Chronic alcohol remodels prefrontal neurons and disrupts NMDA receptor-mediated fear extinction encoding

Alcoholism is frequently co-morbid with posttraumatic stress disorder (PTSD) but it is unclear how alcohol impacts neural circuits mediating recovery from trauma. We found that chronic intermittent ethanol (CIE) impaired fear extinction and remodeled the dendritic arbor of medial prefrontal cortical...

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Detalles Bibliográficos
Autores principales: Holmes, Andrew, Fitzgerald, Paul J., MacPherson, Kathryn P., DeBrouse, Lauren, Colacicco, Giovanni, Flynn, Shaun M., Masneuf, Sophie, Pleil, Kristen E., Li, Chia, Marcinkiewcz, Catherine A., Kash, Thomas L., Gunduz-Cinar, Ozge, Camp, Marguerite
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2012
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471649/
https://www.ncbi.nlm.nih.gov/pubmed/22941108
http://dx.doi.org/10.1038/nn.3204
Descripción
Sumario:Alcoholism is frequently co-morbid with posttraumatic stress disorder (PTSD) but it is unclear how alcohol impacts neural circuits mediating recovery from trauma. We found that chronic intermittent ethanol (CIE) impaired fear extinction and remodeled the dendritic arbor of medial prefrontal cortical (mPFC) neurons in mice. CIE impaired extinction encoding by infralimbic (IL) mPFC neurons in vivo, and functionally downregulated burst-mediating NMDA GluN1 receptors. These findings suggest alcohol may increase risk for trauma-related anxiety disorders by disrupting mPFC-mediated extinction of fear.

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