{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Becker HC"],"funding":["BLRD VA","National Institute on Alcohol Abuse and Alcoholism","NIAAA NIH HHS","National Institutes of Health","U.S. Department of Veterans Affairs"],"pagination":["215-225"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10247903"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["94(3)"],"pubmed_abstract":["<h4>Background</h4>There is high comorbidity of posttraumatic stress disorder (PTSD) and alcohol use disorder with few effective treatment options. Animal models of PTSD have shown increases in alcohol drinking, but effects of stress history on subsequent vulnerability to alcohol relapse have not been examined. Here we present a mouse model of PTSD involving chronic multimodal stress exposure that resulted in long-lasting sensitization to stress-induced alcohol relapse, and this sensitized stress response was blocked by oxytocin (OT) administration.<h4>Methods</h4>Male and female mice trained to self-administer alcohol were exposed to predator odor (TMT) + yohimbine over 5 consecutive days or left undisturbed. After reestablishing stable alcohol responding/intake, mice were tested under extinction conditions, and then all mice were exposed to TMT or context cues previously associated with TMT before a reinstatement test session. Separate studies examined messenger RNA expression of Oxt and Oxtr in hypothalamus following chronic stress exposure. A final study examined the effects of systemic administration of OT on stress-induced alcohol relapse in mice with and without a history of chronic stress experience.<h4>Results</h4>Chronic stress exposure produced long-lasting sensitization to subsequent stress-induced alcohol relapse that also generalized to stress-related context cues and transcriptional changes in hypothalamic OT system. OT injected before the reinstatement test session completely blocked the sensitized stress-induced alcohol relapse effect.<h4>Conclusions</h4>Collectively, these results provide support for the therapeutic potential of OT, along with highlighting the value of utilizing this model in evaluating other pharmacological interventions for treatment of PTSD/alcohol use disorder comorbidity."],"journal":["Biological psychiatry"],"pubmed_title":["Oxytocin Reduces Sensitized Stress-Induced Alcohol Relapse in a Model of Posttraumatic Stress Disorder and Alcohol Use Disorder Comorbidity."],"pmcid":["PMC10247903"],"funding_grant_id":["IK6 BX006299","U01 AA 014095","F31 AA026483","R01 AA026536","U24 AA029968","P50 AA010761","U24 AA020929","I01 BX000813","U01 AA014095"],"pubmed_authors":["Lopez MF","King CE","Becker HC","Griffin WC"],"additional_accession":[]},"is_claimable":false,"name":"Oxytocin Reduces Sensitized Stress-Induced Alcohol Relapse in a Model of Posttraumatic Stress Disorder and Alcohol Use Disorder Comorbidity.","description":"<h4>Background</h4>There is high comorbidity of posttraumatic stress disorder (PTSD) and alcohol use disorder with few effective treatment options. Animal models of PTSD have shown increases in alcohol drinking, but effects of stress history on subsequent vulnerability to alcohol relapse have not been examined. Here we present a mouse model of PTSD involving chronic multimodal stress exposure that resulted in long-lasting sensitization to stress-induced alcohol relapse, and this sensitized stress response was blocked by oxytocin (OT) administration.<h4>Methods</h4>Male and female mice trained to self-administer alcohol were exposed to predator odor (TMT) + yohimbine over 5 consecutive days or left undisturbed. After reestablishing stable alcohol responding/intake, mice were tested under extinction conditions, and then all mice were exposed to TMT or context cues previously associated with TMT before a reinstatement test session. Separate studies examined messenger RNA expression of Oxt and Oxtr in hypothalamus following chronic stress exposure. A final study examined the effects of systemic administration of OT on stress-induced alcohol relapse in mice with and without a history of chronic stress experience.<h4>Results</h4>Chronic stress exposure produced long-lasting sensitization to subsequent stress-induced alcohol relapse that also generalized to stress-related context cues and transcriptional changes in hypothalamic OT system. OT injected before the reinstatement test session completely blocked the sensitized stress-induced alcohol relapse effect.<h4>Conclusions</h4>Collectively, these results provide support for the therapeutic potential of OT, along with highlighting the value of utilizing this model in evaluating other pharmacological interventions for treatment of PTSD/alcohol use disorder comorbidity.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Aug","modification":"2026-06-03T05:35:34.231Z","creation":"2026-04-24T03:14:47.748Z"},"accession":"S-EPMC10247903","cross_references":{"pubmed":["36822933"],"doi":["10.1016/j.biopsych.2022.12.003"]}}