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)

Activation of the GABA(A)-benzodiazepine receptor complex has previously been shown to inhibit the release of alpha-melanocyte-stimulating hormone (alpha-MSH) from proopiomelanocortin (POMC) neurons of the hypothalamus. To examine whether long-term activation of the GABA(A) receptor may also modulate the expression of the POMC gene in hypothalamic neurons, we have investigated the effect of chronic treatment with the centraltype benzodiazepine receptor agonist clonazepam, alone or in combination with the GABA(A) receptor agonist muscimol, on POMC mRNA levels in four anatomical subdivisions of the arcuate nucleus of the rat hypothalamus, using quantitative in situ hybridization. Clonazepam treatment produced a significant decrease in POMC mRNA levels in all the regions of the arcuate nucleus with the exception of the most rostral one. Administration of both clonazepam and muscimol induced a marked reduction of mRNA levels in all the subdivisions of the arcuate nucleus. Chronic treatment with muscimol and clonazepam also induced a significant decrease in POMC mRNA level in the pars intermedia of the pituitary. These results, together with previous data, indicate that activation of the GABA(A)-benzodiazepine receptor complex inhibits the expression of the POMC gene as well as the release of POMC-derived mature peptides in both hypothalamic neurons and pituitary melanotrophs.
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PMID:Activation of the GABA(A)-benzodiazepine receptor complex inhibits proopiomelanocortin gene expression in the rat arcuate nucleus. 1991 29

The older of two siblings began to have spasms and partial seizures at 1 month of age. Head magnetic resonance imaging showed an abnormal area in the left temporo-parieto-occipital region. Interictal electroencephalogram (EEG) showed a suppression-burst pattern. Adrenocorticotropic hormone stopped the spasms, but the seizures continued. Clonazepam, carbamazepine, zonisamide, and clobazam were ineffective. She underwent focal resection at age 8 months. Postoperatively, the seizures disappeared. Histopathologically, the lesion appeared to be focal cortical dysplasia type IIa. The younger sibling had spasms from birth. Head magnetic resonance imaging showed left hemi-megalencephaly. Interictal EEG showed a suppression-burst pattern. Phenobarbital, valproic acid, and zonisamide were ineffective. He underwent hemispherotomy at age 2 months and became seizure free. The histopathological features were consistent with those of hemi-megalencephaly. The siblings' EEG and clinical courses had some similarities. These siblings' conditions may have the same genetic background.
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PMID:Two siblings with cortical dysplasia: Clinico-electroencephalographic features. 2601 18