Chronic ethanol consumption exacerbates future stress‐enhanced fear learning, an effect mediated by dorsal hippocampal astrocytes

التفاصيل البيبلوغرافية
العنوان: Chronic ethanol consumption exacerbates future stress‐enhanced fear learning, an effect mediated by dorsal hippocampal astrocytes
المؤلفون: Gillian A. Barkell, Shveta V. Parekh, Jacqueline E. Paniccia, Alia J. Martin, Kathryn J. Reissner, Darin J. Knapp, Stacey L. Robinson, Todd E. Thiele, Donald T. Lysle
المصدر: Alcoholism: Clinical and Experimental Research. 46:2177-2190
بيانات النشر: Wiley, 2022.
سنة النشر: 2022
مصطلحات موضوعية: Alcoholism, Psychiatry and Mental health, Ethanol, Astrocytes, Animals, Medicine (miscellaneous), Fear, RNA, Messenger, Toxicology, Hippocampus, Rats
الوصف: Alcohol use disorder (AUD) and post-traumatic stress disorder (PTSD) are highly comorbid, yet there is a lack of preclinical research investigating how prior ethanol (EtOH) dependence influences the development of a PTSD-like phenotype. Furthermore, the neuroimmune system has been implicated in the development of both AUD and PTSD, but the extent of glial involvement in this context remains unclear. A rodent model was developed to address this gap in the literature.We used a 15-day exposure to the 5% w/v EtOH low-fat Lieber-DeCarli liquid diet in combination with the stress-enhanced fear learning (SEFL) paradigm to investigate the effects of chronic EtOH consumption on the development of a PTSD-like phenotype. Next, we used a reverse transcription quantitative real-time polymerase chain reaction to quantify mRNA expression of glial cell markers GFAP (astrocytes) and CD68 (microglia) following severe footshock stress in EtOH-withdrawn rats. Finally, we tested the functional contribution of dorsal hippocampal (DH) astrocytes in the development of SEFL in EtOH-dependent rats using astrocyte-specific GResults demonstrate that chronic EtOH consumption and withdrawal exacerbate future SEFL. Additionally, we found significantly increased GFAP mRNA expression in the dorsal and ventral hippocampus and amygdalar complex following the severe stressor in EtOH-withdrawn animals. Finally, the stimulation of the astroglial GCollectively, results indicate that prior EtOH dependence and withdrawal combined with a severe stressor potentiate future enhanced fear learning. Furthermore, DH astrocytes significantly contribute to this change in behavior. Overall, these studies provide insight into the comorbidity of AUD and PTSD and the potential neurobiological mechanisms behind increased susceptibility to a PTSD-like phenotype in individuals with AUD.
تدمد: 1530-0277
0145-6008
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::049e72879baf5e381aa1cb54442faf14
https://doi.org/10.1111/acer.14963
حقوق: CLOSED
رقم الأكسشن: edsair.doi.dedup.....049e72879baf5e381aa1cb54442faf14
قاعدة البيانات: OpenAIRE