ArticleAlcoholism, clinical and experimental research2015
Ethanol produces corticotropin-releasing factor receptor-dependent enhancement of spontaneous glutamatergic transmission in the mouse central amygdala.
Article in Alcoholism, clinical and experimental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Central amygdala neuroimmune signaling in alcohol use disorder.Addiction neuroscience · 2025Article
- Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025Review
- Central amygdala corticotropin-releasing factor neurons promote hyponeophagia but do not control alcohol drinking in mice.Molecular psychiatry · 2022Article
- Astrocytes play a critical role in mediating the effect of acute ethanol on central amygdala glutamatergic transmission.Neuropharmacology · 2022Article
- Subregional Differences in Alcohol Modulation of Central Amygdala Neurocircuitry.Frontiers in molecular neuroscience · 2022Review
- The Rewarding and Anxiolytic Properties of Ethanol within the Central Nucleus of the Amygdala: Mediated by Genetic Background and Nociceptin.The Journal of pharmacology and experimental therapeutics · 2020Article
- Chronic alcohol disrupts hypothalamic responses to stress by modifying CRF and NMDA receptor function.Neuropharmacology · 2020Article
- Driving the Downward Spiral: Alcohol-Induced Dysregulation of Extended Amygdala Circuits and Negative Affect.Alcoholism, clinical and experimental research · 2019Review
- The center of the emotional universe: Alcohol, stress, and CRF1 amygdala circuitry.Alcohol (Fayetteville, N.Y.) · 2018Review
- Targeted overexpression of CRH receptor subtype 1 in central amygdala neurons: effect on alcohol-seeking behavior.Psychopharmacology · 2018Article
- Ethanol Modulates Glutamatergic Transmission and NMDAR-Mediated Synaptic Plasticity in the Agranular Insular Cortex.Frontiers in pharmacology · 2018Article
- Review
- Presynaptic Ethanol Actions: Potential Roles in Ethanol Seeking.Handbook of experimental pharmacologyArticle
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundEthanol (EtOH) modulation of central amygdala (CeA) neurocircuitry plays a key role in the development of alcoholism via activation of the corticotropin-releasing factor (CRF) receptor (CRFR) system. Previous work has predominantly focused on EtOH × CRF interactions on the CeA GABA circuitry; however, our laboratory recently showed that CRF enhances CeA glutamatergic transmission. Therefore, this study sought to determine whether EtOH modulates CeA glutamate transmission via activation of CRF signaling.
methodsThe effects of EtOH on spontaneous excitatory postsynaptic currents (sEPSCs) and basal resting membrane potentials were examined via standard electrophysiology methods in adult male C57BL/6J mice. Local ablation of CeA CRF neurons (CRF(CeAhDTR) ) was achieved by targeting the human diphtheria toxin receptor (hDTR) to CeA CRF neurons with an adeno-associated virus. Ablation was quantified post hoc with confocal microscopy. Genetic targeting of the diphtheria toxin active subunit to CRF neurons (CRF(DTA) mice) ablated CRF neurons throughout the central nervous system, as assessed by quantitative reverse transcriptase polymerase chain reaction quantification of CRF mRNA.
resultsAcute bath application of EtOH significantly increased sEPSC frequency in a concentration-dependent manner in CeA neurons, and this effect was blocked by pretreatment of co-applied CRFR1 and CRFR2 antagonists. In experiments utilizing a CRF-tomato reporter mouse, EtOH did not significantly alter the basal membrane potential of CeA CRF neurons. The ability of EtOH to enhance CeA sEPSC frequency was not altered in CRF(CeAhDTR) mice despite a ~78% reduction in CeA CRF cell counts. The ability of EtOH to enhance CeA sEPSC frequency was also not altered in the CRF(DTA) mice despite a 3-fold reduction in CRF mRNA levels.
conclusionsThese findings demonstrate that EtOH enhances spontaneous glutamatergic transmission in the CeA via a CRFR-dependent mechanism. Surprisingly, our data suggest that this action may not require endogenous CRF.
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