Effects of food availability and administration of orexigenic and anorectic agents on elevated ethanol drinking associated with drinking in the dark procedures.
about
Requirement of central ghrelin signaling for alcohol rewardGut-brain peptides in corticostriatal-limbic circuitry and alcohol use disordersRole of appetite-regulating peptides in the pathophysiology of addiction: implications for pharmacotherapyPeripherally circulating ghrelin does not mediate alcohol-induced reward and alcohol intake in rodentsPreclinical studies of alcohol binge drinkingPersistent escalation of alcohol drinking in C57BL/6J mice with intermittent access to 20% ethanol.Genome-wide gene expression analysis identifies K-ras as a regulator of alcohol intake"Drinking in the Dark" (DID): a simple mouse model of binge-like alcohol intakeCRF-1 antagonist and CRF-2 agonist decrease binge-like ethanol drinking in C57BL/6J mice independent of the HPA axis.Ghrelin receptor antagonism decreases alcohol consumption and activation of perioculomotor urocortin-containing neuronsExperimental traumatic brain injury alters ethanol consumption and sensitivity.Ghrelin-Derived Peptides: A Link between Appetite/Reward, GH Axis, and Psychiatric Disorders?Modeling binge-like ethanol drinking by peri-adolescent and adult P rats.Commentary: studies on binge-like ethanol drinking may help to identify the neurobiological mechanisms underlying the transition to dependence.The complexity of alcohol drinking: studies in rodent genetic modelsThe neurobiology of binge-like ethanol drinking: evidence from rodent models.Rodent models and mechanisms of voluntary binge-like ethanol consumption: Examples, opportunities, and strategies for preclinical research.CRF1 receptor signaling regulates food and fluid intake in the drinking-in-the-dark model of binge alcohol consumption.Repeated cycles of binge-like ethanol (EtOH)-drinking in male C57BL/6J mice augments subsequent voluntary EtOH intake but not other dependence-like phenotypesSelection for drinking in the dark alters brain gene coexpression networks.Deletion of agouti-related protein blunts ethanol self-administration and binge-like drinking in mice.Repeated binge-like ethanol drinking alters ethanol drinking patterns and depresses striatal GABAergic transmission.The protective effects of the melanocortin receptor (MCR) agonist, melanotan-II (MTII), against binge-like ethanol drinking are facilitated by deletion of the MC3 receptor in mice.Neurobiology of consummatory behavior: mechanisms underlying overeating and drug use.Binge ethanol-drinking potentiates corticotropin releasing factor R1 receptor activity in the ventral tegmental area.Pre-clinical evidence that corticotropin-releasing factor (CRF) receptor antagonists are promising targets for pharmacological treatment of alcoholism."Drinking in the dark" (DID) procedures: a model of binge-like ethanol drinking in non-dependent mice.Genetics and genomics of alcohol responses in Drosophila.Rat animal models for screening medications to treat alcohol use disorders.
P2860
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P2860
Effects of food availability and administration of orexigenic and anorectic agents on elevated ethanol drinking associated with drinking in the dark procedures.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
Effects of food availability a ...... inking in the dark procedures.
@en
type
label
Effects of food availability a ...... inking in the dark procedures.
@en
prefLabel
Effects of food availability a ...... inking in the dark procedures.
@en
P2093
P2860
P1476
Effects of food availability a ...... inking in the dark procedures.
@en
P2093
Angela M Lyons
Dennis R Sparta
Emily G Lowery
Todd E Thiele
P2860
P304
P356
10.1111/J.1530-0277.2008.00784.X
P577
2008-11-01T00:00:00Z