Literature DB >> 15834231

Vasoactive intestinal peptide and corticotropin-releasing hormone increase beta-endorphin release and proopiomelanocortin messenger RNA levels in primary cultures of hypothalamic cells: effects of acute and chronic ethanol treatment.

Michael M Poplawski1, Nadka Boyadjieva, Dipak K Sarkar.   

Abstract

BACKGROUND: beta-Endorphin (beta-EP) neurons are involved in ethanol's action on a variety of brain functions, including positive reinforcement. These neurons are innervated by vasoactive intestinal peptide (VIP)-containing and corticotropin-releasing hormone (CRH)-containing neurons in the hypothalamus. Whether these neuropeptides affect beta-EP neuronal function in the presence or absence of ethanol has not previously been determined.
METHODS: The authors determined the effects of VIP and CRH on gene expression and peptide release from beta-EP neurons in primary cultures of mediobasal hypothalamic cells. The effects of receptor antagonists on VIP- and CRH-induced beta-EP release was determined. Furthermore, the authors studied the effects of acute and chronic treatment with ethanol on the response of beta-EP neurons to VIP and CRH. Real-time reverse-transcription polymerase chain reaction was used for messenger RNA (mRNA) detection, and radioimmunoassay was used for hormone measurements.
RESULTS: We show that beta-EP neurons responded concentration dependently to VIP and CRH treatments by increasing both beta-EP release and proopiomelanocortin mRNA expression. Simultaneous treatment with a nonspecific receptor antagonist reduced the ability of CRH or VIP to induce beta-EP release from mediobasal hypothalamic cells. Acute treatment with ethanol increased beta-EP neuronal gene expression and the secretory response to CRH and VIP. However, previous exposure to chronic ethanol reduced the CRH and VIP responses of these neurons.
CONCLUSIONS: These results indicate that VIP and CRH stimulate beta-EP release from hypothalamic cells in primary cultures and that the stimulatory and adaptive responses of beta-EP neurons to ethanol may involve alteration in the responsiveness of beta-EP-secreting neurons to CRH and VIP.

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Year:  2005        PMID: 15834231     DOI: 10.1097/01.alc.0000158834.11252.2e

Source DB:  PubMed          Journal:  Alcohol Clin Exp Res        ISSN: 0145-6008            Impact factor:   3.455


  6 in total

1.  Period 2 gene deletion abolishes beta-endorphin neuronal response to ethanol.

Authors:  Maria Agapito; Nadia Mian; Nadka I Boyadjieva; Dipak K Sarkar
Journal:  Alcohol Clin Exp Res       Date:  2010-06-25       Impact factor: 3.455

2.  Induction of type 2 iodothyronine deiodinase in the mediobasal hypothalamus by bacterial lipopolysaccharide: role of corticosterone.

Authors:  Edith Sánchez; Praful S Singru; Csaba Fekete; Ronald M Lechan
Journal:  Endocrinology       Date:  2008-01-24       Impact factor: 4.736

3.  Opioid receptors and the discriminative stimulus effects of ethanol in squirrel monkeys: Mu and delta opioid receptor mechanisms.

Authors:  Donna M Platt; Kristen M Bano
Journal:  Eur J Pharmacol       Date:  2010-10-15       Impact factor: 4.432

Review 4.  Integration of the circadian and stress systems: influence of neuropeptides and implications for alcohol consumption.

Authors:  Cybele C P Wong; Gunter Schumann
Journal:  J Neural Transm (Vienna)       Date:  2012-05-31       Impact factor: 3.575

5.  Influence of beta-Endorphin on anxious behavior in mice: interaction with EtOH.

Authors:  Judith E Grisel; Jessica L Bartels; Stephani A Allen; Victoria L Turgeon
Journal:  Psychopharmacology (Berl)       Date:  2008-07-05       Impact factor: 4.530

6.  Dibutyryl-cAMP affecting fat deposition of finishing pigs by decreasing the inflammatory system related to insulin sensitive or lipolysis.

Authors:  Xianyong Ma; Wei Fang; Zongyong Jiang; Li Wang; Xuefen Yang; Kaiguo Gao
Journal:  Genes Nutr       Date:  2016-06-03       Impact factor: 5.523

  6 in total

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