Neuropeptide Y opposes alcohol effects on gamma-aminobutyric acid release in amygdala and blocks the transition to alcohol dependence
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Background During the transition to alcohol and drug addiction, neuromodulator systems in the extended amygdala are recruited to mediate aspects of withdrawal and relapse via convergence on inhibitory gamma-aminobutyric acid (GABA) neurons in central amygdala (CeA).Methods This study investigated the role of neuropeptide Y (NPY) in excessive alcohol drinking by making rats dependent on alcohol via alcohol vapor inhalation. This study also utilized intracellular and whole-cell recording techniques to determine the effects of NPY on GABAergic inhibitory transmission in CeA, synaptic mechanisms involved in these NPY effects, and NPY interactions with alcohol in the CeA of alcohol-naive and alcohol-dependent rats.Results Chronic NPY treatment blocked excessive operant alcohol-reinforced responding associated with alcohol dependence, as well as gradual increases in alcohol responding by intermittently tested nondependent control animals. Neuropeptide Y decreased baseline GABAergic transmission and reversed alcohol-induced enhancement of inhibitory transmission in CeA by suppressing GABA release via actions at presynaptic Y(2) receptors.Conclusions These results highlight NPY modulation of GABAergic signaling in central amygdala as a promising pharmacotherapeutic target for the treatment of alcoholism. Gamma-aminobutyric acid neurons in the CeA likely constitute a major point of convergence for neuromodulator systems recruited during the transition to alcohol dependence.
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For alcohol, NPY administration directly in the brain blocks the increase in self-administration in alcohol-preferring rats and in alcohol dependence, blocks the transition to excessive drinking with development of dependence, and blocks the increase in GABA release in the CeA produced by alcohol.
“For alcohol, NPY administration directly in the brain blocked the increase in self-administration in alcoholpreferring rats and in alcohol dependence, blocked the transition to excessive drinking with the development of dependence, and blocked the increase in GABA release in the CeA that was produced by alcohol”
From Drug Addiction: Hyperkatifeia/Negative Reinforcement as a Framework for Medications Development (2021) · cites this paper as Gilpin et al., 2011
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References 44 · Cited by 116
- Authors
- Gilpin, N. W., Misra, K., Herman, M. A., Cruz, M. T., Koob, G. F., & Roberto, M.
- Affiliations
- Scripps Research Institute (US)
- Corresponding author
- Gilpin, Nicholas W.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 69
- Issue
- 11
- Pages
- 1091-1099
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC3090491
- OpenAlex
- W2115234743
- Cited by
- 116
- References
- 44
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 5 · 2022: 8 · 2021: 8 · 2020: 4 · 2019: 9 · 2018: 7 · 2017: 7 · 2016: 7 · 2015: 8 · 2014: 13 · 2013: 10 · 2012: 11
- FWCI
- 5.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (AA016436, AA016985, AA015566, AA06420, AA08459, AA012602)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- neuropeptide Y, gamma-aminobutyric acid release, central amygdala, alcoholism, alcohol withdrawal, alcohol relapse, Y2 receptor, presynaptic inhibition, GABAergic neurotransmission, excessive alcohol drinking
- MeSH terms
- Ethanol, Amygdala, Analysis of Variance, Animals, Conditioning, Operant, gamma-Aminobutyric Acid, Male, Synaptic Transmission, Neurons, Neuropeptide Y, Self Administration, Rats, Wistar, Patch-Clamp Techniques, Alcohol-Related Disorders, Rats, Inhibitory Postsynaptic Potentials, Miniature Postsynaptic Potentials
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