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

The endogenous opioid met-enkephalin intraventricularly adminstered to the rat at the dose of 100 microgram raised rectal temperature, whereas 400 microgram of the pentapeptide caused a diphasic effect, i.e., hypothermia followed by hyperthermia. Met-enkephalin was ineffective when administered i.p. The effects on temperature were substantially similar to those elicited, for both routes of administration, by morphine, which may either raise or lower rat temperature depending on the dose. More naloxone was required to antagonize thermic effects of met-enkephalin than morphine. Finally, there was a lack of effects on temperature for met-enkephalin centrally administered to morphine-tolerant animals, thus providing further evidence, in vivo, of cross tolerance between opiates and naturally occurring ligands of opiate receptors.
 ...
PMID:Effects of Met-enkephalin on body temperature of normal and morphine-tolerant rats. 9 98

The behavioral effects of beta-endorphin, [D-Ala2, D-Leu5]-enkephalin and morphine were investigated in golden hamsters and in rats. In golden hamsters, beta-endorphin and [D-Ala2, D-Leu5]-enkephalin induced loss of righting reflex, whereas morphine caused no such effect. Both opiate peptides and morphine caused the inhibition of tail-flick response and catalepsy in rats. beta-Endorphin was the most potent, followed by [D-Ala2, D-Leu5]-enkephalin and then by morphine. The catalepsy induced in rats by [D-Ala2, D-Leu5]-enkephalin was different from that of beta-endorphin and morphine in that it produced catalepsy without muscular rigidity. beta-Endorphin and [D-Ala2, D-Leu5]-enkephalin caused hypothermia in golden hamsters; morphine was less active in altering the body temperature. beta-Endorphin caused hypothermia at high doses and hyperthermia at low doses in rats. These heterogenous behavioral responses indicate that multiple types of receptors mediate the effects of opiates in the central nervous system.
 ...
PMID:Behavioral activities of opioid peptides and morphine sulfate in golden hamsters and rats. 11 44

The endogenous morphinomimetic brain peptides Met5-enkephalin and alpha-, beta-, and gamma-endorphins have been evaluated in rats after intracerebrospinal fluid injection. beta-Endorphin produces marked, prolonged muscular rigidity and immobility similar to a catatonic state, counteracted by the opiate antagonist naloxone; this effect occurs at molar doses 1/100 to 1/400 that at which the other peptides or morphine block the response to painful stimuli. All peptides evoked dose-related, naloxone-reversible, wet-dog shakes in rats that had not been exposed to drugs. beta-Endorphin produced hypothermia, whereas gamma-endorphin produced hyperthermia. Such potent and divergent responses to naturally occurring subtances suggest that alterations in their homeostatic regulation could have etiological significance in mental illness.
 ...
PMID:Endorphins: profound behavioral effects in rats suggest new etiological factors in mental illness. 18 94

The effects of intraventricular administration of beta-endorphin on thermoregulatory responses of unanesthetized rats to different ambient temperatures (Ta) of 8, 22 and 30 degrees C were assessed. Administration of beta-endorphin produced a fall in rectal temperature at both Ta 8 and 22 degrees C. The hypothermia in response to beta-endorphin was brought about by both cutaneous vasodilation (as indicated by an increase in both the tail and the foot skin temperatures) and decreases in metabolic heat production. However, at Ta 30 degrees C, administration of beta-endorphin produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermic effect induced by beta-endorphin was greatly attenuated by either the depletion of brain serotonin levels (with 5,6-dihydroxytryptamine and p-chlorophenylanine) or the blockade of opiate receptors (with naloxone). The data indicate that beta-endorphin leads to hypothermia in rats by increasing sensible heat loss and decreasing metabolic heat production, probably via the release of endogenous serotonin within brain.
 ...
PMID:Serotoninergic mechanisms of beta-endorphin-induced hypothermia in rats. 23 Apr 53

The antinociceptive and hypothermic effects of intracisternal administration of 11 endogenous neuropeptides and morphine were evaluated in mice. Of the substances tested, only neurotensin (NT) and beta-endorphin exerted significant antinociceptive and hypothermic effects; NT was the most potent in inducing hypothermia whereas beta-endorphin was the most potent antinociceptive agent via this route of administration. Both NT, and beta-endorphin were, on a molar basis, considerably more potent antinociceptive agents than morphine, [Met]enkephalin, or [Leu]enkephalin. NT-induced analgesia and hypothermia both were significantly dose-dependent. Substance P was found to produce significant hyperalgesia and hyperthermia. Bombesin produced a significant hypothermic effect, whereas somatostatin and luteinizing hormone-releasing hormone (luliberin) produced hyperthermia. None of the other peptides studies [bradykinin, thyrotropin-releasing factor (thyroliberin), melanocyte-stimulating hormone release-inhibiting factor (melanostatin), somatostatin, [Met]enkephalin, and [Leu]enkephalin] produced any significant alterations in colonic temperature or response to a noxious stimulus with the doses tested. These data demonstrate that NT and beta-endorphin, two endogenous brain peptides, are potent in inducing hypothermia and in producing an antinociceptive state.
 ...
PMID:Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine. 29 52

1. The effects of beta-endorphin and morphine on thermoregulatory responses of unanaesthetized rabbits to different ambient temperatures (Ta) of 2, 22 and 32 degrees C were assessed. 2. Intraventricular administration of either beta-endorphin or morphine produced dose-dependent hypothermia at 2 and 22 degrees C Ta. At 2 degrees C Ta the hypothermia was brought about solely by a decrease in metabolic heat production. At 22 degrees C Ta the hypothermia was due to a decrease in metabolism and an increase in peripheral blood flow. However, at 32 degrees C Ta, there were no changes in rectal temperature in response to either beta-endorphin or morphine application. 3. Hypothermic effects of the administration of beta-endorphin or morphine were greatly antagonized by pretreatment of animals with either an opiate antagonist naloxone or a serotonin depletor 5,6-dihydroxytryptamine. 4. These findings indicate that the hypothermic responses to beta-endorphin or morphine in rabbits may be mediated through central serotonergic mechanisms. The hypothermia was due to a decrease in heat production and/or an increase in heat loss.
 ...
PMID:Metabolic, respiratory, vasomotor and body temperature responses to beta-endorphin and morphine in rabbits. 52 21

Repeated intracisternal injections of human beta-endorphin lead to development of tolerance with respect to the catalepsy, analgesia, and hypothermia which are seen following a single injection. The initial injection of beta-endorphin results in increases in the dopamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in neostriatum, as well as increases in the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in hypothalamus and brainstem and a decrease in 5-HIAA in hippocampus. In the present study, we report changes in metabolism of dopamine and serotonin in specific brain areas during the development of tolerance to beta-endorphin. Thus, the development of tolerance to beta-endorphin with respect to catalepsy, analgesia, and hypothermia may be mediated by development of tolerance to the effects of beta-endorphin on brain dopamine and serotonin release.
 ...
PMID:Alterations in brain dopamine and serotonin metabolism during the development of tolerance to human beta-endorphin in rats. 74 24

To explore 5-HT1A receptor responsivity in panic disorder (PD), hypothermic, neuroendocrine and behavioral responses to the selective partial 5-HT1A receptor agonist ipsapirone (IPS) were investigated in patients with primary PD and healthy controls. Fourteen patients and matched controls received a single oral dose of 0.3 mg/kg IPS or placebo under double-blind, random-assignment conditions. IPS induced hypothermia and corticotropin (ACTH)/cortisol release but had only minimal effects on behavior. Compared with controls, the patients with PD exhibited significantly attenuated thermoregulatory and neuroendocrine responses to IPS. Although the healthy subjects reported increased drowsiness and the PD patients rated themselves more nervous and less calm following administration of IPS, no consistent changes in ratings of anxiety or panic symptoms were recorded. The impaired hypothermic and ACTH/cortisol responses following 5-HT1A receptor activation reflects subsensitivity of both the pre- and post-synaptic 5-HT1A receptor-effector system, thus supporting the hypothesis that a 5-HT1A receptor-related serotonergic dysfunction may be linked to the pathophysiology of PD. Future studies of 5-HT1A receptor-effector complex function in conjunction with assessment of the responsivity of other subtypes (e.g. 5-HT2, 5-HT3) should promote the evaluation of 5-HT system integrity in anxiety disorders and its involvement in anxiolytic drug effects.
 ...
PMID:5-HT1A receptor-effector system responsivity in panic disorder. 134 19

This study shows inhibition of the increase in locomotor activity induced by ethanol (2 g/kg i.p.) in mice by a low dose (0.1 mg/kg i.p.) of the non-opioid beta-endorphin fragment ORG 5878 (des-enkephalin-gamma-endorphin). ORG 5878 (0.1 mg/kg i.p.) also significantly antagonised the large increase in electroshock seizure threshold produced by ethanol (1.5 g/kg i.p.). In contrast, the hypothermia induced by ethanol (2 g/kg i.p.) was not altered by ORG 5878 (0.1 mg/kg i.p.). The effects of ORG 5878 showed an abnormal dose-response relationship, in that a high dose (1 mg/kg i.p.) did not significantly suppress any of the behavioural effects of ethanol examined although there was some indication that it attenuated the stimulant action of ethanol. ORG 5878 (0.1, 1 mg/kg i.p.) did not have any intrinsic effects on locomotion, seizure threshold or body temperature in mice. These results are the first demonstration that ORG 5878 may act as an ethanol antagonist in some paradigms.
 ...
PMID:Attenuation of the behavioural effects of ethanol in mice by des-enkephalin-gamma-endorphin (ORG 5878). 141 12

Six met-enkephalin derivatives substituted in position 4 with D-4-chlorophenylalanine or D-4-fluorophenylalanine were obtained. Their antinociceptive activity was determined after icv administration to rats by tail immersion test. Cataleptic activity and the influence of the analogs obtained on the body temperature were also estimated. All compounds exerted analgesic activity, which was decreased significantly by naloxone. Almost all compounds appeared cataleptic, some of them caused hypothermia.
 ...
PMID:Opiate-like peptides. Part XIII. Synthesis and analgesic activity of met-enkephalin analogs substituted in position 4 with D-4-halogenophenylalanine. 166 48


1 2 3 4 5 6 7 8 Next >>