Psychopharmacology最新文献

{"title":"A mindfulness-based intervention to reduce altered brain reward function in cannabis use disorder: a double-blind, active and passive, randomised controlled fMRI trial.","authors":"Emillie Beyer, Martine Skumlien, Govinda Poudel, Arush Honnedevasthana Arun, Eugene McTavish, Hannah Thomson, Hannah Sehl, Rebecca Segrave, Adam Clemente, Izelle Labuschagne, Peter Rendell, Gill Terrett, Lisa-Marie Greenwood, Victoria Manning, Tom P Freeman, Sunjeev K Kamboj, Chao Suo, Valentina Lorenzetti","doi":"10.1007/s00213-026-07073-0","DOIUrl":"https://doi.org/10.1007/s00213-026-07073-0","url":null,"abstract":"<p><p>Cannabis Use Disorder (CUD) affects ~ 50 million individuals worldwide and is associated with alterations in brain reward pathways. Mindfulness-based interventions (MBIs) show promise in reducing substance use and aberrant brain function in substance use disorders (SUD), but the effects on CUD or brain reward function have not been investigated. To examine whether a 2-week MBI vs. active control (i.e., closely matched relaxation) and passive control (i.e., no intervention) affected brain reward function in CUD using the Monetary Incentive Delay fMRI task, 49 individuals with moderate-to-severe CUD were randomised to: a 2-week MBI (n = 18), active control condition (n = 15), or passive control condition (n = 16), and assessed before and after the intervention. The effect of intervention-by-time was analysed using an exploratory whole-brain approach and a priori regions-of-interest approach (ROIs; ventral striatum, dorsal caudate, putamen, insula, cingulate, and orbitofrontal cortices). Whole-brain results revealed significant intervention-by-time effects. Post-MBI, there was: decreased cerebellum activity while anticipating monetary cues, increased parietal activity while receiving monetary wins, and decreased fusiform/superior frontal gyri (SFG) activity while receiving monetary wins. Post-relaxation, activity increased in several regions (i.e., hippocampus, insula, parietal cortex, fusiform, and SFG) during the receipt of monetary wins. Post-no intervention, activity increased in the cerebellum while anticipating monetary cues, and decreased in other areas (i.e., parietal cortex, hippocampus, and insula) while receiving monetary wins. There were no significant intervention-by-time effects using the ROI approach. Overall, MBI, matched relaxation, and no intervention may share changes in partially overlapping brain regions in distinct directions.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147842041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on the improvement effect and mechanism of resveratrol on cognitive impairment in tau mutant adenovirus-induced alzheimer's disease model mice.","authors":"Shuting Chen, Kexuan Zhao, Zhidan Shi, Chu Zhang, Hao Wu, Meng Tian, Yi Sun, Ling He","doi":"10.1007/s00213-026-07048-1","DOIUrl":"https://doi.org/10.1007/s00213-026-07048-1","url":null,"abstract":"<p><strong>Rationale: </strong>Tau protein hyperphosphorylation and neuroinflammation playimportant roles in the onset and progression of Alzheimer's disease (AD). SIRT1has been implicated in the regulation of synaptic plasticity, cognitive function, andmemory, and is associated with the modulation of autophagy-and inflammation-related signaling pathways, including AMPK/mTOR/ULK1 and NF-κB. Resveratrol(RSV) has been reported to ameliorate cognitive impairment in AD models,primarily in the context of Aβ-related pathology; however, its potential effects andunderlying mechanisms in Tau-driven pathology remain incompletely understood.</p><p><strong>Objectives: </strong>To investigate the effect of RSV on cognitive impairment in mice withTau mutation-induced Alzheimer's disease, and to explore its effects on autophagyand neuroinflammation.</p><p><strong>Methods: </strong>Tauopathy models were established using AAV-P301L-Tau. Cognitivefunction was assessed via behavioral tests; Hippocampal injury was evaluatedAccepted manuscriptACCEPTED MANUSCRIPTusing HE and Nissl staining, while autophagy was assessed byimmunofluorescence staining. Mechanisms were examined using Western blot,qRT-PCR, and CCK-8 assays.</p><p><strong>Results: </strong>RSV treatment was associated with attenuation of neuronal damage,reduction of p-Tau accumulation, and improvement of cognitive impairment in ADmice. Consistent trends were observed in vitro, where RSV treatment wasassociated with increased cell viability and modulation of autophagy-relatedmarkers in AAV-P301L-Tau-induced BV2 cells. In addition, RSV administration wasaccompanied by coordinated changes in signaling components related to SIRT1,AMPK/mTOR/ULK1, and NF-κB pathways, along with reduced expression ofinflammatory mediators.</p><p><strong>Conclusions: </strong>RSV treatment was associated with coordinated modulation ofsignaling components related to the AMPK/mTOR/ULK1 and NF-κB pathways,together with improvements in cognitive performance in AD mice. These findingssupport the potential therapeutic relevance of RSV in Tau-drivenneurodegenerative pathology, while further studies are required to clarify theunderlying mechanisms.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological effect of (±)-trans-3-methylfentanyl and (±)-cis-3-methylfentanyl.","authors":"Yuanyuan Chen, Miaojun Lai, Wenjie Qiao, Xuena Zhang, Xuesong Shi, Yizhao Xu, Mengchan Xia, Peng Xu, Bin Di, Xiangyu Li","doi":"10.1007/s00213-026-07078-9","DOIUrl":"https://doi.org/10.1007/s00213-026-07078-9","url":null,"abstract":"<p><strong>Rational: </strong>(±)-trans-3-methylfentanyl and (±)-cis-3-methylfentanyl are stereoisomeric analogues of 3-methylfentanyl. Although both exhibit high potency as µ-opioid receptor (MOR) agonists, their pharmacological profiles, such as analgesic potency, differ markedly. Current experimental data remain limited primarily to analgesia and MOR binding affinity.</p><p><strong>Objectives: </strong>To comprehensively evaluate and compare the acute toxicity and the potency of abuse liability of (±)-trans-3-methylfentanyl and (±)-cis-3-methylfentanyl.</p><p><strong>Methods: </strong>Acute toxicity was assessed using the up-and-down procedure in mice. The potency of abuse liability was evaluated through four complementary paradigms: conditioned place preference (CPP), drug self-administration (SA), drug discrimination, and naloxone-precipitated withdrawal. In addition, dopamine D2 receptor (D2R) binding affinity was quantified in vitro using surface plasmon resonance (SPR), complementing in vivo behavioral findings.</p><p><strong>Results: </strong>The median lethal dose (LD₅₀) of (±)-trans-3-methylfentanyl and (±)-cis-3-methylfentanyl was identical and was 101 mg/kg (s.c.). The minimum doses to induce CPP were 30 µg/kg for (±)-trans-3-methylfentanyl and 3 µg/kg for (±)-cis-3-methylfentanyl, indicating a 10-fold higher potency of (±)-cis-3-methylfentanyl in inducing reward-associated learning. Conversely, in SA experiments, the peak dose to induce SA was 0.05 µg/kg/infusion for (±)-trans-3-methylfentanyl and 0.25 µg/kg/infusion for (±)-cis-3-methylfentanyl, demonstrating that the trans-isomer exhibits fivefold greater reinforcing potency. Drug discrimination experiment revealed that the discriminative stimulus potency of (±)-trans-3-methylfentany (ED₅₀ = 0.29 µg/kg) was 1.4 times lower than that of (±)-cis-3-methylfentany (ED₅₀ = 0.20 µg/kg). Repeated administration of (±)-trans-3-methylfentanyl and (±)-cis-3-methylfentanyl produced naloxone-precipitated withdrawal symptoms, confirming physical dependence liability. Notably, (±)-trans-3-methylfentanyl showed higher D2R binding affinity than (±)-cis-3-methylfentanyl in the SPR experiment.</p><p><strong>Conclusions: </strong>This study provides the first integrated assessment of acute toxicity and multifaceted abuse liability across key behavioral and molecular endpoints for these two stereoisomers. The divergent structure-activity relationships observed, particularly the inverse potency patterns in CPP versus SA and differential D2R engagement, highlight the critical influence of stereochemistry on neuropharmacological outcomes. These findings advance mechanistic understanding of fentanyl analogue action and inform future risk assessment and structure-based design of opioid therapeutics.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147820082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A history of chronic adolescent stress attenuates cued fear-potentiated startle in adult female Wistar rats.","authors":"Amy J Wegener, Molly M Hyer, Zuby Okafor, Grace Young, Chloe Burns, Emilie Bjerring, Samya Dyer, Paul Howell, Susie Turkson, Tanja Jovanovic, Gretchen N Neigh","doi":"10.1007/s00213-026-07077-w","DOIUrl":"https://doi.org/10.1007/s00213-026-07077-w","url":null,"abstract":"<p><strong>Rationale: </strong>Post-traumatic stress disorder (PTSD) is a stress and trauma-related disorder that is largely characterized by hyperarousal to fear-based cues. N-methyl-D-aspartate (NMDA) receptors are key mediators of fear learning behaviors. Altered NMDA receptor signaling is a hallmark of PTSD pathology that impacts fear memory learning and extinction processes.</p><p><strong>Objectives: </strong>In the current study, we tested whether exposing adolescent rats to a mixed modality stress paradigm of repeated restraint, social defeat, and individual housing (chronic adolescent stress; CAS) decreased immunoreactivity of the NMDA subunit NR2B in the central amygdala in adulthood. We sought to determine the impact of a peripherally administered NMDA receptor agonist D-cycloserine (DCS) intervention to enhance extinction of learned fear in CAS animals.</p><p><strong>Methods: </strong>Upon reaching adulthood, CAS animals were exposed to a cued fear-potentiated startle paradigm. DCS was administered immediately following the first of two extinction sessions with the goal of enhancing extinction learning.</p><p><strong>Results: </strong>CAS females expressed impaired fear extinction compared to non-stressed females, but were not influenced by the DCS intervention. Males overall were able to successfully learn fear extinction regardless of stress history, however, DCS treatment may have increased fear potentiated startle responsivity in males with a history of stress.</p><p><strong>Conclusions: </strong>These data suggest that chronic stress during adolescence modifies NMDA receptor expression, but functional impacts on cued fear learning differ by sex and require additional approaches to better understand the mechanisms underlying stress-induced impairments in fear learning behaviors.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147819928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic risk for schizophrenia modulates WIN 55,212-2 reward: Evidence from a heterozygous transmembrane domain neuregulin 1 mutant mouse model.","authors":"Rose Chesworth, Georgia Watt, Jaime Howard, Georgina Ding, Tim Karl","doi":"10.1007/s00213-026-07080-1","DOIUrl":"https://doi.org/10.1007/s00213-026-07080-1","url":null,"abstract":"<p><strong>Background: </strong>Cannabis abuse rates are up to ten times higher in individuals with schizophrenia than the general population, but it is unclear what is driving this high level of comorbidity. Genetic predisposition for schizophrenia may increase the risk of cannabis abuse; however, there is limited empirical support for this.</p><p><strong>Methods: </strong>We investigated this question using a well-established genetic mouse model of schizophrenia risk, the heterozygous transmembrane domain neuregulin 1 mutant (Nrg1 TM HET) mouse, which also shows behavioural and neural susceptibility to cannabis components. WIN 55,212-2 (WIN), a cannabinoid 1 (CB1) receptor agonist, was used to model the rewarding and aversive properties of cannabis. We first validated a conditioned place preference protocol to determine rewarding and aversive doses of WIN administration in C57BL/6J mice, the background strain of our schizophrenia mouse model. We then investigated the effects of these WIN dose regimes on place preference and locomotion in male and female Nrg1 TM HET mice and their control wildtype-like littermates.</p><p><strong>Results: </strong>We found that low dose WIN (0.1 mg/kg) was rewarding in wildtype-like, but not in Nrg1 TM HET mice of both sexes. Conversely, male and female mice of both genotypes found high dose WIN (3 mg/kg) aversive. While all mice showed a similar locomotor response to low dose WIN administration, male Nrg1 TM HET mice showed an earlier development of locomotor tolerance to high dose WIN, with no differences in WIN-induced locomotor sedation in female mice.</p><p><strong>Conclusion: </strong>Our findings suggest that genetic risk for schizophrenia can modulate the rewarding properties of the CB1 receptor agonist WIN and support the hypothesis that comorbidity between schizophrenia and cannabis use disorder may in part be driven by shared genetic risk factors.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147819978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Speech-based system for detecting alcohol intoxication using optimized deep learning.","authors":"S Abirami, V Vasudevan, S Dhanasekaran","doi":"10.1007/s00213-026-07065-0","DOIUrl":"https://doi.org/10.1007/s00213-026-07065-0","url":null,"abstract":"<p><p>In this research, we propose a highly accurate speech-based system for detecting alcohol intoxication, utilizing deep learning algorithms to classify speech as either sober or intoxicated. The core of this system is the Dense Residual Recurrent Network (D2R_Net), which combines dense residual blocks for spatial feature extraction with Gated Recurrent Units (GRUs) for modeling temporal dependencies in speech data. This architecture is further optimized using the Iterative Parrot Optimization (ItPaO) algorithm, a novel hyperparameter tuning method designed to enhance the model's convergence and classification accuracy. The speech data is first pre-processed into log-Mel spectrograms, which allow the model to capture key auditory patterns altered by alcohol consumption. Through extensive experimentation, the proposed system outperformed existing models, with a balanced accuracy of 98.51% and specificity reaching 98.2%. The optimized model is highly efficient, requiring minimal computational resources while providing robust and scalable performance, making it ideal for deployment in real-world scenarios. This non-invasive, cost-effective alcohol detection system is poised to revolutionize public safety applications, such as monitoring drivers, event security, and healthcare settings.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147820080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Memory impairment and chronic high-dose Δ9-THC/cannabis exposure: a narrative review of molecular mechanisms underlying neurotoxic effects.","authors":"Habibeh Mashayekhi-Sardoo, Ali Ahmad Azadbakht, Mahdiyeh Hedayati-Moghadam, Ahmad Golkar, Yousef Baghcheghi","doi":"10.1007/s00213-026-07070-3","DOIUrl":"https://doi.org/10.1007/s00213-026-07070-3","url":null,"abstract":"<p><strong>Rationale: </strong>The increasing potency of cannabis and the growing prevalence of chronic, high-dose use have raised concerns about its potential neurotoxic effects on cognitive functions, particularly memory. While low-dose cannabinoids have demonstrated therapeutic benefits, the molecular basis of memory impairment under high-dose exposure remains insufficiently clarified.</p><p><strong>Objectives: </strong>This narrative review aims to elucidate the molecular mechanisms underlying memory impairment associated with chronic, high-dose Δ9-tetrahydrocannabinol (Δ9-THC) and cannabis exposure, and to distinguish these effects from the beneficial outcomes observed at lower doses.</p><p><strong>Methods: </strong>A narrative review methodology was employed to synthesize evidence from both human studies and murine models, focusing on molecular, cellular, and neurobiological pathways involved in memory dysfunction.</p><p><strong>Results: </strong>Chronic high-dose activation of the endocannabinoid system (ECS) induces acascade of adverse molecular events, including neuroinflammation, oxidative stress, and activation of apoptotic pathways. Significant dysregulation of key neurotransmitter systems was also observed. Importantly, high-dose Δ9-THC disrupts neuroplasticity by impairing hippocampal neurogenesis, synaptogenesis, and dendritic remodeling, thereby compromising mechanisms essential for memory formation and consolidation. Adolescents and elderly individuals were identified as particularly vulnerable populations.</p><p><strong>Conclusions: </strong>Chronic exposure to highdose Δ9-THC is strongly associated with memory impairment through interconnected molecular pathways. These findings provide a mechanistic framework linking cannabis exposure to cognitive deficits and highlight the need for longitudinal human studies and the development of targeted therapeutic interventions.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147820033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunotherapy for depression: targeting cytokine pathways in major depressive disorder.","authors":"Chenyang Long, Guirui Zhang, Zihao Jiang, Feifeng Yang, Jin Wang","doi":"10.1007/s00213-026-07022-x","DOIUrl":"https://doi.org/10.1007/s00213-026-07022-x","url":null,"abstract":"","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating the evidence for repressed memory recovery in psychedelic contexts.","authors":"Anne-Fiona Griesfeller, Lotte Kooman, Lilian Kloft-Heller, Samuli Kangaslampi, Johannes G Ramaekers, Henry Otgaar","doi":"10.1007/s00213-026-07076-x","DOIUrl":"https://doi.org/10.1007/s00213-026-07076-x","url":null,"abstract":"<p><strong>Rationale: </strong>Reports of resurfaced repressed memories during psychedelic experiences have circulated for decades and still emerge today. However, the veracity of repressed memories remains debated, and the mechanisms through which psychedelics might recover alleged repressed memories are unclear.</p><p><strong>Objectives: </strong>This scoping review aimed to provide an overview of the literature on repressed memory in the context of psychedelics. It examined how repressed memory was defined, which substances were predominantly discussed, which mechanisms were proposed to explain their effects, and whether these mechanisms were empirically supported.</p><p><strong>Methods: </strong>A scoping review was conducted in line with PRISMA-ScR guidelines. Web of Science, PubMed, PsycINFO and Google Scholar were searched for relevant publications. Fifty-three sources met eligibility criteria. Data were charted on study design, psychedelic substance, definitions of repressed memory, results, and proposed mechanisms.</p><p><strong>Results: </strong>Most publications focused on lysergic acid diethylamide (LSD) in relation to repressed memory. Few sources provided a definition of repressed memory. Proposed mechanisms on how psychedelics might influence repressed memory included psychoanalytical reductions of defensive memory blockades and neurobiological alterations of executive control. However, empirical support for these mechanisms was limited.</p><p><strong>Conclusions: </strong>The included literature did not offer a coherent explanation on how psychedelics could recover repressed memories, nor consistent evidence that they did so reliably. Future work should provide clear definitions of repressed memory in the context of psychedelics, test proposed effects of psychedelics on memory and executive control across multiple psychedelic substances, include placebo-controlled designs, and account for the potential occurrence of false memories.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"17β-Estradiol alleviates cognitive deficits by modulating fear memory reconsolidation in a PTSD rat model.","authors":"Han Wang, Han Lin, Zilong Zhong, Baoying Jiang, Siyi Li, Jiahao Tang, Xiaoping Zhou, Guohui Zhu, Yang Liu, Wenhao Han, Jinhua Dou, Lin Sun","doi":"10.1007/s00213-026-07068-x","DOIUrl":"https://doi.org/10.1007/s00213-026-07068-x","url":null,"abstract":"","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}