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)

Experiments were conducted to determine if endogenously produced beta-endorphin and met-enkephalin exert a physiological inhibition on luteinizing hormone-releasing hormone (LHRH) release in the central nervous system of sheep. Twenty-two mature ewes were implanted with unilateral guide tubes, through which matched infusion cannulae could be inserted without discomfort once daily for intracerebral (i.c.) infusion of three anti-opioid treatments: naloxone (50 micrograms in 20 microliters), sheep antisheep beta-endorphin (ABE; 20 microliters of 1:25) or sheep anti-met-enkephalin (AME; 20 microliters of 1:25) and of two control treatments: nonimmune sheep serum (20 microliters of 1:25) or sheep antiporcine thyroglobulin (20 microliters of 1:25). To detect abrupt disinhibition of LHRH release by anti-opioid treatments, serum luteinizing hormone (LH) was quantified at 10-min intervals for 1-2 h before and after each i.c. infusion. Complete trials consisted of 3-4 different anti-opioid or control i.c. infusions once daily at a single site over a period of 2-3 days during the luteal phase of recurring estrous cycles. Results were statistically evaluated within each ewe since complete trials were replicated 2-5 times within each ewe and because no 2 ewes could have i.c. infusions in identical locations. Anatomical generalizations were possible when LH responses to anti-opioid treatments were similar for several ewes with i.c. infusion sites in comparable brain regions. However, it was not possible to make such generalizations when infusion sites were not comparable in other ewes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracerebral immunoneutralization of beta-endorphin and met-enkephalin disinhibits release of pituitary luteinizing hormone in sheep. 212 63

Both opioid peptides such as beta-endorphin and met-enkephalin and nonopioid peptides such as vasopressin and oxytocin increase pain thresholds in rodents. Antisera raised against each of these peptides have been developed for use in immunocytochemical and radioimmunoassay procedures. The present study assessed whether central administration of antisera raised against beta-endorphin (ABE), met-enkephalin (AME), arginine, vasopressin (AAVP) or oxytocin (AOT) altered tail-flick latencies elicited by three different levels of radiant heat, jump thresholds, core body temperatures and locomotor activity. ABE induced a transient hyperalgesia on the tail-flick test at thermal levels at which beta-endorphin administration would elicit an analgesic effect. While met-enkephalin increases tail-flick latencies elicited by high thermal levels, AME failed to alter latencies at this level, but rather induced a short-acting hyperalgesia at a low thermal level. While vasopressin increased tail-flick latencies at high thermal levels, AAVP produced reciprocal decreases. Yet AAVP inexplicably induced analgesic effects at moderate and low thermal levels. Finally, while oxytocin increased latencies at high thermal levels, AOT failed to alter latencies. Rather, it decreased latencies at the moderate thermal level and increased latencies at the low thermal level. Neither jump thresholds nor core body temperatures were affected by any antiserum pretreatment. While activity levels were unaffected by either ABE, AME or AAVP pretreatment, AOT decreased activity in a fashion complementry to oxytocin-induced hyperactivity and seizures. There data are discussed in terms of tonic versus phasic influences of these peptides upon pain perception.
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PMID:Pain threshold changes in rats following central injection of beta-endorphin, met-enkephalin, vasopressin or oxytocin antisera. 609 76