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- W2054221346 endingPage "888" @default.
- W2054221346 startingPage "873" @default.
- W2054221346 abstract "Alcohol use disorders are characterized by compulsive drug-seeking and drug-taking, loss of control in limiting intake, and withdrawal syndrome in the absence of drug. The central amygdala (CeA) and neighboring regions (extended amygdala) mediate alcohol-related behaviors and chronic alcohol-induced plasticity. Acute alcohol suppresses excitatory (glutamatergic) transmission whereas chronic alcohol enhances glutamatergic transmission in CeA. Acute alcohol facilitates inhibitory (GABAergic) transmission in CeA, and chronic alcohol increases GABAergic transmission. Electrophysiology techniques are used to explore the effects of neuropeptides/neuromodulators (CRF, NPY, nociceptin, dynorphin, endocannabinoids, galanin) on inhibitory transmission in CeA. In general, pro-anxiety peptides increase, and anti-anxiety peptides decrease CeA GABAergic transmission. These neuropeptides facilitate or block the action of acute alcohol in CeA, and chronic alcohol produces plasticity in neuropeptide systems, possibly reflecting recruitment of negative reinforcement mechanisms during the transition to alcohol dependence. A disinhibition model of CeA output is discussed in the context of alcohol dependence- and anxiety-related behaviors." @default.
- W2054221346 created "2016-06-24" @default.
- W2054221346 creator A5043734937 @default.
- W2054221346 creator A5060479945 @default.
- W2054221346 date "2012-02-01" @default.
- W2054221346 modified "2023-10-01" @default.
- W2054221346 title "Neuropeptide modulation of central amygdala neuroplasticity is a key mediator of alcohol dependence" @default.
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