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)

Acute intracisternal administration of human beta-endorphin produced catalepsy and increased striatal concentrations of 3,4-dihydroxyphenylacetic acid (DOPA) and homovanillic acid (HVA). All of these effects were blocked by naloxone. Apomorphine, a dopamine receptor antagonist, also prevented beta-endorphin-induced catalepsy and the increase in striatal DOPAC and HVA. The combination of subcataleptic doses of haloperidol and beta-endorphin produced catalepsy and large increases in striatal DOPAC and HVA. These data provide evidence for a role for nigrostriatal dopamine neurons in beta-endorphin-induced catalepsy. The apparent increase in striatal dopamine turnover following beta-endorphin administration may be compensatory.
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PMID:Dopaminergic mediation of beta-endorphin-induced catalepsy. 56 67

The aim of this paper is to study the effect of 1, 2 or 3 months' administration of chlorpromazine (CPZ), thioridazine (TDZ) (2 or 6 mg/kg) or haloperidol (HAL) (0.25 or 1 mg/kg) IP on the level of leu- and met-enkephalin (ENK) in striatum. A dose- and time-dependent increase of striatal ENK level was observed after chronic administration of the neuroleptics (NL), but 8 days after withdrawal of chronically administered NL striatal ENK was decreased. Apomorphine pretreatment significantly attenuated the elevation in ENK produced by chronic injections of NL. In perfusion fluid obtained from the lateral ventricle of animals treated 1 month with HAL a dose-dependent increase of ENK levels was observed, which was augmented by potassium ions. It is concluded that: 1) Chronic administration of neuroleptic drugs that block dopamine receptors increases the level and the release of striatal enkephalins; 2) The results support the hypothesis that activation of dopaminergic neurons tonically inhibits the synthesis of enkephalins in the striatum.
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PMID:Chronic treatment with chlorpromazine, thioridazine or haloperidol increases striatal enkephalins and their release from rat brain. 188 95

Apomorphine (Apo), a D1/D2 Dopamine (DA) agonist, at high doses (500 micrograms/kg) induces a short-lasting insomnia, antagonized by a secondary injection of corticotropin-like intermediate lobe peptide (CLIP, 10 ng); these effects are also observed with hypophysectomized (hypoX) rats. The administration of the serotonin (5-HT) agonist 8-hydroxy-2-di-n-propylamino-tetralin (8-OHDPAT, 0.3 mg/kg) induces also an insomnia which, unlike Apo, is followed by a significant PS rebound. CLIP, again, antagonizes the 8-OHDPAT-induced insomnia. Finally, Bromocriptine (5 mg/kg), an agonist for both DA and 5-HT, induces first an insomnia (antagonized by CLIP), followed by a PS rebound; these effects persist in hypoX rats.
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PMID:Proopiomelanocortin (POMC)-derived peptides and sleep in the rat. Part 2--Aminergic regulatory processes. 196 3

Rats subjected to diencephalic hemisection were s.c. treated with alpha-MSH (20 micrograms/rat daily) or with [Nle4,D-Phe7]alpha-MSH (10 micrograms/rat every other day) for two weeks starting on day 3 after lesion. Apomorphine-induced (1 mg/kg s.c.) rotational behavior was studied on days 7, 14 and 21 after lesion, and a sensorimotor test battery was carried out on days 3, 10, 17 and 24 after lesion. [Nle4,D-Phe7]alpha-MSH greatly reduced rotational behavior and significantly improved sensorimotor performance. Histological studies showed that treatment with alpha-MSH and, even more markedly, with [Nle4,D-Phe7]alpha-MSH reduced the size of the lesion and the pseudoinflammatory reaction, and caused a marked proliferation and hypertrophy of astroglia. Binding studies showed that no supersensitivity of striatal dopamine receptors developed on the lesioned side of alpha-MSH- and [Nle4,D-Phe7]alpha-MSH-treated rats. The present results seem to further support the trophic role of MSH peptides on nerve tissue.
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PMID:[Nle4,D-Phe7]alpha-MSH improves functional recovery in rats subjected to diencephalic hemisection. 284 81

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

The effect of alpha-MSH on coat color was examined in viable yellow mice (C3H/He-A*vy). These mice normally grow a coat of darkly pigmented hair at puberty. This darkening effect was also evident in hair that grew in a region that had been plucked at 13 days of age. Administration of alpha-MSH increased the darkness of this hair and the hair which grew naturally in an unplucked area. However, the natural coat darkening that occurred at puberty was not associated with an increase in plasma immunoreactive alpha-MSH levels. Moreover, although bromocryptine, a dopamine agonist that inhibits alpha-MSH release from the pituitary reduced the darkness of the coat that grew after plucking the reduction in coat darkening was unrelated to changes in plasma alpha-MSH. Nevertheless, this effect of bromocryptine was reversed when alpha-MSH was administered together with the drug. Apomorphine had no effect on coat darkening and produced only a slight decrease in plasma alpha-MSH. Melatonin reduced coat darkening slightly but, like apomorphine, had little effect on plasma alpha-MSH concentrations. Although alpha-MSH may have a physiological role in coat darkening in the C3H/He-A*vy mouse at puberty the response seems to be unrelated to an increase in circulating alpha-MSH. Thus, other factors, such as changes in melanocyte sensitivity to alpha-MSH or inhibitory mechanisms that prevent coat darkening during prepubertal and adult life may be involved in regulation of coat color in the viable yellow mouse.
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PMID:Alpha-MSH and coat color changes in the mouse. 653 Dec 69

Previous studies have indicated that 30 min of swimming in room temperature water is a potent stimulus for the secretion of beta-endorphin (beta E) from the intermediate lobe (IL) of the pituitary in rodents. Repeated daily challenge with this paradigm over days to weeks leads to a progressive increase in proopiomelanocortin (POMC)-derived IL peptides and POMC mRNA levels as well as an increase in the stimulated secretion of beta E in response to rechallenge with swim. The current studies were undertaken to examine the possible role of dopamine systems in mediating swim stress-induced changes in IL beta E biosynthesis and release. Confirming previous results, a 30 min swim stress exposure caused plasma concentrations of beta E to increase several fold. Apomorphine (APO), a dopaminergic agonist, completely blocked this effect, suggesting that dopamine receptors may mediate the acute IL response to swim stress. Animals that swam once daily for 14 days displayed elevated beta E levels in both the IL and plasma 24 h after the last swim session. In these animals, repeated administration of APO did not reverse swim-stress-induced changes in beta E. Immediately following an acute-swim rechallenge, animals which had been previously swim-stressed for 14 days demonstrated significantly greater beta E release than naive animals. Again, an acute injection of APO inhibited the acute increase in IL secretion, suggesting that repeatedly swum animals are still responsive to the acute effects of APO even though repeated coadministration of APO with swim exposure had no effect on IL beta E peptide stores or plasma beta E concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dopamine regulation of swim stress induction of the pituitary intermediate lobe proopiomelanocortin system. 825 90

Erection is basically a spinal reflex that can be initiated by recruitment of penile afferents, but also by visual, olfactory, and imaginary stimuli. The reflex involves both autonomic and somatic efferents and is modulated by supraspinal influences. Several central transmitters involved in the erectile control have been identified. Dopamine, acetylcholine, nitric oxide (NO), and peptides, such as oxytocin and adrenocorticotropic/alpha-melanocyte-stimulating hormone, seem to have a facilitatory role, whereas serotonin may be either facilitatory or inhibitory, and enkephalins are inhibitory. Peripherally, the balance between contractant and relaxant factors controls the degree of contraction of the smooth muscle of the corpora cavernosa and determines the functional state of the penis. Noradrenaline contracts both corpus cavernosum and penile vessels via stimulation of alpha(1)-adrenoceptors. Neurogenic NO is considered the most important factor for relaxation of penile vessels and corpus cavernosum. The role of other mediators released from nerves or endothelium has not been definitely established. Erectile dysfunction (ED) may be due to inability of penile smooth muscles to relax. This inability can have multiple causes. However, patients with ED respond well to the pharmacological treatments that are currently available. The drugs used are able to substitute, partially or completely, the malfunctioning endogenous mechanisms that control penile erection. Most drugs have a direct action on penile tissue facilitating penile smooth muscle relaxation, including prostaglandin E(1), NO donors, phosphodiesterase inhibitors, and alpha-adrenoceptor antagonists. Dopamine receptors in central nervous centers participating in the initiation of erection have been targeted for the treatment of ED. Apomorphine, administered sublingually, is the first of such drugs.
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PMID:Pharmacology of penile erection. 1154 36