Regulation of alcohol drinking by ventral striatum and extended amygdala circuitry.

Neuropharmacology

Department of Behavioral Neuroscience, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, OR, 97239, USA; VA Portland Health Care System, 3710 SW US Veterans Hospital Rd, Portland, OR, 97239, USA. Electronic address:

Published: July 2022

Alcohol use disorder is a complex psychiatric disorder that can be modeled in rodents using a number of drinking paradigms. Drinking-in-the-dark (DID) is widely used to model the binge/intoxication stage of addiction, and chronic intermittent ethanol vapor procedures (CIE) are used to induce dependence and model withdrawal/negative affect induced escalation of drinking. We discuss experiments showing the ventral striatum (vStr) and extended amygdala (EA) are engaged in response to ethanol in rodents through c-Fos/Fos immunoreactivity studies. We also discuss experiments in rodents that span a wide variety of techniques where the function of vStr and EA structures are changed following DID or CIE, and the role of neurotransmitter and neuropeptide systems studies in these ethanol-related outcomes. We note where signaling systems converge across regions and paradigms and where there are still gaps in the literature. Dynorphin/κ-opioid receptor (KOR) signaling, as well as corticotropin releasing factor (CRF)/CRF receptor signaling were found to be important regulators of drinking behaviors across brain regions and drinking paradigms. Future research will require that females and a variety of rodent strains are used in preclinical experiments in order to strengthen the generalizability of findings and improve the likelihood of success for testing potential therapeutics in human laboratory studies.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9677601PMC
http://dx.doi.org/10.1016/j.neuropharm.2022.109074DOI Listing

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