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)

We examined the effect of chronic administration (14 days) of haloperidol (2 mg/kg/day) or sulpiride (100 mg/kg/day), on the mRNA levels of various genes in the rat striatum and pituitary by quantitative in situ and Northern blot hybridizations. In the pituitary, haloperidol and sulpiride induced similar increases of mRNAs of pro-opiomelanocortin (POMC) (+65% and +73%), prolactin (PRL) (+821% and +840%) and growth hormone (GH) (+32% and +47%), but sulpiride induced a greater increase of D2R mRNA (+125%) than haloperidol (+92%). In the striatum, sulpiride and haloperidol had different effects: sulpiride induced a higher increase than haloperidol of both preproenkephalin A (PPA) mRNA (+67% versus +47%) and D2 dopamine receptor (D2R) mRNAs (+72% versus +40%). Moreover, haloperidol and sulpiride had opposite effects on substance P (SP) mRNA. Haloperidol decreased the amount of SP mRNA by 20% while sulpiride increased it by 20%. The D1 dopamine receptor (D1R) mRNA level was not significantly modified after either treatment. Our results demonstrate that the effect of a chronic haloperidol treatment on striatal dopamine receptors and neuropeptide mRNA levels is different to that of sulpiride, whereas it is similar on pituitary hormones mRNA levels.
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PMID:Differential influence of haloperidol and sulpiride on dopamine receptors and peptide mRNA levels in the rat striatum and pituitary. 751 29

Opioid peptides and their receptors are present in the placenta of many species. Dopamine plays an important role in the regulation of opioid release in the nervous system and it may play a similar role in placenta since dopamine receptors are also present in this tissue. The aim of the present work was to examine the effect of dopamine on the basal release of rat placental opioids. The effect of several dopamine receptor agonists and antagonists was tested on the release of immunoreactive beta-endorphin and immunoreactive dynorphin from perfused rat placenta fragments. We found that dopamine and apomorphine stimulated the secretion of immunoreactive beta-endorphin in a dose-dependent manner. The selective D1 dopamine receptor agonist (+/-)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride or SKF-38393 reproduced the effect of dopamine while the selective D1 dopamine receptor antagonist R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl 1,2,3,4,5-tetrahydro-1 H-benzazepine hydrochloride or SCH-23390, prevented the dopamine- and SKF-38393-induced increase of immunoreactive beta-endorphin secretion. The selective and potent D2 dopamine receptor agonist (+/-)-2-(N-phenylethyl-N-propyl) amino-5-hydroxytetralin hydrochloride or PPHT had no effect on immunoreactive beta-endorphin. Finally, none of the agonists tested had any effect on the in vitro secretion of placental immunoreactive dynorphin. Our results suggest that dopamine affects the basal release of placental opioids in an opioid and dopamine receptor-specific manner, its effect being different from the effect it exerts on beta-endorphin in the rat neurointermediate pituitary lobe.
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PMID:Dopamine affects the in vitro basal secretion of rat placenta opioids in an opioid and dopamine receptor type-specific manner. 896 Aug 64

Mice lacking the D2 dopamine receptor (D2(-/-)) and congenic to the C57BL/6J background were tested for opioid-mediated locomotor activity to examine the involvement of the D2 dopamine receptor in opioid pharmacology. Morphine-stimulated locomotor activity did not significantly differ between the two genotypes. The opioid antagonist naloxone dose-dependently decreased spontaneous motor activity in wild-type mice but was without significant effect in D2(-/-) mice. The magnitude of food-conditioned increases in locomotor activity in wild-type mice and D2(-/-) mice was similar but naloxone did not decrease conditioned motor activity in D2(-/-) mice. Spontaneous locomotor activity of mice lacking the endogenous opioids beta-endorphin and/or enkephalin was also tested and we found that naloxone did not reduce activity in mice specifically lacking enkephalin. We suggest that the D2 dopamine receptor is necessary for modulation of spontaneous locomotor activity stimulated by the endogenous opioid enkephalin.
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PMID:Naloxone's suppression of spontaneous and food-conditioned locomotor activity is diminished in mice lacking either the dopamine D(2) receptor or enkephalin. 1612 19

There is increasing evidence that the same brain reward circuits involved in perpetuating drug abuse are involved in the hedonic urges and food cravings observed clinically in overweight and obese subjects. A polymorphism of the D2 dopamine receptor which renders it less sensitive to dopamine stimulation has been proposed to promote self-stimulatory behavior such as consuming alcohol, abusing drugs, or binging on foods. It is important to determine how this polymorphism may interact with other well-known candidate genes for obesity including polymorphisms of the leptin receptor gene and the opiomelanocortin gene. Leptin is a proinflammatory cytokine as well as a long-term signal maintaining body fat. Upper-body obesity stimulates systemic inflammation through the action of multiple cytokines including leptin throughout many organs including the brain. The association of numerous diseases including diabetes mellitus, heart disease, as well as depression with chronic low-grade inflammation due to abdominal obesity has raised the possibility that obesity-associated inflammation affecting the brain may promote addictive behaviors leading to a self-perpetuating cycle that may affect not only foods but addictions to drugs, alcohol, and gambling. This new area of interdisciplinary research holds the promise of developing new approaches to treating drug abuse and obesity.
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PMID:Addictive genes and the relationship to obesity and inflammation. 2149 88