<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sha, Kai</style></author><author><style face="normal" font="default" size="100%">Choi, Seung-Hoon</style></author><author><style face="normal" font="default" size="100%">Im, Jeongdae</style></author><author><style face="normal" font="default" size="100%">Lee, Gyunghee G</style></author><author><style face="normal" font="default" size="100%">Loeffler, Frank</style></author><author><style face="normal" font="default" size="100%">Park, Jae H</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Regulation of ethanol-related behavior and ethanol metabolism by the Corazonin neurons and Corazonin receptor in Drosophila melanogaster.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS One</style></secondary-title><alt-title><style face="normal" font="default" size="100%">PLoS ONE</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acetaldehyde</style></keyword><keyword><style  face="normal" font="default" size="100%">Alcohol Dehydrogenase</style></keyword><keyword><style  face="normal" font="default" size="100%">Aldehyde Dehydrogenase</style></keyword><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyclic AMP-Dependent Protein Kinases</style></keyword><keyword><style  face="normal" font="default" size="100%">Drosophila melanogaster</style></keyword><keyword><style  face="normal" font="default" size="100%">Drosophila Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Ethanol</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, Reporter</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Neurons</style></keyword><keyword><style  face="normal" font="default" size="100%">Neuropeptides</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Neuropeptide</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription, Genetic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">e87062</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Impaired ethanol metabolism can lead to various alcohol-related health problems. Key enzymes in ethanol metabolism are alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH); however, neuroendocrine pathways that regulate the activities of these enzymes are largely unexplored. Here we identified a neuroendocrine system involving Corazonin (Crz) neuropeptide and its receptor (CrzR) as important physiological regulators of ethanol metabolism in Drosophila. Crz-cell deficient (Crz-CD) flies displayed significantly delayed recovery from ethanol-induced sedation that we refer to as hangover-like phenotype. Newly generated mutant lacking Crz Receptor (CrzR(01) ) and CrzR-knockdown flies showed even more severe hangover-like phenotype, which is causally associated with fast accumulation of acetaldehyde in the CrzR(01) mutant following ethanol exposure. Higher levels of acetaldehyde are likely due to 30% reduced ALDH activity in the mutants. Moreover, increased ADH activity was found in the CrzR(01) mutant, but not in the Crz-CD flies. Quantitative RT-PCR revealed transcriptional upregulation of Adh gene in the CrzR(01) . Transgenic inhibition of cyclic AMP-dependent protein kinase (PKA) also results in significantly increased ADH activity and Adh mRNA levels, indicating PKA-dependent transcriptional regulation of Adh by CrzR. Furthermore, inhibition of PKA or cAMP response element binding protein (CREB) in CrzR cells leads to comparable hangover-like phenotype to the CrzR(01) mutant. These findings suggest that CrzR-associated signaling pathway is critical for ethanol detoxification via Crz-dependent regulation of ALDH activity and Crz-independent transcriptional regulation of ADH. Our study provides new insights into the neuroendocrine-associated ethanol-related behavior and metabolism.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24489834?dopt=Abstract</style></custom1></record></records></xml>