-17) and des-enkephalin-gamma-endorphin (DE gamma E, beta E 6-17), showed that these peptides suppressed the plasma prolactin levels, when prolactin release was slightly stimulated. However, DE gamma E dose-dependently enhanced plasma prolactin levels, when prolactin release was low. Subchronic treatment with DE gamma E for 4 days made prolactin release more sensitive to the inhibitory action of small doses of apomorphine. Neither DT gamma E nor DE gamma E affected prolactin release by hemipituitary glands and cultured pituitary cells. They did also not affect the dopamine-induced inhibition of prolactin release in vitro. It is suggested that gamma-endorphin increases prolactin secretion by interfering with dopaminergic systems in the pituitary and that DT gamma E and DE gamma E have a modulatory action on prolactin secretion.
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PMID:Non-opiate beta-endorphin fragments and dopamine-V. gamma-Type endorphins and prolactin secretion in rats. 618 42

Dopamine causes a dose-dependent contraction of the rat rectum in vitro followed by a relaxation. This contraction can be inhibited by apomorphine and phenylephrine. This inhibition can be attenuated by the beta-endorphin (beta E) fragments 2-17 (des-Tyr1-gamma-endorphin, DT gamma E) and 6-17 (des-enkephalin-gamma-endorphin, DE gamma E). beta E 6-17 seems to be the shortest sequence with full activity in this respect since a shorter fragment (beta E 10-17) was less effective. The atypical neuroleptics oxypertine, sulpiride, and clozapine, the classic neuroleptic haloperidol and metoclopramide have a similar action to DE gamma E. The peptides and atypical neuroleptics do not affect the dopamine response per se while the classic neuroleptics haloperidol and metoclopramide enhance the dopamine response. The effects of the alpha-type endorphins are opposite to those of the gamma-type endorphins, since des-Tyr1-alpha-endorphin (DT alpha E, beta E 2-16) and des-enkephalin-alpha-endorphin (DE alpha E, beta E 6-16) enhance the phenylephrine-induced decreased responsiveness to dopamine. Structure-activity studies revealed that the active moiety of the alpha-endorphin fragments probably resides in the 6-9 region. In addition the alpha-type endorphins directly inhibit the dopamine response. It is concluded that the rat rectum may be used to analyse neuroleptic-like action. In this model alpha- and gamma-endorphin fragments may directly or indirectly influence the interaction of dopamine with the rectum. Because of the strong similarities between the effects of gamma-type endorphins and that of neuroleptics the results support the purported neuroleptic-like action of gamma-type endorphins. The influence of alpha-type endorphins and gamma-type endorphins on the apomorphine or phenylephrine induced decreased responsiveness to dopamine, although opposite, seems to be mediated by an influence on different dopamine sensitive systems.
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PMID:Opposite interactions between alpha- and beta-endorphin fragments with dopamine mediated responses on the rat rectum in vitro. 618 56

The influence of different neuropeptides related to pro-opiomelanocortin were tested on acquisition of heroin self-administration in rats. The animals were allowed to self-administer heroin intravenously on a continuous reinforcement schedule during 6 h daily sessions on 5 consecutive days. Treatment was performed subcutaneously 1 h before each daily session. It was found that the opioid peptides alpha-, gamma- and beta-endorphin hardly influenced acquisition of heroin self-administration, while the non-opioid fragments of alpha- and gamma- endorphin modulated this behavioral response. In fact, beta-endorphin (beta E) 2-9 tended to facilitate the rate of acquisition, while the gamma-type endorphins, des-Tyr1-gamma-endorphin (beta E 2-17) and des-enkephalin-gamma-endorphin (beta E 6-17), decreased heroin intake. Concerning the ACTH/MSH related peptides, a decreasing effect of heroin intake was found following treatment with (D-Phe7)-ACTH 4-10, with a high dose of the ACTH 4-9 analog Org 2766 and with gamma 2-MSH, while ACTH 1-24, ACTH 4-10 and a low dose of Org 2766 did not significantly influence self-injecting behavior. It is concluded that pro-opiomelanocortin serves as a precursor molecule for peptide fragments, which modulate the acquisition of heroin self-administration in rats.
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PMID:The influence of neuropeptides related to pro-opiomelanocortin on acquisition of heroin self-administration of rats. 631 60