Neuropsychopharmacology最新文献

{"title":"Traumatic stress recruits an excitatory orbitofrontal–amygdala pathway to drive maladaptive aggression","authors":"Mikaela L. Aholt, Jessica T. Jacobs, Magdalene P. Adjei, Nooshin Mojahed, Elana Qasem, Sandria W. Athul, Buffy Ellsworth, Jacob C. Nordman","doi":"10.1038/s41386-026-02432-z","DOIUrl":"10.1038/s41386-026-02432-z","url":null,"abstract":"Traumatic stress is a reliable predictor of heightened aggression, yet the mechanisms linking stress exposure to aggression remain poorly understood. We previously found that traumatic stress activates the posterior ventral segment of the medial amygdala (MeApv) to drive persistent increases in aggressive behavior. However, why traumatic stress would engage an aggression-promoting pathway is unclear. To address this, we mapped the inputs to the MeApv and identified a population of excitatory, but not inhibitory, neurons in Layer 5 of the medial orbitofrontal cortex (mOFC). The OFC is classically viewed as an inhibitory brake on amygdala-driven impulses, yet emerging evidence suggests it can also facilitate context-dependent emotional responses. Notably, traumatic stress is known to disrupt OFC function and its connectivity with the amygdala, implicating this circuit in pathological aggression. Using fiber photometry, we found that traumatic stress selectively activates these MeApv-projecting excitatory mOFC (mOFCMeApv) neurons as well as their downstream MeApv outputs. Chemogenetic inhibition of the excitatory mOFCMeApv neurons during traumatic stress exposure prevented the subsequent increase in aggression while preserving non-aggressive social behavior. Together, these findings identify an excitatory cortical–amygdala pathway that is necessary for stress-induced aggression and support a model in which traumatic stress recruits, rather than suppresses, OFC output to drive maladaptive behavior.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 9","pages":"1610-1622"},"PeriodicalIF":7.6,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41386-026-02432-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147849162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Judith L. Rapoport, M.D. 1933–2026","authors":"Stanley I. Rapoport","doi":"10.1038/s41386-026-02427-w","DOIUrl":"10.1038/s41386-026-02427-w","url":null,"abstract":"","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 8","pages":"1526-1526"},"PeriodicalIF":7.6,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41386-026-02427-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148292571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal control during prenatal oxycodone exposure: differential effects of voluntary versus involuntary self-administration on offspring substance use vulnerability in rats","authors":"Chantal CA Aaron, Kerri E. Budge, Sara B. Isgate, Fair M. Vassoler, Elizabeth M. Byrnes","doi":"10.1038/s41386-026-02422-1","DOIUrl":"10.1038/s41386-026-02422-1","url":null,"abstract":"Prenatal opioid exposure is a growing clinical concern, yet the impact of maternal control over drug intake on long-term offspring outcomes remains unclear. Here, we utilized a translational rat model to examine how the mode of oxycodone administration during pregnancy influences substance use vulnerability in adult offspring. Female Sprague-Dawley rats (n = 10-11/group) were assigned to one of three groups: voluntary intravenous self-administration (Oxycodone-Lead), yoked non-contingent oxycodone delivery (Oxycodone-Yoked), or yoked saline control (Saline-Yoked). The dam self-administered oxycodone in 6h sessions for three weeks, 5 days/week, prior to conception and then daily throughout gestation. Offspring were cross-fostered to drug-naïve dams at birth. In adulthood, male and female offspring were evaluated for oxycodone (0.1 mg/kg/infusion) and cocaine (0.5 mg/kg/infusion) intravenous self-administration using fixed ratio (7 sessions FR1; 5 sessions FR5) and progressive ratio schedules (3 sessions), as well as drug-seeking under extinction conditions (1 session). Despite equivalent overall drug exposure, offspring of Oxycodone-Yoked dams exhibited enhanced motivated responding and drug-seeking behaviors. Female Oxycodone-Yoked offspring showed increased intake and motivated responding specifically for oxycodone, while Oxycodone-Yoked offspring of both sexes displayed augmented cocaine seeking and drug-seeking under extinction. Pearson’s correlations between maternal intake and offspring behavior were sex- and drug-specific and were only observed in the Oxycodone-Yoked group. These findings indicate that maternal control over drug intake, rather than opioid exposure per se, plays a critical role in shaping neurodevelopmental trajectories underlying substance use vulnerability. This study highlights the importance of considering patterns of maternal opioid use when assessing long-term developmental risks.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 9","pages":"1529-1537"},"PeriodicalIF":7.6,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41386-026-02422-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147849152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synaptic plasticity in cocaine-seeking ensembles of the nucleus accumbens core","authors":"Levi T. Flom, Skylar L. Hodgins, German Gutierrez Erives, Jordan M. Russelavage, Samuel M. Hyken, Zhaojie Zhang, Christopher E. Vaaga, Ana-Clara Bobadilla","doi":"10.1038/s41386-026-02425-y","DOIUrl":"10.1038/s41386-026-02425-y","url":null,"abstract":"Cue-induced seeking engages neuronal ensembles within the nucleus accumbens core (NAcore), with neuronal ensembles defined here as neurons coactivated during specific behavioral experiences that have been implicated in cued-reinstatement. Although transient synaptic plasticity has been widely observed in unidentified ensemble and non-ensemble neuronal populations in the NAcore during reinstatement, its expression within behaviorally relevant ensembles remains unclear. Here, we used c-Fos-TRAP2-based tagging to characterize structural and functional synaptic plasticity within ensembles during cocaine-seeking in mice following cocaine intravenous self-administration, extinction, and cue-induced reinstatement. Structural plasticity was measured via spine confocal imaging, and functional changes were evaluated by AMPA/NMDA ratios using whole-cell electrophysiology across reinstatement time points. Ensemble neurons exhibited increased dendritic spine head diameter during cue-induced reinstatement and were functionally potentiated relative to non-ensemble neurons. Spine classification showed reduced mature spines during reinstatement in both ensemble and non-ensemble cells, suggesting morphological remodeling rather than new spine formation. Non-ensemble neurons showed no change in spine head diameter during reinstatement but did exhibit an increased AMPA/NMDA ratio during cued-reinstatement. Paired-pulse ratio analysis suggested that yoked-cocaine exposure decreased presynaptic vesicle release probability, while operant cocaine exposure had no effect. Ensemble neurons showed an elevated AMPA/NMDA ratio following cocaine exposure, regardless of whether intake was yoked or contingent. Together, these findings suggest that ensemble and non-ensemble neurons undergo distinct forms of synaptic plasticity during cue-induced reinstatement. By distinguishing ensemble-specific structural plasticity from non-ensemble functional plasticity, this study refines the current understanding of mechanisms underlying cue-induced relapse. In preclinical models of substance use disorder drug seeking is associated with cue-induced reactivation of neuronal ensembles in the nucleus accumbens core. While transient synaptic plasticity has been extensively described in non-selective neuronal populations pooling recordings of both ensemble and non-ensemble neurons of the nucleus accumbens core, ensemble-specific plasticity remains unclear. Here, we combined c-Fos-TRAP2 tagging, confocal imaging, and slice electrophysiology to show that structural synaptic plasticity is selectively expressed in behaviorally relevant ensembles. By linking ensemble identity with structural and functional plasticity during cue-induced cocaine seeking, these findings refine current models of relapse and identify plasticity within the ensemble as a potential target for therapeutic intervention.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 11","pages":"2197-2205"},"PeriodicalIF":7.6,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41386-026-02425-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147826041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sequence termination cues drive automated habit-like strategy via dopamine-mediated processes","authors":"Robin Magnard, Yifeng Cheng, Joanna Zhou, Haley Province, Nathalie Thiriet, Patricia H. Janak, Youna Vandaele","doi":"10.1038/s41386-026-02420-3","DOIUrl":"10.1038/s41386-026-02420-3","url":null,"abstract":"Mesolimbic dopamine (DA) neurons are central to cue-guided reward seeking and action sequence learning. Yet, the mechanisms by which cue-induced DA neural activity drives goal-directed or habitual sequence execution remain unknown. We designed two novel tasks to isolate the effect of sequence-delineating cues on DA-driven behavioral strategies and learning. In the lever insertion fixed-ratio 5 task (LI5), the lever insertion marked sequence initiation. In the lever retraction fixed-ratio 5 task (LR5), the lever retraction served as both sequence termination and reward-predictive cue. We found that sequence initiation and termination cues differentially affect reward expectation during action sequences, with only the termination cue contributing to greater outcome devaluation insensitivity, automaticity and behavioral chunking. Mesolimbic fiber photometry recording revealed that this habit-like behavior was associated with a rapid backpropagation in DA signals from the reward to the immediately preceding cue and with attenuated DA reward prediction error signals, which reflected greater behavioral inflexibility. Finally, in absence of external cues, brief optogenetic stimulation of VTA DA neurons at sequence termination was sufficient to drive automaticity and, to some extent, behavioral chunking. Our results highlight the critical role of cue-evoked DA signals at sequence termination in driving the development of automated, habit-like sequence execution.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 11","pages":"2269-2279"},"PeriodicalIF":7.6,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147825968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant cortico-striato-limbic functional connectivity to alcohol cues in co-occurring bipolar disorder and alcohol use disorder","authors":"William H. Mellick, Bryan K. Tolliver, Raymond F. Anton, James J. Prisciandaro","doi":"10.1038/s41386-026-02418-x","DOIUrl":"10.1038/s41386-026-02418-x","url":null,"abstract":"Reward brain circuitry dysfunction is a hypothesized mechanism of bipolar disorder and alcohol use disorder co-occurrence (BD + AUD) that remains largely untested. This neuroimaging study represents the first investigation of functional connectivity in BD + AUD. Following a two-by-two factorial design (N = 90), individuals with BD + AUD (n = 22), AUD alone (n = 20), BD alone (n = 23), and healthy control participants (n = 25) were administered a fMRI alcohol-cue reactivity paradigm. Generalized psychophysiological interaction (PPI) modeling (p < 0.001; p-FDR < 0.05) was performed for regions of interest, including the right dorsal anterior insula, inferior frontal gyrus, and bilateral amygdala and dorsal striatum (i.e., caudate body). Extracted beta weights were explored for bivariate associations with key behavioral correlates (AUD age of onset, alcohol craving and dependence severity, abstinence duration, and impulsivity) (p < 0.05). BD + AUD individuals exhibited cue-modulated hyperconnectivity between the left dorsal striatum and right posterior cingulate cortex (p-FDR = 0.045) versus the AUD and BD groups, who both exhibited hypoconnectivity between these regions versus healthy participants. Additionally, there were main effects of AUD and BD (p-FDR ≤ 0.040) on cue-modulated functional connectivity of the right dAI (↓ middle frontal gyrus [MFG]) and left amygdala (↑ right superior temporal gyrus, anterior cingulate cortex, and MFG), respectively. Select functional connectivity data were associated with trait characteristics of AUD in BD + AUD (r ≥±0.50, p ≤ 0.026) but not AUD. A distinct pattern of cortico-striato-limbic functional connectivity and brain-behavior relationships was found to characterize BD + AUD with implications for treatment development. Namely, leveraging neuromodulation techniques that can effectively normalize the identified circuitry disruptions could represent a novel path for treatment advances in BD + AUD.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 8","pages":"1378-1386"},"PeriodicalIF":7.6,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41386-026-02418-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147826350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Energy-dependent modulation of nucleus accumbens output via K-ATP channel activity","authors":"Simone Astori, Olivia Zanoletti, Jocelyn Grosse, Carmen Sandi","doi":"10.1038/s41386-026-02429-8","DOIUrl":"10.1038/s41386-026-02429-8","url":null,"abstract":"Mitochondria are central to neuronal bioenergetics, supporting the high metabolic demands required for synaptic signaling and network activity. Yet how neurons adapt their activity to rapid fluctuations in energy supply—and how such adaptations shape behavior—remains poorly understood. We previously showed that acute pharmacological manipulation of mitochondrial complex activity in the nucleus accumbens (NAc) affects motivated behaviors, which led us to hypothesize that medium spiny neurons (MSNs) can rapidly adjust their output in response to bioenergetic levels. To test this hypothesis, we examined how acute mitochondrial inhibition alters MSN function using mouse brain slices. Inhibition of mitochondrial complex I with the selective inhibitor rotenone reduced MSN intrinsic excitability, an effect that was counteracted by intracellular ATP replenishment. We next asked whether ATP-sensitive potassium (K-ATP) channels, canonical regulators of membrane excitability under metabolic stress, contribute to these responses. Histological analyses revealed specific expression of Kir6.2 subunits in both D1- and D2-MSNs, as compared to non-MSNs, and electrophysiological recordings showed that K-ATP channel activation blockade prevented rotenone-induced reductions in MSN excitability. In behavioral assays, complex I inhibition impaired effort-related performance, an effect that was rescued by K-ATP channel blockade. These findings identify K-ATP channels in MSNs as key mediators that sense acute changes in neuronal energy state and translate them into rapid adjustments in NAc excitability and behavior.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 11","pages":"2238-2247"},"PeriodicalIF":7.6,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41386-026-02429-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147825941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Vitamin A deficiency induces sex-specific reward processing alterations through a dysregulation of the mesolimbic dopamine transmission in mice","authors":"Pauline Couty, Sonya Yung, Ilona Dulapt, Loreleï Berger, Adrien Santoro, Lola Hardt, Anna Petitbon, Fabien Ducrocq, Roman Walle, Julien Catanese, Serge Alfos, Jean-Christophe Helbling, Maria-Florencia Angelo, Charlotte Sabran, Patrick Borel, Guillaume Ferreira, Clémentine Bosch-Bouju, Pierre Trifilieff, Katia Touyarot","doi":"10.1038/s41386-026-02424-z","DOIUrl":"10.1038/s41386-026-02424-z","url":null,"abstract":"","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 7","pages":"1352-1354"},"PeriodicalIF":6.6,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41386-026-02424-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147795232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute dose-dependent effects of 4-bromo-2,5-dimethoxyphenethylamine (2C-B) compared with 3,4-methylenedioxymethamphetamine (MDMA) and psilocybin in a double-blind, placebo-controlled study in healthy participants","authors":"Denis Arikci, Joran Borgulya, Isabelle Straumann, Patrick Vizeli, Dino Luethi, Jan Thomann, Deborah Rudin, Ina Vukalovic, Anne Eckert, Matthias E. Liechti, Friederike Holze","doi":"10.1038/s41386-026-02428-9","DOIUrl":"10.1038/s41386-026-02428-9","url":null,"abstract":"Based on its in vitro profile and preliminary evidence, 4-bromo-2,5-dimethoxyphenethylamine (2C-B) may have psychoactive properties that are similar to 3,4-methylenedioxymethamphetamine (MDMA) and psilocybin, which are investigated for the treatment of posttraumatic stress disorder and depressive disorders. We compared acute effects of 2C-B (10, 20, and 30 mg), 125 mg MDMA, and 25 mg psilocybin in 24 healthy participants (12 women, 12 men) using a double-blind, randomized, placebo-controlled, crossover design. Outcome measures included acute subjective effects, autonomic effects, adverse effects, effects on emotional and cognitive empathy, plasma oxytocin and neurophysin I concentrations, and pharmacokinetics up to 9 h. 2C-B produced dose-dependent subjective effects, with the 30 mg dose exerting comparable “any drug effects” to MDMA but lower “any drug effects” than psilocybin. Only psilocybin induced “bad drug effects” and “anxiety” compared with placebo. The 30 mg dose of 2C-B induced psychedelic-type alterations of state of consciousness and increased emotional empathy similarly to MDMA. The average subjective effect duration of 30 mg 2C-B was 4.9 h and similar to MDMA (4.8 h) and shorter than psilocybin (6.1 h). MDMA produced the highest cardiovascular stimulation, followed by psilocybin and 2C-B. Only MDMA increased plasma oxytocin and neurophysin I concentrations. 2C-B exhibited dose-proportional pharmacokinetics, with a plasma elimination half-life of ~1.3 h. The 30 mg dose of 2C-B induced entactogenic and psychedelic effects similarly to MDMA and psilocybin, respectively. MDMA is more cardiostimulant than psilocybin and 2C-B. At the tested dose-level, psilocybin is more distressing than MDMA and 2C-B. These results may assist with dose-finding for future 2C-B research and provide a direct comparison with standard doses of the prototypical compounds MDMA and psilocybin. Trial registration: ClinicalTrials.gov identifier: NCT05523401.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 8","pages":"1511-1518"},"PeriodicalIF":7.6,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41386-026-02428-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147795102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lasting effects of early-life oxytocin treatment on LTP and episodic memory in a mouse model of Fragile X syndrome","authors":"Jasmine Chavez, Aliza A. Le, Julie C. Lauterborn, Brittney M. Cox, Yousheng Jia, Gary Lynch, Christine M. Gall","doi":"10.1038/s41386-026-02423-0","DOIUrl":"10.1038/s41386-026-02423-0","url":null,"abstract":"Deficits in episodic memory are a debilitating feature of Fragile X syndrome (FXS) and other congenital autism spectrum disorders (ASDs). There is evidence that oxytocin (OXT) treatments can improve sociability in persons with ASD and related animal models, encouraging the idea that benefits might extend to cognitive function. We tested this possibility in male FXS model, Fmr1-knockout (KO) mice. Intranasal treatments with OXT or saline were given daily during the second or fifth postnatal week, and effects on social behavior, spatial and episodic memory, and hippocampal synaptic plasticity were assessed in adulthood. Saline-treated Fmr1-KOs exhibited profound deficits in social recognition, object location memory, what-when-where components of episodic memory and long-term potentiation (LTP) in both the CA3-CA1 and lateral perforant path (LPP) systems; NMDAR-mediated components of LPP responses were also impaired. OXT treatments during the second week postnatal normalized all of these functions in Fmr1-KOs assessed in adulthood; this included restoration of initial stages of CA3-CA1 LTP and granule cell NMDAR-mediated currents. In hippocampal slices from naïve adult male Fmr1-KO mice, bath-applied OXT treatment restored LTP in CA1 but not the LPP, indicating pathway-specific effects. Intranasal OXT treatments during the 5th week postnatal did not have enduring effects in either genotype. The present evidence that early OXT treatment corrects a broad range of cognitive and synaptic plasticity deficits in Fmr1-KO mice identifies a clinically plausible strategy for normalizing hippocampal function in ASD and FXS, and highlights the presence of a critical developmental window for effective intervention.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"51 11","pages":"1958-1968"},"PeriodicalIF":7.6,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13536618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147795165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}