| Name | beta endorphin |
|---|---|
| Synonyms | Beta endorphin; endorphin; B endorphin; Beta endorphin |
| Name | methyl bromide |
|---|---|
| CAS | bromomethane |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 2454493 | Amir S: Anaphylactic shock: catecholamine actions in the responses to opioid antagonists. Prog Clin Biol Res. 1988;264:265-74. The pathophysiological consequences of endorphin release in anaphylactic shock were investigated through pharmacological studies using opiate antagonists (naloxone, naltrexone, natrexone methyl bromide) as well as agonists (morphine, beta-endorphin). |
83(1,1,1,3) | Details |
| 2137676 | Hargreaves KM, Flores CM, Dionne RA, Mueller GP: The role of pituitary beta-endorphin in mediating corticotropin-releasing factor-induced antinociception. Am J Physiol. 1990 Feb;258(2 Pt 1):E235-42. Furthermore, the effect of CRF was antagonized by 1) naltrexone, 2) naltrexone methyl bromide, and 3) passive immunization with anti-beta-endorphin antiserum. |
34(0,1,1,4) | Details |
| 2935140 | Introini IB, McGaugh JL, Baratti CM: Pharmacological evidence of a central effect of naltrexone, morphine, and beta-endorphin and a peripheral effect of met- and leu-enkephalin on retention of an inhibitory response in mice. Behav Neural Biol. 1985 Nov;44(3):434-46. The peripheral-acting opioid receptor blocker, naltrexone methyl bromide (MR 2263) (0.01-10.00 mg/kg), did not significantly influence retention latencies of either shocked or unshocked mice. |
2(0,0,0,2) | Details |
| 2823789 | Baratti CM: The impairment of retention induced by pentylenetetrazol in mice may be mediated by a release of opioid peptides in the brain. Behav Neural Biol. 1987 Sep;48(2):183-96. On the contrary, neither naltrexone methyl bromide (0.01, 0.10, or 10.0 mg/kg, ip), a quaternarium analog of naltrexone, nor MR2266 (0.01 or 0.10 mg/kg, ip), a putative kappa opiate receptor antagonist, modified the behavioral effects of PTZ. Administration of beta-endorphin (0.01 or 0.10 microgram/kg, ip) 10 min prior to testing attenuate the retrograde amnesia caused by PTZ. |
2(0,0,0,2) | Details |
| 3104708 | Buydens P, Velkeniers B, Golstein J, Finne E, Vanhaelst L: Opioid modulation of induced prolactin secretion. Life Sci. 1987 Mar 23;40(12):1207-14. A beta-endorphin (beta EP) injection in the third ventricle stimulated PRL secretion and induced furthermore a PRL secretory reaction to TRH injected intravenously 20 min later. Pretreatment with naloxone methyl bromide (Br-naloxone), a quaternary naloxone derivative, which does not cross the blood-brain barrier, had no effect on the PRL response to beta EP but prevented the conjugated effect of beta EP and TRH on PRL secretion. |
1(0,0,0,1) | Details |
| 2087144 | Baratti CM, de Erausquin GA, Faiman CP: Brain opioid peptides may participate in the reversal of pentylenetetrazol-induced amnesia. Methods Find Exp Clin Pharmacol. 1990 Sep;12(7):451-6. The effect was reversed by any of the following treatments given 1 h prior to testing: a) a beta-endorphin injection (0.1 microgram/kg, i.p.), b) PTZ injection, or c) exposure to a novel experience (10 min in a stainless steel box with a wire mesh top). All treatments had a similar time course of effectiveness (up to at least 3 h) and their effects were blocked by naltrexone (0.1 mg/kg, i.p.) but not by naltrexone methyl bromide (10 mg/kg, i.p.). |
1(0,0,0,1) | Details |
| 6722534 | Amir S: Naloxone improves, and morphine exacerbates, experimental shock induced by release of endogenous by compound 48/80. Brain Res. 1984 Apr 9;297(1):187-90. In mice, fatal shock induced by release of endogenous by compound 48/80 was reversed by the intracerebroventricular (i.c.v.) administration of the opiate antagonist naloxone (10-25 micrograms) but not by the systemic administration of the selective peripherally acting antagonist, naltrexone methyl bromide (1-5 mg/kg). The results suggest possible involvement of central opiate (endorphin) mechanisms in the pathophysiology of fatal shock in mice. |
1(0,0,0,1) | Details |