ArticleBiological psychiatry2015
Anhedonia, Reduced Cocaine Reward, and Dopamine Dysfunction in a Rat Model of Posttraumatic Stress Disorder.
Article in Biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- Attenuating trauma- and cocaine-related intrusions by blocking memory reconsolidation with minocycline: protocol for a transdiagnostic randomized controlled trial.European journal of psychotraumatology · 2026Trial
- Behavioral Domain-Specific Effects of Positive Modulation of α5 and α6 GABAPharmacology research & perspectives · 2026Article
- Article
- Sexually dimorphic effects of single prolonged stress on conditioned suppression behavior in Long Evans rats with no detection of altered mRNA expression of VGLUT1, GAD1, and Arc in the ventral hippocampus.Frontiers in behavioral neuroscience · 2026Article
- Time-Dependent Therapeutic Effect of S-Ketamine on PTSD Mediated by VTA-OFC Dopaminergic Neurocircuit.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neuropeptide S pathway in PTSD and neuropsychiatric disorders: A review.Biomolecules & biomedicine · 2025Review
- Quality of life in hospitalized COVID-19 patients: the role of psychosocial, inflammatory, and dopaminergic pathways.Frontiers in psychology · 2025Article
- Does Trauma Change the Way Individuals with Post-Traumatic Stress Disorder (PTSD) Deal with Positive Stimuli?Behavioral sciences (Basel, Switzerland) · 2024Article
- Time-course analysis of frontal gene expression profiles in the rat model of posttraumatic stress disorder and a comparison with the conditioned fear model.Neurobiology of stress · 2023Article
- Stress to inflammation and anhedonia: Mechanistic insights from preclinical and clinical models.Neuroscience and biobehavioral reviews · 2023Review
- Impact of Mephedrone on Fear Memory in Adolescent Rats: Involvement of Matrix Metalloproteinase-9 (MMP-9) and N-Methyl-D-aspartate (NMDA) Receptor.International journal of molecular sciences · 2023Article
- The neural circuits and molecular mechanisms underlying fear dysregulation in posttraumatic stress disorder.Frontiers in neuroscience · 2023Review
- Exploring gene-drug interactions for personalized treatment of post-traumatic stress disorder.Frontiers in computational neuroscience · 2023Article
- Diosgenin normalization of disrupted behavioral and central neurochemical activity after single prolonged stress.Frontiers in pharmacology · 2023Article
- Chronic fluoxetine enhances extinction therapy for PTSD by evaluating brain glucose metabolism in rats: an [Annals of nuclear medicine · 2022Article
- Trauma Cue-Elicited Alcohol Craving as a Function of Adult Versus Childhood-Onset Interpersonal Traumatic Events in Young Adult Drinkers.Journal of studies on alcohol and drugs · 2022Article
- Ventral tegmental area dopaminergic action in music therapy for post-traumatic stress disorder: A literature review.Frontiers in psychology · 2022Review
- Anhedonia in Posttraumatic Stress Disorder: Prevalence, Phenotypes, and Neural Circuitry.Current topics in behavioral neurosciences · 2022Review
- Repeated cocaine exposure prior to fear conditioning induces persistency of PTSD-like symptoms and enhancement of hippocampal and amygdala cell density in male rats.Brain structure & function · 2021Article
- The Neurocircuitry of Posttraumatic Stress Disorder and Major Depression: Insights Into Overlapping and Distinct Circuit Dysfunction-A Tribute to Ron Duman.Biological psychiatry · 2021Review
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5 authors.
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Abstract
backgroundPosttraumatic stress disorder (PTSD) co-occurs with substance use disorders at high rates, but the neurobiological basis of this relationship is largely unknown. PTSD and drug addiction each involve dysregulation of brain reward circuitry; therefore, the identification of pathology of the mesolimbic dopamine system may aid in understanding their functional relationship. Dopamine reward dysfunction also may be relevant to the mechanisms underlying the PTSD symptoms of anhedonia and emotional numbing.
methodsSingle-prolonged stress (SPS) was used as a rat model of PTSD, and a series of behavioral and neuropharmacologic assays were applied to assess the impact of SPS on reward, cocaine intake, and components of the striatal dopamine system.
resultsExposure to SPS increased anhedonia-like behaviors and decreased the rewarding properties of cocaine compared with control handling. Altered cocaine intake during extended access self-administration sessions was observed in rats exposed to SPS, further suggesting a difference in the reinforcing properties of cocaine following severe stress. SPS reduced tissue content of dopamine and its metabolites in the striatum, as well as altered striatal dopamine transporter and D2, but not D1, receptor densities.
conclusionsThese results support a role for altered dopaminergic transmission in reduced reward function in PTSD. Pathology of the dopamine system and the degradation of reward processes may contribute to PTSD symptomology and have implications for co-occurring psychiatric disorders such as substance abuse or depression.
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