Behavioural Brain Research最新文献

{"title":"Neural dynamics of constraint relaxation and problem representation changes in single-trial insight problem solving: An fNIRS study","authors":"Reiji Ohkuma ,&nbsp;Yuto Kurihara ,&nbsp;Toru Takahashi ,&nbsp;Rieko Osu","doi":"10.1016/j.bbr.2025.115813","DOIUrl":"10.1016/j.bbr.2025.115813","url":null,"abstract":"<div><div>Insight problem solving involves overcoming an impasse when a solution seems unreachable, often experienced as an ‘Aha!’ moment. In such solving, shifting from an incorrect representation imposed by constraints to a correct representation through constraint relaxation is critical. Prior research compared brain activity when constraint relaxation and representation change occurred versus when they did not occur, but neural activity before and after such changes within trials has remained underexplored. This study examines neural correlates of problem solving progress, focusing on transitions from impasse—defined by an incorrect, constrained representation—to the state immediately preceding the ‘Aha!’ moment when constraints relax and correct representation emerges. Functional near-infrared spectroscopy (fNIRS) monitored brain activity during a slot machine task. Task performance and eye movement data identified the representations adopted by participants and whether constraint relaxation occurred. Participants were categorized into a success group, which reached the solution, and a failure group, which did not. In the success group, the state just before ‘Aha!’ showed increased oxygenated hemoglobin in the right dorsolateral prefrontal cortex (DLPFC) and superior temporal gyrus (STG) compared with the impasse state. In contrast, the failure group showed increased activity in the right angular gyrus. These results suggest that right DLPFC activation supports constraint relaxation via executive function and working memory, and right STG activation facilitates the transition to a new representation. Integrating fNIRS measures of right DLPFC/STG activation with eye tracking indices of saccade direction shifts enables detection of constraint relaxation preceding the ‘Aha!’ moment.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115813"},"PeriodicalIF":2.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032542","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":"Neuroimaging Biomarkers in Postpartum Depression: A Comprehensive Review of Structural, Functional, and Metabolic Alterations.","authors":"Linfeng Yang, Qingqing Wang, Rui Yang, Boyao Chen, Lingfei Guo","doi":"10.1016/j.bbr.2025.115810","DOIUrl":"https://doi.org/10.1016/j.bbr.2025.115810","url":null,"abstract":"<p><p>Postpartum Depression (PPD) is a significant perinatal mood disorder affecting many new mothers in the first postpartum year. It is characterized by emotional, cognitive, and behavioral changes, often leading to delayed diagnosis due to nonspecific symptoms. PPD arises from a complex interplay of neuroendocrine, genetic, and psychosocial factors. Advances in neuroimaging have revealed structural, functional, and metabolic brain alterations associated with PPD. Specifically, structural MRI studies have shown gray matter volume changes in regions such as the dorsolateral prefrontal cortex and anterior insula, as well as white matter integrity changes in tracts like the internal capsule and cingulum. Functional MRI studies have revealed abnormal activity in regions including the amygdala, hippocampus, and prefrontal cortex, with altered functional connectivity within networks such as the default mode network. Metabolic studies using MRS and PET have identified imbalances in neurotransmitters like serotonin, glutamate, and GABA, as well as changes in brain metabolism.This review synthesizes these findings, highlighting potential biomarkers and implications for targeted treatments. Future research should focus on multimodal approaches, larger sample sizes, and longitudinal studies to further elucidate PPD's neurobiological basis and improve diagnosis and treatment.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"115810"},"PeriodicalIF":2.3,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145028860","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":"Downregulation of Nrf2 deteriorates cognitive impairment in APP/PS1 mice by inhibiting mitochondrial biogenesis through the PPARγ/PGC1α signaling pathway","authors":"Weigang Luo ,&nbsp;Wei Bu ,&nbsp;Guisong Zhang ,&nbsp;Yujuan Dong ,&nbsp;Yuling Wang ,&nbsp;Jinyang Wang ,&nbsp;Cuicui Liu ,&nbsp;Xiaokai Hu ,&nbsp;Yanan Jia ,&nbsp;Huiling Ren","doi":"10.1016/j.bbr.2025.115805","DOIUrl":"10.1016/j.bbr.2025.115805","url":null,"abstract":"<div><h3>Background</h3><div>Mitochondrial dysfunction is considered to be an important pathogenesis of cognitive impairment in Alzheimer's disease(AD). Activation of Nrf2 can improve cognitive impairment in AD mice, but the underlying mechanism remains to be elucidated. This research aims to investigate the intrinsic molecular mechanism of Nrf2 in mitochondrial biogenesis related to cognitive impairment of AD mice.</div></div><div><h3>Methods</h3><div>APP/PS1 mice were used as AD model mice, and Nrf2 down-regulated mouse model was established by injecting lentivirus into hippocampus. Morris water maze test was used to evaluate the learning and memory ability of mice. The biochemical assays were used to detect the expression of Nrf2, mitochondrial biogenesis-related genes, and Aβ protein.Transmission electron microscopy was used to observe the number of mitochondria and synaptic structure in neurons. Chromatin immunoprecipitation was used to observe the binding of Nrf2 protein to the PGC1α promoter; Co-Immunoprecipitation was used to observe the interaction between PPARγ protein and PGC1α protein.</div></div><div><h3>Results</h3><div>Downregulation of Nrf2 reduced mitochondrial biogenesis, aggravated Aβ protein deposition and synaptic damage, and in turn aggravated cognitive impairment in mice. Compared with control mice, AD model mice had reduced levels of Nrf2, PPARγ, PGC1α, NRF1, TFAM protein, mitochondrial number and MAP2, increased Aβ protein deposition, and worsened synaptic damage and cognitive impairment. Lentivirus-induced Nrf2 downregulation downregulates PPARγ, PGC1α, NRF1, and TFAM protein expression, reduces mitochondrial number and MAP2 levels, and aggravates Aβ protein deposition, synaptic damage, and cognitive impairment. Nrf2 protein bound to the PGC1α gene promoter, and PPARγ protein interacted with PGC1α protein.</div></div><div><h3>Conclusion</h3><div>Nrf2 can directly regulate PGC1α transcription, and can also regulate PPARγ followed by binding to the PGC1α protein, thereby modulating mitochondrial biogenesis.Nrf2 downregulation reduces the expression of PPARγ and PGC1α proteins, thereby reducing their interaction. This suppression impairs mitochondrial biogenesis, exacerbates mitochondrial dysfunction, intensifies Aβ deposition and synaptic damage, and ultimately worsens cognitive impairment in AD mice.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115805"},"PeriodicalIF":2.3,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145010429","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":"Gratitude increases the sharing willingness to micro-charity information: An fNIRS study","authors":"Xianling Su ,&nbsp;Qi Gao ,&nbsp;Mingzhu Fu ,&nbsp;Changfeng Wang ,&nbsp;Weihao Ye","doi":"10.1016/j.bbr.2025.115807","DOIUrl":"10.1016/j.bbr.2025.115807","url":null,"abstract":"<div><div>Micro-charity, with its ease of dissemination, is an effective way to support public welfare. Gratitude has been shown to promote prosocial behavior. However, its specific role in driving micro-charity sharing, particularly the underlying neural correlates, remains unclear. To address this, the present study used functional near-infrared spectroscopy (fNIRS) to explore the neural correlates underlying gratitude on micro-charity sharing in Chinese college students (<em>N</em> = 27). A modified charitable decision task was used to measure sharing willingness under control and gratitude conditions. Specifically, the participants were asked to indicate their willingness to share the viewed micro-charity appeals on their personal social media platforms. Gratitude was induced using an established essay-writing paradigm. Self-report results showed that gratitude increased willingness to share micro-charity information on social media platforms. Under the gratitude condition, fNIRS findings revealed enhanced activity in bilateral dorsolateral prefrontal cortex (DLPFC) and frontopolar cortex (FPC), potentially reflecting reward processing during decision evaluation. Gratitude also strengthened functional connectivity among the main regions of interest (ROIs: bilateral DLPFC, FPC and MTG). In addition, activation in regions associated with mentalizing (right middle temporal gyrus, right MTG) was positively correlated with sharing willingness. Taken together, our findings elucidate gratitude’s positive impact on micro-charity sharing and reveal its underlying neural mechanisms.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115807"},"PeriodicalIF":2.3,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013787","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":"The effects of multimodal distractors on sign-trackers and goal-trackers attention","authors":"Noémie Thériault,&nbsp;Mathieu J. Bourque,&nbsp;Frédéric Huppé-Gourgues","doi":"10.1016/j.bbr.2025.115800","DOIUrl":"10.1016/j.bbr.2025.115800","url":null,"abstract":"<div><div>During Pavlovian conditioning, Sign-Tracker (ST), Goal-Tracker (GT), and Intermediate (IN) phenotypes emerge, as characterized by the degree to which an individual attributes incentive salience to reward-associated cues. These operationally defined phenotypes differ in other respects: In human studies, STs tend to favor bottom-up attention, while GTs tend to favor top-down attention. There is some limited evidence that rats exhibit similar patterns during Pavlovian conditioning. To substantiate this model, we tested the hypothesis that introducing light and auditory distractors would disproportionately impair the signal detection performance of ST rats, given their propensity for bottom-up attention processing, as opposed to GT rats, who rely more on top-down strategies. To this end, we assessed detection performance in 86 Long-Evans rats by introducing both visual and auditory distractors of varying intensities. This approach aimed to investigate the limits of attentional control among ST, GT, and IN rats across six variants of a sustained attention task. Although distractors impaired performance, contrary to initial expectations, the extent of this impairment varied across phenotypes and tasks, indicating a more nuanced relationship between attentional mechanisms and susceptibility to distractions than previously posited. The present results suggest the occurrence of a complex interplay of attentional mechanisms that may not align completely with the ST/GT dichotomy as traditionally presented. These findings have potential implications for understanding individual differences in attentional control and susceptibility to distractions, which could relate to addiction vulnerability.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115800"},"PeriodicalIF":2.3,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013799","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":"Dose optimization of NMDA for rat model of infantile spasms: Approach using EEG, behavior (Seizure) and histopathology","authors":"Muskan Uniyal ,&nbsp;Arushi Sandhu ,&nbsp;Aniket Gupta ,&nbsp;Kajal Rawat,&nbsp;Anil Kumar,&nbsp;Sakshi Singh,&nbsp;Lekha Saha","doi":"10.1016/j.bbr.2025.115808","DOIUrl":"10.1016/j.bbr.2025.115808","url":null,"abstract":"<div><div>Infantile Epileptic Spasms Syndrome (IESS), also referred to as West syndrome, is a severe epileptic disorder that emerges during early childhood. It is marked by characteristic epileptic spasms, developmental stagnation or regression, and a distinctive electroencephalogram (EEG) pattern known as hypsarrhythmia. To better understand the underlying mechanisms of IESS, various genetic and chemically induced animal models have been developed. Among these, the N-methyl-D-aspartate (NMDA) induced model is widely used, although it is often associated with high toxicity and mortality. In the study, we optimized the NMDA dose to reduce toxicity while maintaining the pathological features of IS. The validity of the model was assessed through EEG recordings, behavioural assessments, and brain histopathology. EEG analysis in the NMDA treated group revealed prominent abnormalities, including irregular wave patterns and elevated interictal activity. Histological examination showed signs of neuronal damage, such as nuclear pyknosis, in the model group. Behavioural tests assessing locomotion, memory, stereotypic activity, and anxiety like behaviour did not show significant differences between control and NMDA exposed rats. These findings demonstrate that a reduced and optimised dose of NMDA can reliably induce IS-like features in rats, offering a safer and effective model for future preclinical research.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115808"},"PeriodicalIF":2.3,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145003780","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":"Glutamate modulation of physiological and behavioral responses to restraint stress: Participation of supraoptic nucleus of the hypothalamus","authors":"Silvana Lopes-Azevedo ,&nbsp;Gabriela Marie Ferreira Suzuki ,&nbsp;Cristiane Busnardo ,&nbsp;América Augusto Scopinho ,&nbsp;Melina Matthiesen ,&nbsp;José Antunes-Rodrigues ,&nbsp;Fernando Morgan Aguiar Corrêa","doi":"10.1016/j.bbr.2025.115802","DOIUrl":"10.1016/j.bbr.2025.115802","url":null,"abstract":"<div><h3>Aims</h3><div>Acute restraint stress (RS) has been reported to activate the supraoptic nucleus of the hypothalamus (SON). The aim of the present study was to evaluate the role of glutamatergic neurotransmission in the SON on autonomic [mean arterial pressure (MAP), heart rate (HR), and tail cutaneous temperature], neuroendocrine (plasma levels of corticosterone, oxytocin, and vasopressin), and behavioral responses to RS.</div></div><div><h3>Methods</h3><div>Male Wistar rats with bilateral SON cannulas received microinjections of NMDA or non-NMDA receptor antagonists or vehicle before restraint stress, and the effects on cardiovascular, tail temperature, hormonal, and behavioral responses were evaluated</div></div><div><h3>Results</h3><div>Microinjection of DL-AP7 or NBQX into the SON reduced MAP increases and tail temperature decreases induced by RS. Also, NBQX enhanced RS-evoked tachycardia. SON treatment with DL-AP7 or NBQX reduced RS-induced increases in oxytocin, without affecting vasopressin plasma levels. Morever, NBQX enhanced RS-induced increases in plasma corticosterone level. DL-AP7 inhibited the RS-caused delayed anxiogenic-like effect.</div></div><div><h3>Conclusion</h3><div>NMDA and non-NMDA glutamate receptors in the SON facilitate pressor response and oxytocin release during RS. In addition, non-NMDA receptors exert an inhibitory influence RS-induced increases in heart rate and corticosterone release, whereas NMDA receptors contribute to the delayed expression of anxiety-like behaviors.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"495 ","pages":"Article 115802"},"PeriodicalIF":2.3,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145003779","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":"Relationship between anxiety and tinnitus development in a rat model","authors":"Jack W. Zimdahl ,&nbsp;Kady J. Braack ,&nbsp;Jennifer Rodger ,&nbsp;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}

{"title":"Neuroprotective role of GLT-1/EAAT2 in glutamate-induced excitotoxicity","authors":"Yi Zhang,&nbsp;Wen Liu,&nbsp;Tao Huang,&nbsp;Lingling Liu,&nbsp;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 ,&nbsp;Amol Pable ,&nbsp;Raj Katariya ,&nbsp;Manasi Tadas ,&nbsp;Mayur Kale ,&nbsp;Milind Umekar ,&nbsp;Nandkishor Kotagale ,&nbsp;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}