ArticleAddiction biology2016
Chronic ethanol exposure decreases CB1 receptor function at GABAergic synapses in the rat central amygdala.
Article in Addiction biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 42 citations in OpenAlex.
- Adolescent ethanol exposure reduces central amygdala GABA transmission but preserves noradrenergic signaling in adulthood.Neuropharmacology · 2026Article
- Chronic alcohol consumption sex-dependently affects IL-6 modulation of GABAergic synapses in the central amygdala of rhesus macaques.Brain, behavior, and immunity · 2026Article
- Knockdown of the type 1 cannabinoid receptor in the central amygdala increases both spontaneous and water deprivation-induced sodium intake in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Central amygdala neuroimmune signaling in alcohol use disorder.Addiction neuroscience · 2025Article
- Article
- Chronic ethanol induces a pro-inflammatory switch in interleukin-1β regulation of GABAergic signaling in the medial prefrontal cortex of male mice.Brain, behavior, and immunity · 2023Article
- Role of Cannabinoid CB2 Receptor in Alcohol Use Disorders: From Animal to Human Studies.International journal of molecular sciences · 2022Review
- The Synaptic Interactions of Alcohol and the Endogenous Cannabinoid System.Alcohol research : current reviews · 2022Review
- CB1 receptor neutral antagonist treatment epigenetically increases neuropeptide Y expression and decreases alcohol drinking.Neuropharmacology · 2021Article
- Importance of sex and trauma context on circulating cytokines and amygdalar GABAergic signaling in a comorbid model of posttraumatic stress and alcohol use disorders.Molecular psychiatry · 2021Article
- Neurobiological aspects of pain in the context of alcohol use disorder.International review of neurobiology · 2021Article
- Cannabinoids in Audiogenic Seizures: From Neuronal Networks to Future Perspectives for Epilepsy Treatment.Frontiers in behavioral neuroscience · 2021Review
- Multiple sources of internal calcium stores mediate ethanol-induced presynaptic inhibitory GABA release in the central nucleus of the amygdala in mice.Psychopharmacology · 2020Article
- Evidence for incentive salience sensitization as a pathway to alcohol use disorder.Neuroscience and biobehavioral reviews · 2019Review
- Endocannabinoid Signaling in the Central Amygdala and Bed Nucleus of the Stria Terminalis: Implications for the Pathophysiology and Treatment of Alcohol Use Disorder.Alcoholism, clinical and experimental research · 2019Review
- Driving the Downward Spiral: Alcohol-Induced Dysregulation of Extended Amygdala Circuits and Negative Affect.Alcoholism, clinical and experimental research · 2019Review
- Synaptic GABAergic transmission in the central amygdala (CeA) of rats depends on slice preparation and recording conditions.Physiological reports · 2019Article
- Distinct functions of endogenous cannabinoid system in alcohol abuse disorders.British journal of pharmacology · 2019Review
- IL-1β expression is increased and regulates GABA transmission following chronic ethanol in mouse central amygdala.Brain, behavior, and immunity · 2019Article
- Central Amygdala Circuits Mediate Hyperalgesia in Alcohol-Dependent Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The endogenous cannabinoids (eCBs) influence the acute response to ethanol and the development of tolerance, dependence and relapse. Chronic alcohol exposure alters eCB levels and Type 1 cannabinoid receptor (CB1 ) expression and function in brain regions associated with addiction. CB1 inhibits GABA release, and GABAergic dysregulation in the central nucleus of the amygdala (CeA) is critical in the transition to alcohol dependence. We investigated possible disruptions in CB1 signaling of rat CeA GABAergic transmission following intermittent ethanol exposure. In the CeA of alcohol-naive rats, CB1 agonist WIN 55,212-2 (WIN) decreased the frequency of spontaneous and miniature GABAA receptor-mediated inhibitory postsynaptic currents (s/mIPSCs). This effect was prevented by CB1 antagonism, but not Type 2 cannabinoid receptor (CB2 ) antagonism. After 2-3 weeks of intermittent ethanol exposure, these WIN inhibitory effects were attenuated, suggesting ethanol-induced impairments in CB1 function. The CB1 antagonist AM251 revealed a tonic eCB/CB1 control of GABAergic transmission in the alcohol-naive CeA that was occluded by calcium chelation in the postsynaptic cell. Chronic ethanol exposure abolished this tonic CB1 influence on mIPSC, but not sIPSC, frequency. Finally, acute ethanol increased CeA GABA release in both naive and ethanol-exposed rats. Although CB1 activation prevented this effect, the AM251- and ethanol-induced GABA release were additive, ruling out a direct participation of CB1 signaling in the ethanol effect. Collectively, these observations demonstrate an important CB1 influence on CeA GABAergic transmission and indicate that the CeA is particularly sensitive to alcohol-induced disruptions of CB1 signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.