Jack W. Zimdahl , Kady J. Braack , Jennifer Rodger , Wilhelmina H.A.M. Mulders
{"title":"Relationship between anxiety and tinnitus development in a rat model","authors":"Jack W. Zimdahl , Kady J. Braack , Jennifer Rodger , Wilhelmina H.A.M. Mulders","doi":"10.1016/j.bbr.2025.115803","DOIUrl":"10.1016/j.bbr.2025.115803","url":null,"abstract":"<div><div>Tinnitus, the auditory perception of sound without an external environmental stimulus, affects 15 % of the human population and is associated with hearing loss. Interestingly, anxiety may be a significant risk factor in tinnitus pathophysiology potentially due to underlying common neural circuits of the auditory and limbic systems. The current study aimed to investigate the effects of stress-induced anxiety on tinnitus development in a rat model. Neonatal dexamethasone (DEX) exposure was used to mimic early life stress with the aim of inducing an anxiety-like phenotype in adulthood. These animals were then exposed to an acoustic trauma (AT) to investigate proportion and time to tinnitus development. DEX exposure (<em>n</em> = 18) induced changes in anxiety-like behaviour, compared to vehicle control animals (<em>n</em> = 15), with increased anxiety-like behaviour in acoustic startle response tests but not in the Elevated Plus Maze. There was no difference in the proportion of animals that developed behavioural signs of tinnitus between DEX and control groups, however, animals that developed behavioural signs of tinnitus had higher levels of anxiety prior to AT. Furthermore, neuronal recordings in the medial geniculate nucleus, a region crucial in the gating of non-salient auditory information, indicated that rats with behavioural signs of tinnitus had elevated spontaneous and burst firing rates compared to rats without behavioural signs of tinnitus. Overall, these findings further illuminate our understanding of the relationship between anxiety and susceptibility to tinnitus development, and are consistent with the body of clinical literature highlighting the correlation between anxiety and tinnitus percept.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115803"},"PeriodicalIF":2.3,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yi Zhang, Wen Liu, Tao Huang, Lingling Liu, Xiuping Chen
{"title":"Neuroprotective role of GLT-1/EAAT2 in glutamate-induced excitotoxicity","authors":"Yi Zhang, Wen Liu, Tao Huang, Lingling Liu, Xiuping Chen","doi":"10.1016/j.bbr.2025.115804","DOIUrl":"10.1016/j.bbr.2025.115804","url":null,"abstract":"<div><div>Glutamate-mediated excitotoxicity represents a common pathomechanism in neurological disorders. As the predominant glutamate transporter in the central nervous system, glutamate transporter 1 (GLT-1, known as EAAT2 in humans) plays a crucial role in maintaining glutamate homeostasis and preventing excitotoxicity through its Na⁺-dependent transport mechanism. Key functions of GLT-1 include reducing extracellular glutamate concentration, regulating calcium homeostasis, suppressing oxidative stress, preserving mitochondrial integrity, and modulating neuroinflammatory processes by limiting microglial activation. This review systematically examines the role of GLT-1 in cerebral ischemia/reperfusion injury, neurodegenerative diseases, epilepsy, chronic pain, and psychiatric disorders. Furthermore, the therapeutic potential of GLT-1 is explored, encompassing pharmacological activators (e.g., ceftriaxone), gene therapy approaches (e.g., adeno-associated virus (AAV)-mediated GLT-1 overexpression), and non-coding RNA-based strategies. Future research should focus on elucidating the precise regulatory networks of GLT-1 and developing targeted therapies with enhanced specificity and minimal off-target effects.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115804"},"PeriodicalIF":2.3,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Therapeutic potential of agmatine in alcohol use disorder: Preclinical insights and future directions","authors":"Poonam Dhaigude , Amol Pable , Raj Katariya , Manasi Tadas , Mayur Kale , Milind Umekar , Nandkishor Kotagale , Brijesh Taksande","doi":"10.1016/j.bbr.2025.115793","DOIUrl":"10.1016/j.bbr.2025.115793","url":null,"abstract":"<div><div>Alcohol Use Disorder (AUD) is a major global health challenge characterized by the recurrence of alcohol consumption, withdrawal symptoms, and significant social, economic, and health-related burdens. Despite conventional treatments such as cognitive behavioral therapy and medications like disulfiram and naltrexone, the majority of patients do not achieve adequate relief due to the multifactorial nature of this disorder, including mental health issues and neuroadaptive changes. Recent studies demonstrated that chronic alcohol consumption results in the disruption of both the production and signaling of endogenous agmatine, a neuromodulator synthesized from L-arginine. Agmatine modulates the neurotransmitter systems, particularly at NMDA and imidazoline sites, which are associated with neuroinflammation and neuroplasticity. Moreover, in preclinical models, altered agmatine metabolism is related to changes in alcohol seeking behavior, highlighting its potential as a novel therapeutic candidate. Furthermore, agmatine may mitigate the behavioral and biochemical effects of alcohol-induced neurotoxicity, indicating its potential role in improving tolerance management and withdrawal symptoms. Integration of agmatine into a multimodal treatment strategy could lead to comprehensive personalized interventions in patients with AUD, addressing both neurochemical imbalances and the psychosocial complexity associated with this disorder. Thus, this review explores the potential of agmatine in addressing psychological factors underlying AUD, offering a novel and optimistic treatment option for advancing future therapeutic approaches. However, comprehensive clinical trials are essential to confirm these benefits and to establish optimal dosing regimens and a long-term safety profile in human settings.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115793"},"PeriodicalIF":2.3,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Amber L. LaCrosse, Molly C. Jacobson, Andrew G. Hubl, Caden J. Natale, Jan M. Hoffmann, Autumn B. Stage, Isabella E. Enger, Andrew R. Donar, Megan K. McManey, Adam J. Prus
{"title":"Effects of naltrexone on gabapentin reward and buprenorphine combinations in male mice","authors":"Amber L. LaCrosse, Molly C. Jacobson, Andrew G. Hubl, Caden J. Natale, Jan M. Hoffmann, Autumn B. Stage, Isabella E. Enger, Andrew R. Donar, Megan K. McManey, Adam J. Prus","doi":"10.1016/j.bbr.2025.115801","DOIUrl":"10.1016/j.bbr.2025.115801","url":null,"abstract":"<div><div>Gabapentin (GBP), an anticonvulsant approved for seizures and neuropathic pain, is frequently co-prescribed with buprenorphine (BUP), a partial mu-opioid receptor (MOR) agonist, to manage withdrawal and pain in individuals with opioid use disorder (OUD). While GBP is generally considered safe, emerging evidence suggests abuse potential when combined with opioids. This study used the conditioned place preference (CPP) paradigm to assess the rewarding effects of GBP alone and in combination with BUP. Male mice underwent standard CPP procedures. Treatment groups included GBP (100 or 300 mg/kg) alone or combined with BUP (1.0 mg/kg). Naltrexone (NAL; 10.0 mg/kg), an opioid receptor antagonist, was co-administered with each treatment to assess MOR involvement. Drugs and saline were alternated over eight consecutive days. GBP induced significant CPP at both doses, but only the 100 mg/kg effect was prevented by NAL. BUP-induced CPP was prevented by NAL. Co-administration of GBP and BUP at either dose produced a CPP, which persisted despite NAL treatment. Both opioid and non-opioid systems may contribute to the rewarding effects of GBP and GBP-BUP combinations. These findings raise important concerns about the abuse potential of GBP, particularly when co-prescribed with BUP, and underscore the need for cautious clinical use and further investigation into non-opioid mechanisms of reward.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115801"},"PeriodicalIF":2.3,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145005889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Li-Tsung Lin , Hui-An Lin , Chyi-Huey Bai , Sheng-Feng Lin
{"title":"Flanker task assessment of inhibitory control in ICU survivors: Preliminary insights into cognitive impairment","authors":"Li-Tsung Lin , Hui-An Lin , Chyi-Huey Bai , Sheng-Feng Lin","doi":"10.1016/j.bbr.2025.115791","DOIUrl":"10.1016/j.bbr.2025.115791","url":null,"abstract":"<div><h3>Background and purpose</h3><div>Cognitive assessment tools for ICU survivors often lack sensitivity to detect subtle impairments. This study examines whether combining standard screening instruments with computerized inhibitory control measures enhances post-ICU cognitive evaluation.</div></div><div><h3>Methods</h3><div>In this prospective cohort study conducted at a university-affiliated hospital, participants included ICU survivors aged ≥ 40 years, functionally independent prior to admission, and alert upon ICU discharge. Assessments included the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and a computerized Flanker task evaluating response accuracy and reaction time. The Stroop task was used to validate agreement with the Flanker task.</div></div><div><h3>Results</h3><div>Among 34 participants, median MMSE and MoCA scores were 25.5 and 24, respectively. Cognitive scores ≥ 25 were observed in 55.9 % (MMSE) and 44.1 % (MoCA). Participants in the highest MoCA tertile (>26) demonstrated preserved attention and inhibitory control. MoCA scores were more strongly associated with Flanker task accuracy than MMSE, particularly in the combined condition (adjusted β = 2.7 per MoCA point, p = 0.026; β = 27.2 for MoCA ≥ 25 vs <25, p = 0.026) versus MMSE (adjusted β = 2.8 per point, p = 0.044; β = 20.6 for MMSE ≥ 25 vs <25, p = 0.074). Bland–Altman analysis indicated strong agreement between Flanker and Stroop task accuracy in high-performing individuals.</div></div><div><h3>Conclusions</h3><div>Integrating the Flanker task with MoCA may offer a more nuanced assessment of post-ICU cognitive function. This combined approach enhances detection of cognitive deficits and supports early intervention strategies in ICU recovery care.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115791"},"PeriodicalIF":2.3,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144999539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Frontal alpha asymmetry and heart rate variability as markers of conditional heart-brain interaction in test anxiety","authors":"Swathy Parameswaran, Venkatesh Balasubramanian","doi":"10.1016/j.bbr.2025.115792","DOIUrl":"10.1016/j.bbr.2025.115792","url":null,"abstract":"<div><div>Test Anxiety (TA) is known to impair the heart-brain interaction affecting both the central and autonomic nervous systems. The impairment is often assumed to be uniform, overlooking individual variability in stress response. This study explores how heart–brain dysregulation in TA may manifest conditionally, shaped by individual differences. Frontal alpha asymmetry (FAA), reflecting predisposition to avoidance and anxiety, and heart rate variability (HRV), indicating regulatory capacity, are employed as markers to examine individual variations.</div><div>Fifty-seven healthy university students (M = 22.07 ± 2.61 years) participated in a 30-minute mock test before their university assessment, during which TA, avoidance, FAA, and HRV metrics were recorded. A moderated mediation model was then utilized to examine the relationship between heart-brain interaction and avoidance in test anxiety, testing for the conditionality of this interaction.</div><div>While the overall moderated mediation model was non-significant, significant direct and indirect effects of HRV metrics on avoidance were observed at higher negative FAA values (B = 0.8805, p < 0.05). In contrast, at higher FAA levels, the indirect effect diminishes, and neither FAA (Estimate = 1.8565, p = 0.3559) nor its interaction with tonic RMSSD (Estimate = −0.3153, p = 0.3919) significantly predicts avoidance, suggesting reduced reliance on autonomic regulation.</div><div>Results highlight that heart-brain impairment in TA is conditional, manifesting specifically in individuals with a predisposition to anxiety (negative FAA). The findings further suggest that a baseline disposition to anxiety can override the heart’s regulatory activation in a stress response. While previous works suggest general heart-brain impairment, this study specifies that such impairment is primarily observed in individuals with a predisposition to anxiety.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115792"},"PeriodicalIF":2.3,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of attenuated TrkB signaling on the medial prefrontal cortex during early brain development: A comparative study using the maternal separation model","authors":"Ken-Ichi Ohta , Hidetoshi Ujihara , Haruki Kumei , Shingo Suzuki , Hikari Otabi , Katsuhiko Warita , Takanori Miki","doi":"10.1016/j.bbr.2025.115790","DOIUrl":"10.1016/j.bbr.2025.115790","url":null,"abstract":"<div><div>Early life stress (ELS) is known to cause long-lasting social and cognitive deficits, but the underlying mechanisms remain unclear. We previously reported that maternal separation (MS), a widely used ELS model, induces transient downregulation of brain-derived neurotrophic factor (BDNF) expression in the medial prefrontal cortex (mPFC) during early postnatal development. In this study, we investigated whether this transient suppression of BDNF-TrkB signaling contributes to the reduction in inhibitory neurons and behavioral alterations observed in the MS model. We first confirmed that a single administration of ANA-12, a TrkB antagonist, at postnatal day (PD) 7 suppressed TrkB phosphorylation and downstream signaling in Sprague-Dawley rats. Using this dosage, repeated ANA-12 administration from PD 7–14 decreased the number of inhibitory neurons, particularly parvalbumin-positive interneurons, in adolescence (PD 35), which resembled the changes observed in the MS model. However, these reductions returned to control levels by young adulthood (8 weeks). Behaviorally, ANA-12 treatment impaired working memory in the Y-maze but did not induce social deficits in the modified three-chamber test (3-CST). Furthermore, neural activity during the 3-CST was comparable to that of controls. These findings suggest that early TrkB signaling disruption partially mediates the MS-induced reduction in inhibitory neurons and subsequent cognitive impairment. However, this disruption alone is insufficient to produce persistent social abnormalities. Our findings highlight the complexity of ELS effects and indicate that persistent neural and behavioral alterations likely involve additional mechanisms beyond early TrkB signaling disruption.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115790"},"PeriodicalIF":2.3,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fabrice de Chaumont , Gaëlle Yvenou , Ana Perez Villalba , Yann Hérault , Thomas Bourgeron , Elodie Ey
{"title":"Female C57BL/6 J mice perform distinctive urination behaviour accompanied by ultrasonic vocalisation sequences with a stereotyped temporal organisation.","authors":"Fabrice de Chaumont , Gaëlle Yvenou , Ana Perez Villalba , Yann Hérault , Thomas Bourgeron , Elodie Ey","doi":"10.1016/j.bbr.2025.115788","DOIUrl":"10.1016/j.bbr.2025.115788","url":null,"abstract":"<div><div>Ultrasonic vocalisations (USVs) are widely studied in mice as a marker of social communication. Typically, USVs are recorded during brief social encounters in unfamiliar test cages. In the present study, we explored how freely interacting pairs of C57BL/6<!--> <!-->J adult female mice spontaneously use USVs during long-term monitoring. We discovered that these mice display a previously undescribed behaviour: they emit specific USV sequences while depositing a large volume of urine in a corner of the cage. The most striking feature of USVs accompanying this vocalised urination behaviour was the stereotyped duration of the intervals between acoustically simple USVs. The frequency of this behaviour was highly variable between pairs. Interestingly, when urination was accompanied by the specific USV sequence, it was associated with a significant increase in locomotor activity in both the emitter and the cage mate, compared with urination without USVs. Altogether, these observations and the description of this vocalised urination behaviour highlight the importance of exploring mouse vocalisations at the sequence level to better understand the functions of USVs in different behavioural contexts.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115788"},"PeriodicalIF":2.3,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Early-life cognitive effects of prebiotics and probiotics: A cross-species systematic review","authors":"Saúl Sal-Sarria , Philip W.J. Burnet","doi":"10.1016/j.bbr.2025.115789","DOIUrl":"10.1016/j.bbr.2025.115789","url":null,"abstract":"<div><div>This systematic review evaluated the effects of prebiotic and probiotic interventions on early-life cognitive development in animal models and humans. Following PRISMA 2020 guidelines, 39 studies published between 2015 and 2025 were included from PubMed, Scopus, and Web of Science. In rodents, probiotics -mainly <em>Lactobacillus</em> and <em>Bifidobacterium</em> strains- consistently improved spatial learning, working memory, and cognitive flexibility, particularly under conditions of early-life stress and neuroinflammation. Porcine models showed partial benefits in learning and memory, though several studies reported neutral outcomes. Human trials yielded mixed findings: some demonstrated improvements in language, attention, or adaptive behavior, while others observed no significant cognitive effects. Proposed mechanisms include modulation of neurotransmitter systems, reduced neuroinflammation, restoration of blood-brain barrier integrity, and regulation of the hypothalamic-pituitary-adrenal axis. Overall, preclinical evidence strongly supports the cognitive benefits of microbiota-targeted interventions, but translation to humans remains uncertain due to methodological heterogeneity, species differences, and the limited number of pediatric studies. Future research should focus on longitudinal human trials, direct comparisons between prebiotic, probiotic, and synbiotic approaches, and the inclusion of sex as a biological variable.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115789"},"PeriodicalIF":2.3,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hongzhu Liu , Tong Li , Rui Qin , Lin Li , Congshan Ji , Xianshun Yuan , Baojin Chen , Cuicui Li , Ximing Wang
{"title":"Altered gray matter networks in the co-occurrence of autism spectrum disorder and attention deficit hyperactivity disorder","authors":"Hongzhu Liu , Tong Li , Rui Qin , Lin Li , Congshan Ji , Xianshun Yuan , Baojin Chen , Cuicui Li , Ximing Wang","doi":"10.1016/j.bbr.2025.115787","DOIUrl":"10.1016/j.bbr.2025.115787","url":null,"abstract":"<div><div>Although the comorbidity of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) (ASD+ADHD) is prevalent, the neurobiological mechanisms underlying this combined condition are not yet fully understood. Both ASD and ADHD have been associated with alterations in gray matter (GM) structural networks, suggesting that such altered GM networks may serve as potential markers for identifying this comorbid disorder. In this study, we compared the GM structural networks in ASD+ADHD, ASD without ADHD (ASD-only), ADHD without ASD (ADHD-only), and typically developing controls (TDc). Structural magnetic resonance imaging data of 41 individuals with ASD+ADHD, 53 individuals with ASD-only, 40 individuals with ADHD-only, and 62 TDc were obtained from the Autism Brain Imaging Data Exchange II and the ADHD-200 Sample databases. Graph theory analysis was employed to construct individual GM structural networks for each participant, followed by the calculation of topological metrics based on these networks. Our analysis revealed both common and disorder-specific nodal centralities alterations across the ASD+ADHD, ASD-only, and ADHD-only groups, compared with TDc. A significant correlation was found between the severity of symptoms and altered nodal centralities in the amygdala in the ASD+ADHD group. These findings support the Diagnostic and Statistical Manual of Mental Disorders-5 diagnosis of ASD+ADHD. Moreover, these findings provide novel neurobiological evidence for the ASD+ADHD comorbid state, which could lead to more targeted diagnostic and therapeutic approaches.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115787"},"PeriodicalIF":2.3,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}