Neuropharmacology最新文献

{"title":"Retraction Notice to “Anandamide mediates cognitive judgement bias in rats” [Neuropharmacology 101 (2016) 146–153]","authors":"J. Kregiel , N. Malek , P. Popik , K. Starowicz , R. Rygula","doi":"10.1016/j.neuropharm.2025.110588","DOIUrl":"10.1016/j.neuropharm.2025.110588","url":null,"abstract":"","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110588"},"PeriodicalIF":4.6,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of amylin in feeding and satiation","authors":"Thomas A. Lutz","doi":"10.1016/j.neuropharm.2025.110587","DOIUrl":"10.1016/j.neuropharm.2025.110587","url":null,"abstract":"<div><div>This article summarizes the key literature describing the effects of the pancreatic beta-cell hormone amylin on eating. One of the first described and best investigated effects of amylin on eating is its physiological effect to control meal size by inducing satiation. This effect is very rapid, short-lasting and probably directly reflects the meal-induced increase in circulating amylin levels. Evidence provided by many groups suggests that the effect of amylin on eating is directly mediated by humoral action in the central nervous system rather than by peripheral receptors. It is also clear that the caudal hindbrain, in particular the area postrema, is a key brain region mediating amylin effects, but amylin may also act at different sites in the brain. The latter is particularly true for the effect of amylin to reduce food reward. Hence, amylin not only reduces caloric intake as such but may specifically reduce high fat intake, at least in certain experimental conditions; in people, amylin receptor agonists have been shown to reduce the number of binge eating episodes. In recent years, long-lasting amylin receptor agonists have been developed. Alone or in combination with other gut hormone receptor agonists (in particular the agonist of glucagon-like peptide-1 [GLP-1] receptor, semaglutide), these molecules turned out to be highly promising therapeutic agents for the treatment of obesity.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110587"},"PeriodicalIF":4.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reciprocal c-Abl-GPx1 regulation controls CA1 neuronal viability to oxidative stress via ERK1/2-DRP1-mediated mitochondrial dynamics","authors":"Ji-Eun Kim,&nbsp;Su Hyeon Wang,&nbsp;Tae-Cheon Kang","doi":"10.1016/j.neuropharm.2025.110586","DOIUrl":"10.1016/j.neuropharm.2025.110586","url":null,"abstract":"<div><div>Abelson murine leukemia viral oncogene homolog 1 (c-Abl, also known as ABL1) is a potent selenium-independent regulator of expression and activity of glutathione peroxidase-1 (GPx1) and extracellular signal-regulated kinase 1/2 (ERK1/2). Since GPx1-ERK1/2 pathway modulates dynamin-related protein 1 (DRP1) serine (S) 616 phosphorylation, we investigated whether c-Abl participates in GPx1-ERK1/2 interaction and DRP1-mediated mitochondrial dynamics in CA1 neurons in response to oxidative stress induced by L-buthionine sulfoximine (BSO, an oxidative stress inducer) and status epilepticus (SE). In the present study, BSO enhanced c-Abl tyrosine (Y) 245 phosphorylation, ERK1/2 activity and GPx1 upregulation in the CA1 region under physiological condition. Imatinib (a c-Abl inhibitor) ameliorated BSO-induced c-Abl Y245, but elicited further ERK1/2 phosphorylation without affecting GPx1 expression. <em>GPx1</em> knockdown enhanced BSO-induced c-Abl Y245 phosphorylation, but decreased ERK1/2 activity. BSO also facilitated mitochondrial fission in CA1 neurons by augmenting DRP1 expression and its S616 phosphorylation in the CA1 region, which were diminished by <em>GPx1</em> knockdown and U0126 (an ERK1/2 inhibitor), but reinforced by imatinib. SE increased c-Abl Y245 phosphorylation and mitochondrial length in CA1 neurons, accompanied by reduced GPx1 expression and ERK1/2 phosphorylation. Imatinib and N-acetylcysteine (NAC, an antioxidant) attenuated these post-SE events and CA1 neuronal death. However, <em>GPx1</em> knockdown deteriorated SE-induced CA1 neuronal degeneration accompanied by augmenting c-Abl Y245 phosphorylation and mitochondrial elongation in CA1 neurons. These findings indicate that the impaired reciprocal regulation between c-Abl and GPx1 may cause CA1 neuronal degeneration in response to oxidative stress by abrogating ERK1/2-DRP1-mediated mitochondrial fission.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110586"},"PeriodicalIF":4.6,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144581362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT1-mediated deacetylation and activation of MEK/ERK pathway decreased IL-6 in spinal dorsal horn to promote oxycodone tolerance","authors":"Shenghui Hu ,&nbsp;Fengjia Zhou ,&nbsp;Baoguang Lin ,&nbsp;Tong Jiang ,&nbsp;Xinyu Fan ,&nbsp;Shuohan Xu","doi":"10.1016/j.neuropharm.2025.110585","DOIUrl":"10.1016/j.neuropharm.2025.110585","url":null,"abstract":"<div><div>Oxycodone, an opioid analgesic, exhibits limited clinical utility due to the development of tolerance. This study aims to investigate the role of Sirtuin 1 (SIRT1), a histone deacetylase, in oxycodone-induced analgesic tolerance. Adult ICR mice were administered oxycodone subcutaneously once a day for seven consecutive days. The tail-flick test was used to establish a mouse model of oxycodone tolerance. RT-qPCR was employed to assess the mRNA levels of SIRT1-SIRT7. Western blotting was performed to measure the expression levels of SIRT1, interleukin (IL)-6, H3K9ac, H3K14ac, H3K18ac, total/phosphorylated extracellular signal-regulated kinase (ERK) (1/2), and mitogen-activated protein kinase/ERK kinase (MEK) (1/2). ChIP-qPCR were used to localize SIRT1/IL-6 expression, and to quantify histone acetylation at the IL-6 promoter. Mice developed analgesic tolerance by Day 7 of oxycodone administration. Oxycodone significantly reduced SIRT1 mRNA and protein levels in the lumbar spinal cord. Bioinformatics analysis identified <em>IL-6</em> as the most prominently upregulated gene in the spinal cord. Correspondingly, IL-6 protein levels were elevated, along with increased levels of total H3K9ac (but not H3K14ac or H3K18ac) and enriched H3K9ac at the IL-6 promoter. While total ERK(1/2) and MEK(1/2) levels remained unchanged, their phosphorylated forms were significantly upregulated in tolerant mice. An SIRT1 agonist (SRT1720) inhibited the development of oxycodone tolerance, suppressed IL-6 overexpression, normalized H3K9ac and phospho-ERK/MEK levels, and reduced H3K9ac expression at the IL-6 promoter. Thus, SIRT1 promotes oxycodone tolerance by deacetylating histone H3K9 at the IL-6 promoter and activating the MEK/ERK pathway to upregulate IL-6 expression.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110585"},"PeriodicalIF":4.6,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144562841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hippocampal O-GlcNAc homeostasis sustains memory reconsolidation amidst stress hormone exposure","authors":"Chenran Wang ,&nbsp;Jianhui Wang ,&nbsp;Feng Liu ,&nbsp;Jingying Liu ,&nbsp;Yan Huang ,&nbsp;Mengting Xia ,&nbsp;Hexi Yang ,&nbsp;Zhiyong Xiao ,&nbsp;Wenxia Zhou","doi":"10.1016/j.neuropharm.2025.110582","DOIUrl":"10.1016/j.neuropharm.2025.110582","url":null,"abstract":"<div><div>Memory is not always reliable, inherently malleable. The malleability enables organisms to adapt their behavior based on future predictions, increasing survival odds. O-linked β-N-acetylglucosamine (O-GlcNAc) has emerged as a modulator of memory, notwithstanding, its impact on memory malleability remains to be comprehensively elucidated. Here, we report that the reliable prediction-mediated strengthening or incomplete reminder-mediated updating of original memories, a process called reconsolidation can alter memory malleability, which is impaired in mice (C57BL/6J, males) under stress. Pharmacologically enhancing O-GlcNAc levels afford dynamic and phase-specific protection of reconsolidation. Meanwhile, overexpression of hippocampal O-GlcNAc transferase (OGT), aimed at elevating O-GlcNAc, recapitulated this protective effect. Inhibiting OGT substrate availability negates this protective effect. Interestingly, the concurrent overexpression of hippocampal OGT alongside substrate supplementation, intended to excessively elevate O-GlcNAc, proves ineffective in affording additional protection. It even triggers a reappearance of reconsolidation resistance in the original memory. This protective role of O-GlcNAc, seemingly acting in a buffering-like manner, insulating reconsolidation from aberrant modifications within an optimal range. These data establish hippocampal O-GlcNAc as a potential target for preserving memory malleability.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110582"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144557288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal fentanyl exposure affects social dominance and myelination patterns in the adult mouse brain","authors":"Chioma Uchegbu ,&nbsp;Trinity Nguyen ,&nbsp;Inayat Sood ,&nbsp;Kimberly Blankenship ,&nbsp;Huan He ,&nbsp;Gregg D. Stanwood ,&nbsp;Cynthia Vied ,&nbsp;Devon L. Graham","doi":"10.1016/j.neuropharm.2025.110583","DOIUrl":"10.1016/j.neuropharm.2025.110583","url":null,"abstract":"<div><div>Fentanyl use has reached epidemic proportions, and more adults are administering the drug illicitly. Despite its high use rates, very little is known of the long-term effects following prenatal fentanyl exposure. Using an oral model of lower-dose prenatal fentanyl administration in mice, we found that fentanyl-exposed offspring developed similarly to their saline-exposed counterparts. In adulthood, there were few significant changes in tests of anxiety- and depression-like behavior, cognition, or ambulatory function. However, fentanyl-exposed mice, specifically males, exhibited significant deficits in social dominance and social interaction. RNA sequencing of the amygdala and subsequent examination of myelin basic protein levels suggested that prenatal fentanyl exposure affects myelin-related processes, which may impact the subsequent behavioral changes. These data suggest that <em>in utero</em> fentanyl exposure could significantly alter social-related behaviors, which may be related to aberrant brain myelination and connectivity.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110583"},"PeriodicalIF":4.6,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144522906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting IL-6 as a novel therapeutic approach for alcohol abstinence – related mechanical allodynia","authors":"Vittoria Borgonetti ,&nbsp;Celsey M. St. Onge ,&nbsp;Bryan Cruz ,&nbsp;Cristina Zalfa ,&nbsp;Tali Nadav ,&nbsp;Amanda J. Roberts ,&nbsp;Nicoletta Galeotti ,&nbsp;Michal Bajo ,&nbsp;Marisa Roberto","doi":"10.1016/j.neuropharm.2025.110584","DOIUrl":"10.1016/j.neuropharm.2025.110584","url":null,"abstract":"<div><div>Alcohol use disorder (AUD) is defined by the emergence of negative affective symptoms during withdrawal. Neuroinflammation is a key contributor to AUD, and it is well known to play an essential role in the pathogenesis of pain states. The chronic-intermittent ethanol two-bottle choice (CIE-2BC) paradigm is well-established to generate alcohol-dependent (Dep) and non-dependent (Non-Dep) mice. Our recent work demonstrated that the CIE-2BC model promotes mechanical allodynia in Dep mice, with these mice developing mechanical allodynia during withdrawal. In this study, we examined the role of interleukin-6 (IL-6) in the development of mechanical allodynia by adapting the CIE-2BC mouse model and employing the von Frey test, <em>in situ</em> hybridization (RNAscope), and Multiplex protein analysis of the spinal cord, examining changes in this target including an array of cytokines associated with IL-6 signaling. CIE-2BC escalated alcohol drinking and enhanced mechanical allodynia in Dep versus Non-Dep mice, with Dep females displaying greater alcohol intake. Dep mice displayed increased IL-6 protein in the spinal cord while males additionally had increased <em>Il6</em>^<em>+</em> cell expression versus Non-Dep controls. Systemic treatment of an IL-6 receptor antibody (IL-6R Ab) did not decrease mechanical allodynia during abstinence. Collectively, these data suggest that alcohol exerts sex-dependent effects on spinal IL-6 levels. However, in our study, blocking IL-6 signaling did not reduce alcohol-associated pain sensitivity in a mouse model of comorbid pain and alcohol dependence.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110584"},"PeriodicalIF":4.6,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144522905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Embracing Diversity: Sedative effects vary across drug chemistry and frequency domains","authors":"Jing Guang ,&nbsp;Halen Baker Erdman ,&nbsp;Orilia Ben-Yishay Nizri ,&nbsp;Shimon Firman ,&nbsp;Uri Werner-Reiss ,&nbsp;Vadim Kapuller ,&nbsp;Zvi Israel ,&nbsp;Hagai Bergman","doi":"10.1016/j.neuropharm.2025.110580","DOIUrl":"10.1016/j.neuropharm.2025.110580","url":null,"abstract":"<div><div>Moderate sedation can balance patients' comfort and preserve brain activities during deep brain stimulation neurosurgical procedures; however, the sub-cortical effects of different sedatives are rarely explored. We simultaneously recorded EEG, local field potential (LFP), and spikes (multi- and single-unit) from the dorsolateral frontal cortex and external globus pallidus (GPe), the central nucleus of the basal ganglia, of two female non-human primates. These recordings were carried out after titration of each drug and animal to achieve moderate sedative effects. The recording sessions included three 1-h epochs before, during, and after a continuous infusion of sedative drugs. We tested four sedative drugs (ketamine, propofol, remifentanil, and dexmedetomidine) that mainly affect glutamate, GABA, opiate, and noradrenaline neuromodulation, respectively. These sedative drugs modulate cortical and GPe activity across unique frequency bands. Ketamine increased EEG/LFP power in the beta/gamma bands and decreased theta band power. Propofol, remifentanil, and dexmedetomidine increased the power of the delta band and decreased theta, beta, and gamma bands’ power, respectively. GPe activity often aligns with cortical activity. The inter- and intra-area correlations show similar patterns to the spectrograms. The pattern and synchronization of spiking activity exhibited trends similar to those observed in EEG/LFP signals, although the effects were less pronounced. These results suggest that, similar to sleep, the thalamic-cortical network, plays a crucial role in shaping basal ganglia activity during moderate sedation. EEG activity may, therefore, serve as a reference for selecting sedation protocols in deep brain stimulation procedures.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110580"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibiotic treatment improves gut dysbiosis and depression-like behavior induced by morphine withdrawal","authors":"Dong-yu Yu ,&nbsp;Jing-qi Gao ,&nbsp;Xi-xi Yang ,&nbsp;Fei-fei Gao ,&nbsp;Jun-lin Liu ,&nbsp;Meng-qing Shen ,&nbsp;Bo-yuan Gu ,&nbsp;Yu-xiang Zhang ,&nbsp;Chun-xia Yan","doi":"10.1016/j.neuropharm.2025.110579","DOIUrl":"10.1016/j.neuropharm.2025.110579","url":null,"abstract":"<div><div>Opioid withdrawal poses a significant neuropsychiatric challenge, notably contributing to the onset of depression. Depression intertwines with gut flora richness and diversity, frequently coinciding with synaptic plasticity alterations in the brain. Gut microbiota dysbiosis potentially contributes to withdrawal-triggered depression via gut-brain axis. This research delves into the impact of antibiotic-induced gut microbiota alteration on behavioral and synaptic protein variations in mice subjected to morphine withdrawal-induced depression. A murine model was established using escalating doses of morphine followed by naloxone-precipitated withdrawal. Depression-like behaviors were assessed through tail suspension, sucrose preference, forced swimming tests, while histopathology evaluated ileocolonic inflammation. Synaptic markers, Synaptophysin (SYP) and Synapsin 1 (SYN1), in the hippocampus were analyzed via Western blotting, and gut microbiota composition was assessed through 16S rRNA sequencing. An antibiotic intervention model was employed to explore microbiota-dependent mechanisms. Morphine withdrawal induced characteristic depression-like behaviors, including prolonged immobility in forced swimming and reduced sucrose preference. Microbiota diversity metrics demonstrated significant declines in α-diversity. Histological analysis revealed marked inflammatory infiltration in ileal tissues, accompanied by reduction in hippocampal SYP expression. Antibiotic administration attenuated behavioral impairments, mitigated gut dysbiosis, reduced intestinal inflammation, and partially rescued SYP expression. These findings establish that morphine withdrawal induces intestinal dysbiosis, hippocampal synaptic plasticity deficits and depression-like behaviors, which are reversible through microbiota modulation. The results highlight the antibiotic treatment as a potential therapy for opioid withdrawal sequelae.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110579"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144513638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perinatal fentanyl exposure drives enduring addiction risk and central amygdala gene dysregulation","authors":"Courtney P. Wood ,&nbsp;Yeji Shin ,&nbsp;Maria G. Balaguer ,&nbsp;Paola Campo ,&nbsp;Selen Dirik ,&nbsp;Bryan A. Montoya ,&nbsp;Gregory M.R. Cook ,&nbsp;Gabrielle M. Palermo ,&nbsp;Parsa K. Naghshineh ,&nbsp;Alex Morgan ,&nbsp;Sara R.M.U. Rahman ,&nbsp;Abraham A. Palmer ,&nbsp;Francesca Telese ,&nbsp;Giordano de Guglielmo","doi":"10.1016/j.neuropharm.2025.110581","DOIUrl":"10.1016/j.neuropharm.2025.110581","url":null,"abstract":"<div><div>The use of fentanyl and other opioids during pregnancy is a pressing public health issue due to its association with Neonatal Opioid Withdrawal Syndrome (NOWS) and long-term neurobehavioral deficits. Human epidemiologic studies are confounded by both genetic and environmental factors that differ between exposed and unexposed children. We developed a novel rat model of perinatal fentanyl exposure in heterogeneous stock (HS) rats characterized by high genetic diversity, to investigate NOWS symptoms and its long-term effects on adult fentanyl self-administration, drug-seeking behavior, and central amygdala (CeA) transcriptomic changes, addressing a critical gap in understanding synthetic opioid impacts. Offspring born to fentanyl-exposed dams exhibited reduced survival, lower body weight, spontaneous withdrawal symptoms, and mechanical hypersensitivity during adolescence. These rats displayed negative affect in adolescence, while they showed increased fentanyl self-administration, heightened drug-seeking during reinstatement, and elevated corticosterone levels during withdrawal in adulthood. To explore the molecular underpinnings of these physiological and behavioral outcomes, we conducted RNA-seq in the CeA of adult rats, revealing dysregulated pathways related to GPCR signaling, adaptive immune response and neurodevelopmental processes. These transcriptional changes provide insights into the mechanisms driving addiction vulnerability and stress-related behaviors following early fentanyl exposure. Our findings highlight the lasting impact of perinatal opioid exposure in an experimental system that avoids many of the confounds that plague studies in humans, underscoring the need for preclinical models to study NOWS and its long-term consequences. This model offers translational relevance for developing therapeutic strategies to mitigate NOWS and reduce neuropsychiatric risks associated with perinatal opioid exposure.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"278 ","pages":"Article 110581"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144514183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}