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 effect of lesioning the ipsilateral globus pallidus (GP) on apomorphine-induced circling in nigro-striatal lesioned rats was investigated. A GP electrolesion almost abolished circling whereas a kainic acid lesion partly antagonized circling. Drugs that affect GABA and opiate receptors were injected in GP through a cannula. Circling was antagonized by the GABA antagonists picrotoxin and bicuculline, the GABA agonist muscimol and by baclofen. Opiate receptor agonists including morphine, levorphanol, [D-Ala2, D-Leu5]-enkephalin and beta-endorphin had no effect on circling in GP. Ethylketazocine caused a pronounced, naloxone-reversible slowing of apomorphine circling. Apomorphine-induced circling behaviour may be modulated by GP GABA receptors and kappa-type opiate receptors.
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PMID:Role of globus pallidus GABA and opiate receptors in apomorphine circling in nigro-striatal lesioned rats. 628 99

A variety of behavioral tests were used to characterize the cataleptic state induced by various treatments. Besides catalepsy, posture, locomotion, rigidity and the presence of reflexive responses were assessed. Measures of analgesia and body temperature were taken. The behavioral profiles of beta-endorphin, morphine, etonitazene, haloperidol, arecoline and GABA were compared at the time maximal catalepsy scores were obtained. Results indicated that, for an equivalent degree of catalepsy, the profile of beta-endorphin was similar to that of opiates, except for changes in body temperature; beta-endorphin's profile differed markedly from that of haloperidol, arecoline and GABA. Catalepsy was less pronounced with the latter two drugs. There were similarities in the behavioral profile of haloperidol and arecoline.
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PMID:Similarities of the cataleptic state induced by beta-endorphin and morphine. 629 79

In decerebrate, cerebellectomized cats, a comparison was made between the effects of electrical stimulation in nucleus raphe magnus (NRM) and iontophoretic application of GABA, glycine, met-enkephalin and beta-endorphin on the responses of neurones in the medial brain stem reticular formation to tooth pulp stimulation. NRM stimulation, GABA, glycine and enkephalin produced a short lasting inhibition of tooth pulp evoked responses whilst the time course of the inhibition produced by beta-endorphin was much slower, often lasting up to 1 h following a 3-7 min ejection period. The effects of GABA and glycine could be antagonised by iontophoresis of bicuculline and strychnine respectively whilst intravenous injection of naloxone antagonised the inhibition induced by the opioid peptides. In most neurones tested, inhibition of tooth pulp evoked responses by NRM stimulation was blocked by iontophoretic application of bicuculline but not by strychnine or naloxone (i.v.). We conclude that GABA may act as a transmitter which mediates the inhibitory effects of NRM on the responses of reticular neurones to tooth pulp stimulation. Thus GABA may be involved in stimulation produced analgesia.
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PMID:Actions of GABA, glycine, methionine-enkephalin and beta-endorphin compared with electrical stimulation of nucleus raphe magnus on responses evoked by tooth pulp stimulation in the medial reticular formation in the cat. 630 24

The observation that opiates and endorphins exert euphorogenic effects in normal probands points to a possible involvement of endorphins in different types of affective disorders. There are several powerful arguments that the activation of particular central opiate receptors (e.g. by "opium cure", beta-endorphin, partial agonists, release of endorphins via electroconvulsion) exerts curative effects in endogenous depression. Results from a double-blind investigation of the possible antidepressant action of the opiate partial agonist buprenorphine in patients with endogenous depression revealed a strong antidepressant effect of this substance. A series of anticonvulsants, possibly acting via a GABA-ergic-like mechanism (valproate, dipropylacetamide, carbamazepine and oxcarbazepine), have recently been shown by different groups to possess antimanic and also, partially, antidepressant properties. Furthermore, a synergistic mode of action in the prophylaxis of manic episodes has been observed as concerns valproate and lithium. On the other hand, there is some evidence from both in vitro and in vivo animal experiments that chronic application of lithium results in a modification of the GABA-turnover. The present paper reviews the present state of knowledge concerning the concept of a GABA-dependent regulation of affective states.
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PMID:Current perspectives in the pharmacopsychiatry of depression and mania. 630 56

The proconvulsant actions of high doses of systemic morphine are probably mediated by 3 different systems. One of them produces non-convulsant electrographic seizures and can be activated separately from the others both by intracerebroventricular injections as well as microinjections into discrete subcortical areas. The enkephalins and beta-endorphin, when administered to the same loci, produce similar effects. Pharmacological evidence suggests that specific opiate receptors of the delta-subtype mediate the epileptiform effects produced by this system. The second system mediating proconvulsant effects of systemic morphine is not mediated by stereo-specific opiate receptors. It produces behavioral convulsions, and the GABA-ergic system has been implicated in its action. A third proconvulsant action of systemic morphine can be activated separately from the other two systems by administering this compound with other convulsive agents or manipulations. Specific mu-type opiate receptors are implicated in this effect. In addition to potent proconvulsant effects, systemic morphine also has anticonvulsant properties which are mediated by specific opiate mu-receptors. The conditions under which morphine acts as a proconvulsant rather than an anticonvulsant agent are, as yet, not understood.
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PMID:Pro- and anticonvulsant actions of morphine and the endogenous opioids: involvement and interactions of multiple opiate and non-opiate systems. 631 87

Opioid peptide-like (OPL)-immunoreactivity and (the GABA-biosynthetic enzyme) glutamic acid decarboxylase-like (GAD)-immunoreactivity were localized in rat neostriatum and central amygdaloid nucleus (ACE) using a polyclonal sheep antiserum to rat brain GAD and a monoclonal mouse antibody to the N-terminus of beta-endorphin (3-E7) as primary antisera. PAP-immunohistochemistry revealed GAD-immunoreactivity in the majority of neurons in neostriatum and ACE. OPL-immunoreactivity was observed in numerous neurons in ACE, but only in few neostriatal nerve cells. In double immunofluorescence in the same section OPL- and GAD-immunoreactivity colocalized in few medium size cells in the neostriatum, but in numerous neurons in ACE. The existence of opioid peptide containing GABAergic neurons in ACE and neostriatum is demonstrated.
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PMID:Opioid peptide-like immunoreactivity localized in GABAErgic neurons of rat neostriatum and central amygdaloid nucleus. 666 48

Huntington's Disease (HD) is a progressive degenerative disorder of the central nervous system inherited as an autosomal dominant trait. Clinically, the disorder is characterized by choreoathetosis (with age of onset typically in the late thirties or early forties) and neuropsychiatric disturbance. The striatum is particularly vulnerable to the degenerative disease process, with selective loss of medium spiny neurons and decreased levels of associated neurotransmitters, including substance P. GABA, met-enkephalin and dynorphin. Although the underlying pathophysiology is unknown, recent theories concerning pathogenesis have involved mitochondrial abnormalities and excitotoxin-mediated damage. The gene for HD has recently been discovered and characterized as an unstable CAG trinucleotide repeat sequence on the short arm of chromosome 4 (now known as IT15). The direct test now available for the HD gene has facilitated disease diagnosis, particularly for those with unclear family history or chorea of uncertain origin; presymptomatic testing is also available. Management of affected individuals is unsatisfactory as only symptomatic control is available. However, as the effect of the genetic abnormality may soon be known, specific treatment of the disorder may become available in the near future.
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PMID:Huntington's disease: recent advances in diagnosis and management. 775 74

Our research focusses on the role of brain and hypophysis in the control of background adaptation in the clawed toad, Xenopus laevis. This adaptation is regulated by alpha-melanophorestimulating hormone (alpha-MSH). Previously, it was shown that various neurotransmitters influence alpha-MSH release. Here we report about the origin of these factors. Using retrograde labelling techniques combined with immunocytochemistry, it was found that the inhibitory transmitters dopamine and neuropeptide Y coexist in neurons in the suprachiasmatic nucleus. These neurons project to the pars intermedia and synaptically contact the alpha-MSH-producing melanotrope cells. In the synapses also GABA is present. Tracing of the optic nerve indicated the presence of a direct retinosuprachiasmatic tract. Furthermore, locus coeruleus neurons project to the pars intermedia. They contain the inhibitory transmitter noradrenaline. The stimulatory factors corticotropin-releasing hormone and thyrotropin stimulating hormone originate from the magnocellular nucleus which send its processes to the neural lobe of the hypophysis.
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PMID:Central control of melanotrope cells of Xenopus laevis. 780 85

The ring-A-reduced progesterone derivative 5 alpha-pregnan-3 alpha-ol-20-one (tetrahydroprogesterone) is synthesized under normal physiological conditions in the brain and is a potent modulator of the GABA receptor. This neurosteroid has significant sedative and anxiolytic properties. Corticotropin-releasing hormone plays a major role in stress-induced activation of the hypothalamo-pituitary-adrenal axis, and sustained hyperactivity of hypothalamic corticotropin-releasing hormone-producing neurons may be causally related to both, increased pituitary-adrenal secretion and behavioural symptoms observed in anxiety and affective disorders. We investigated the effect of tetrahydroprogesterone on corticotropin-releasing hormone-induced anxiety, the basal and methoxamine-stimulated release of corticotropin-releasing hormone from hypothalamic organ explants in vitro, and adrenalectomy-induced up-regulation of the gene expression of corticotropin-releasing hormone in the hypothalamic paraventricular nucleus in rats. At doses of 5 and 10 micrograms i.c.v., tetrahydroprogesterone counteracted the anxiogenic action of 0.5 microgram of corticotropin-releasing hormone. Tetrahydroprogesterone did not alter the basal release of corticotropin-releasing hormone in vitro, but suppressed the stimulatory effect of the alpha 1-adrenergic agonist methoxamine on this parameter. Measurements of the steady-state levels of mRNA coding for corticotropin-releasing hormone by quantitative in situ-hybridization histochemistry revealed that tetrahydroprogesterone was equipotent with corticosterone in preventing adrenalectomy-induced up-regulation of peptide gene expression. Systemic administration of tetrahydroprogesterone also restrained adrenalectomy-induced thymus enlargement. These results demonstrate that tetrahydroprogesterone has anxiolytic effects that are mediated through interactions with hypothalamic corticotropin-releasing hormone in both, genomic and non-genomic fashions.
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PMID:The neurosteroid tetrahydroprogesterone counteracts corticotropin-releasing hormone-induced anxiety and alters the release and gene expression of corticotropin-releasing hormone in the rat hypothalamus. 781 4

Corticotropin releasing factor (CRF) is a 41 amino acid peptide implicated in the expression of stress- and fear-enhanced behaviors. CRF potentiates the amplitude of the startle reflex, and this effect is reversed by benzodiazepines (BDZ), suggesting that the startle-enhancing effects of CRF are modulated by changes in the GABA/BDZ receptor complex. In the present study, CRF-potentiated startle is inhibited by alphaxalone, a pregnane steroid anesthetic that is thought to act via the GABA/BDZ receptor complex. Alphaxalone (ALX) does not reduce CRF-potentiated startle by producing a generalized reduction in reactivity, since blockade of CRF-stimulated startle was not accompanied by an ALX-induced reduction in baseline startle amplitude and ALX does not reduce strychnine-potentiated startle. The effects of alphaxalone on CRF-potentiated startle may not be generalized to all CRF-stimulated behaviours, since alphaxalone failed to disrupt CRF-stimulated locomotor activity. CRF-potentiated startle is a useful assay for studying the effects of novel anxiolytic agents, and alphaxalone appears to be a steroid anesthetic with anxiolytic properties in this assay.
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PMID:Alphaxalone, a steroid anesthetic, inhibits the startle-enhancing effects of corticotropin releasing factor, but not strychnine. 786 86


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