Neuropharmacology最新文献

{"title":"AMPK activation mitigates α-synuclein pathology and dopaminergic degeneration in cellular and mouse models of Parkinson's disease","authors":"Yoonha Kim,&nbsp;Jong Sam Lee,&nbsp;Sumin Son,&nbsp;Seobin Park,&nbsp;Hyungkeun Oh,&nbsp;Yoon Kyung Choi,&nbsp;Dong-Eun Kim","doi":"10.1016/j.neuropharm.2025.110700","DOIUrl":"10.1016/j.neuropharm.2025.110700","url":null,"abstract":"<div><div>Parkinson's disease (PD) is characterized by oxidative stress, mitochondrial dysfunction, and pathological accumulation of p-α-Synuclein (p-α-Syn). AMP-activated protein kinase (AMPK) has emerged as a regulator of cellular energy homeostasis, yet its role in PD pathology remains unclear. Here, we examined the effects of AMPK activation in SH-SY5Y neuroblastoma cells and in an MPTP-induced PD mouse model. In both undifferentiated and retinoic acid-differentiated SH-SY5Y cells exposed to 6-hydroxydopamine (6-OHDA), pharmacological AMPK activation with AICAR reduced reactive oxygen species (ROS) production and p-α-Syn aggregation. These effects were associated with enhanced mitophagy, increased lysosomal degradation, and stimulation of mitochondrial biogenesis, collectively restoring mitochondrial integrity and improving dopaminergic features. <em>In vivo</em>, AICAR treatment attenuated nigrostriatal dopaminergic degeneration in MPTP-exposed mice, reduced p-α-Syn accumulation, and preserved tyrosine hydroxylase expression. Moreover, systemic cytokine analysis revealed that AMPK activation suppressed IL-6–mediated inflammation, while modulating IL-1β levels in a context-dependent manner. These results demonstrate that AMPK activation mitigates α-synuclein pathology, preserves mitochondrial function, and protects dopaminergic neurons in both cellular and animal PD models. Our findings support AMPK as a potential therapeutic target for disease modification in PD.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110700"},"PeriodicalIF":4.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186546","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":"Reward-associated cues reduce H-current amplitude in midbrain dopamine neurons","authors":"Cristhian G. Calo-Guadalupe ,&nbsp;Karl Y. Bosque-Cordero ,&nbsp;Joseph Capella-Muñiz ,&nbsp;Daisy Consuegra-García ,&nbsp;Rafael Vazquez-Torres ,&nbsp;Omaris Vélez-Acevedo ,&nbsp;Keven Laboy-Juarez ,&nbsp;Priscila Sanabria ,&nbsp;Carlos A. Jimenez-Rivera","doi":"10.1016/j.neuropharm.2025.110699","DOIUrl":"10.1016/j.neuropharm.2025.110699","url":null,"abstract":"<div><div>Cocaine is a psychoactive substance that targets brain regions involved in motivation and reward learning. Lateral ventral tegmental area (VTA) dopamine (DA) neurons play a critical role in these processes, yet their intrinsic modulations during drug and non-drug self-administration or reward-associated cue learning remain poorly understood. This study employed an Intermittent Access (IntA) cocaine model, both contingent and non-contingent, to examine how reward delivery and associated cues modulate the hyperpolarization-activated cyclic nucleotide-gated (HCN) current (I_h), an intrinsic property regulating neuronal physiology. Male rats were divided into saline and cocaine IntA groups, with yoked controls receiving non-contingent cocaine infusions either paired (Yoked + cue) or unpaired (Yoked - cue) with a light cue to control for contingency and cue exposure. A parallel sucrose self-administration cohort served as a non-addictive reward control. Whole-cell patch-clamp recordings in lateral VTA DA neurons revealed reduced I_h amplitude in the cocaine IntA and Yoked-cocaine + cue groups, accompanied by a hyperpolarizing voltage shift in all cocaine-treated animals. Cocaine IntA enhanced input integration, whereas IntA animals also exhibited reduced membrane capacitance (C_m). Similar I_h reductions were observed in sucrose IntA and Yoked-sucrose + cue groups. These learning-associated changes may enhance DA neurons' ability to signal reward anticipation or saliency. We propose that I_h modulation in VTA DA neurons maintains intrinsic excitability, improves signal-to-noise ratio, and facilitates learning of reward-salient cues—processes essential for motivation toward drug and non-drug rewards. This hypothesis provides insight into how intrinsic plasticity in VTA DA neurons shapes reward learning.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110699"},"PeriodicalIF":4.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182033","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":"Evaluating the reinforcing properties of oxycodone and oxymorphone using intravenous drug self-administration in male rats","authors":"Mina Rashvand ,&nbsp;Douglas Funk ,&nbsp;Paul J. Fletcher ,&nbsp;Sharon Miksys ,&nbsp;Rachel F. Tyndale","doi":"10.1016/j.neuropharm.2025.110698","DOIUrl":"10.1016/j.neuropharm.2025.110698","url":null,"abstract":"<div><div>Oxycodone, a commonly abused opioid, and its metabolite oxymorphone are agonists at the μ-opioid receptor. While oxymorphone is more potent, and clinical data suggests a greater abuse liability, there is little data comparing them in preclinical models. We examined their reinforcing properties using the intravenous (IV) self-administration method. Male Wistar Han rats were implanted with IV catheters and trained to lever press for infusions of oxycodone and oxymorphone. Dose response curves were assessed using fixed ratio (FR) 1, FR3, FR5 and progressive ratio (PR) schedules. Responding was then extinguished and drug priming-induced reinstatement, a model of relapse, was assessed. Microdialysis was used to assess central concentrations of oxymorphone following IV oxycodone. Under FR1 schedules, in both oxycodone and oxymorphone self-administering rats, active lever pressing and infusions earned decreased with increasing dose, while intake increased, however the shape of the dose response curves differed. Oxymorphone, compared to oxycodone, exhibited a leftward shift in the dose-response curve, indicative of higher potency, but also a shallower slope and lower maximal active lever pressing and infusions. On the PR schedule, the highest breakpoint was observed for oxymorphone. Oxycodone (0.25 mg/kg) induced significant drug-priming reinstatement after extinction, while an equipotent dose of oxymorphone (0.025 mg/kg) approached significant reinstatement. After a bolus IV injection of oxycodone, oxymorphone was present in the cerebrospinal fluid at approximately 1/250th the concentration of oxycodone. These findings highlight distinct self-administration patterns between oxycodone, which is metabolized to oxymorphone in vivo, and oxymorphone itself, suggesting differences beyond potency at the μ-opioid receptor.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110698"},"PeriodicalIF":4.6,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145120025","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":"Inhibiting MARS attenuates hyperhomocysteinemia-associated neurodegeneration in Parkinson's disease","authors":"Tao Guo ,&nbsp;Dandan Su ,&nbsp;Juan Huang ,&nbsp;Guohua Zhao ,&nbsp;Xin Fang ,&nbsp;Ting Yu ,&nbsp;Shangqi Sun ,&nbsp;Anyu Bao ,&nbsp;Lihong Bu ,&nbsp;Zhentao Zhang","doi":"10.1016/j.neuropharm.2025.110685","DOIUrl":"10.1016/j.neuropharm.2025.110685","url":null,"abstract":"<div><div>Hyperhomocysteinemia is an independent risk factor for Parkinson's disease (PD). Homocysteine (Hcy) is converted to Hcy thiolactone (HTL) in error-editing reactions catalyzed by methionine-tRNA synthetase (MARS). HTL forms isopeptide bonds with lysine residues of target proteins in a process known as N-homocysteinylation (N-Hcy), which contributes to the neurotoxicity of Hcy in PD pathogenesis. Thus, MARS may represent a potential target for controlling hyperhomocysteinemia-associated neurotoxicity. Here we tested the effect of MARS on protein N-Hcy in cultured cells, MPTP-induced mouse model of PD, and mice injected with α-synuclein PFFs. We found that the protein N-Hcy levels were increased in the brains of PD model mice. MARS knockdown ameliorates protein N-Hcy, oxidative stress, mitochondrial dysfunction, and α-synuclein aggregation in cells. MARS knockdown also alleviated dopaminergic neurodegeneration and behavioral deficits in mice injected with MPTP. In mice injected with α-synuclein fibrils, MARS knockdown attenuated α-synuclein aggregation, dopaminergic neurodegeneration, and motor impairments. These results indicate that inhibition of MARS attenuates PD-like pathology induced by hyperhomocysteinemia.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110685"},"PeriodicalIF":4.6,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150158","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":"Decoding the nitration-phosphorylation switch: 7,8-Dihydroxyflavone rebalances TrkB signaling dynamics for retinal neuroprotection","authors":"Yanping Zhou ,&nbsp;Yifan Feng ,&nbsp;Min Li ,&nbsp;Xi Yang ,&nbsp;Yingxi Zhao ,&nbsp;Xiangwu Chen","doi":"10.1016/j.neuropharm.2025.110697","DOIUrl":"10.1016/j.neuropharm.2025.110697","url":null,"abstract":"<div><h3>Purpose</h3><div>To investigate how 7,8-Dihydroxyflavone (7,8-DHF) coordinates competing post-translational modifications of TrkB, specifically examining its role in modulating the redox-sensitive balance between tyrosine nitration and phosphorylation to achieve neuroprotective efficacy.</div></div><div><h3>Methods</h3><div>The effects of 7,8-DHF on nitric oxide (NO) inhibition, protein nitration, TrkB activation, and downstream signaling were assessed using a male mouse optic nerve crush (ONC) model and 3D retinal explants. Techniques such as Western blotting, ELISA, immunoprecipitation, immunohistochemistry, metabolomics, and molecular docking were used to examine the biochemical and molecular impacts of 7,8-DHF.</div></div><div><h3>Results</h3><div>7,8-DHF reduced NO levels and inducible/neuronal nitric oxide synthase (iNOS/nNOS) expression in 3D retinal cultures and ONC mouse models, with molecular docking indicating its binding to iNOS's active site and metabolomics showing downregulation of the arginine biosynthesis pathway. It also decreased TrkB nitration in vivo and in vitro, with the Y816 residue being critical for this modification. 7,8-DHF enhanced TrkB phosphorylation at Y816 and PLCγ1 activation, inhibited by L-arginine and TrkB blockers. Additionally, 7,8-DHF promoted retinal gangion cell survival and axonal regeneration via TrkB signaling, effects reversed by nitration agents or TrkB blockers.</div></div><div><h3>Conclusion</h3><div>7,8-DHF pioneers a new class of nitration-phosphorylation modulators, converting nitrosative damage into neuroregenerative signals by rebalancing TrkB's modification states. This mechanistic insight opens therapeutic avenues for optic nerve disorders.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110697"},"PeriodicalIF":4.6,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145109965","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":"P2X7R-NF-κB-PDI signal pathway regulates LPS-induced impaired GSH synthesis by modulating ATF4-mediated xCT upregulation, S-nitrosylation of ASCT2 and GSHS expressions in the mouse hippocampus","authors":"Ji-Eun Kim ,&nbsp;Su Hyeon Wang ,&nbsp;Duk-Shin Lee","doi":"10.1016/j.neuropharm.2025.110696","DOIUrl":"10.1016/j.neuropharm.2025.110696","url":null,"abstract":"<div><div>Protein disulfide isomerase (PDI) augments lipopolysaccharide (LPS)-induced nuclear factor-κB (NF-κB) activation by integrating Toll-like receptor 4 (TLR4) and P2X7 receptor (P2X7R) signaling pathways in a positive feedback manner. However, it has been largely unknown whether PDI is involved in altered glutathione (GSH) biosynthesis, which is mediated by P2X7R, in response to LPS. In the present study, LPS-induced NF-κB activation increased PDI expression, but decreased solute carrier 1 A5 (ASCT2) level in the <em>P2X7</em>^<em>+/+</em> mouse hippocampus. <em>PDI</em> knockdown attenuated ASCT2 downregulation and <em>S</em>-nitrosylated (SNO-) ASCT2 level in response to LPS. This LPS-induced NF-κB-PDI activation also increased <em>activating transcription factor 4 (</em>ATF4) expression in astrocytes, which elicited cystine:glutamate transporter (xCT) upregulation, but decreased ASCT2 and GSH synthetase (GSHS) expression. Furthermore, <em>S</em>-nitrosylation of PDI modulated ATF4-mediated xCT upregulation in response to LPS. SN50 (a NF-κB inhibitor), <em>PDI</em> knockdown and <em>ATF4</em> siRNA mitigated the decreased GSH content induced by LPS. Under physiological condition, <em>P2X7R</em> deletion did not affect basal PDI, ATF4, xCT and SNO-ASCT2 levels. However, it increased ASCT2 expression and decreased SNO-PDI level. <em>P2X7R</em> ablation ameliorated (1) PDI, ATF4 and xCT2 upregulations, (2) <em>S</em>-nitrosylation of ASCT2 and PDI and (3) ASCT2 downregulation in response to LPS. These findings indicate that P2X7R-NF-κB-PDI signal pathway may inhibit GSH biosynthesis in response to LPS by modulating expression/<em>S</em>-nitrosylation of ASCT2 and ATF4-mediated xCT regulation in response to LPS.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110696"},"PeriodicalIF":4.6,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091998","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":"Xanomeline treatment attenuates cocaine self-administration in rats and nonhuman primates","authors":"Samuel A. Marsh ,&nbsp;Nicholas Heslep ,&nbsp;Carol A. Paronis ,&nbsp;Jack Bergman ,&nbsp;S. Stevens Negus ,&nbsp;Matthew L. Banks","doi":"10.1016/j.neuropharm.2025.110686","DOIUrl":"10.1016/j.neuropharm.2025.110686","url":null,"abstract":"<div><div>The lack of an FDA-approved pharmacotherapy to combat cocaine use disorder (CUD) is an ongoing and urgent public health challenge. Emerging evidence suggests that the muscarinic acetylcholine system modulates mesolimbic dopamine release and thus may serve as a suitable target for novel CUD medications. The M1/M4-preferring muscarinic agonist xanomeline was recently approved by the Food and Drug Administration for schizophrenia management, and a previous study in male rats suggested that xanomeline treatment attenuated cocaine self-administration in a cocaine-vs-food choice procedure. The present study was conducted to further examine xanomeline treatment effectiveness on cocaine self-administration in male and female rats and nonhuman primates. Both male and female rats and monkeys were trained to self-administer cocaine during daily behavioral sessions. Repeated xanomeline treatment significantly decreased cocaine choice in rats similar to both pharmacological (amphetamine maintenance) and non-pharmacological (increasing alternative reinforcer value) positive controls. In separate groups of monkeys, acute xanomeline pretreatment decreased cocaine-vs-food choice in three out of four monkeys and selectively decreased cocaine-, but not food-maintained responding, under a multiple schedule of cocaine and food reinforcement in three out of four monkeys. Overall, the consistent effectiveness of xanomeline to reduce IV cocaine self-administration in both rodents and nonhuman primate supports its further evaluation as a CUD medication in humans.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110686"},"PeriodicalIF":4.6,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086641","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":"Neuronal ensembles formed rapidly in the prelimbic cortex mediate initial and maintained cocaine-seeking behavior in male and female rats","authors":"Bo W. Sortman ,&nbsp;Samantha Rakela ,&nbsp;Berk Cerci ,&nbsp;Sarah Paprotna ,&nbsp;Jordan Harrow ,&nbsp;Sophie Hao ,&nbsp;Michel van den Oever ,&nbsp;Brandon L. Warren","doi":"10.1016/j.neuropharm.2025.110684","DOIUrl":"10.1016/j.neuropharm.2025.110684","url":null,"abstract":"<div><div>Substance use disorder is a complex neurobiological disease thought to be partially driven by aberrant forms of learning and memory. The cellular basis of memory is hypothesized to be small subsets of interconnected networks formed during the acquisition of behavior called neuronal ensembles. We interrogate neuronal ensembles by utilizing a dual viral approach that expresses Cre^ERT2 under the control of the c-Fos promoter in conjunction with a Cre-dependent inhibitory DREADD. This approach gives us the temporal specificity to target neuronal ensembles formed during the acquisition of cocaine seeking in the prelimbic cortex. First, we demonstrate that neuronal ensembles in the prelimbic cortex are rapidly recruited and mediate cocaine seeking. Second, we show that the neuronal ensembles formed during behavioral acquisition are an enduring population that continues to be behaviorally relevant once rats are well-trained. Finally, through the combination of retrograde tract tracing and Fos immunohistochemistry, we show that neuronal ensembles in the prelimbic cortex recruit the nucleus accumbens core and shell after behavioral acquisition of cocaine self-administration. Collectively, we show that the prelimbic neuronal ensembles that mediate cocaine seeking are highly specific to context and behavioral conditions and recruit downstream projection targets post-acquisition.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110684"},"PeriodicalIF":4.6,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080496","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":"Intranasal AdipoRon improves motor function in a rat model of Parkinson's disease by promoting neurogenesis in the nigrostriatal pathway","authors":"Seyed Zanyar Athari ,&nbsp;Fereshteh Farajdokht ,&nbsp;Mohammad Karimipour ,&nbsp;Mohammad Reza Alipour ,&nbsp;Gisou Mohaddes","doi":"10.1016/j.neuropharm.2025.110687","DOIUrl":"10.1016/j.neuropharm.2025.110687","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a neurodegenerative disorder characterized by drastically reduced synaptic plasticity and neurogenesis, possibly due to abnormal α-synuclein deposition. Boosting endogenous neurogenesis is a potential strategy for halting cell death and restoring brain function. AdipoRon (AR) has been shown to promote progenitor cell proliferation and differentiation in neurological disorders. This study investigated the effect of intranasal (IN) AR on neurogenesis in the nigrostriatal pathway and motor function in a rat PD model. Dopaminergic neuronal degeneration was induced by administering 6-hydroxydopamine (6-OHDA) into the left medial forebrain bundle. One week post-PD induction, hemiparkinsonian rats received either levodopa (10 mg/kg, gavage) or AR (0.1, 1, and 10 μg/rat, IN) for 21 days. To evaluate adult neurogenesis, 5-bromodeoxyuridine (BrdU) was injected for 5 days at the start of treatments. Motor functions were assessed 5 weeks post-6-OHDA injection, and the animals were sacrificed for analysis. The number of BrdU and NeuN/BrdU positive cells in the ipsilateral substantia nigra (SN) was determined. Moreover, the density of tyrosine hydroxylase (TH)-positive fibers and the level of cerebral dopamine neurotrophic factor (CDNF), Zif-268, and synaptophysin (SYP) proteins were examined in the striatum. Our findings indicated that AR dose-dependently restored motor function and increased striatal CDNF, SYP, and Zif-268 protein expression in 6-OHDA-lesioned rats. Besides, AR 10 μg enhanced the number of NeuN + cells in the SN and dopaminergic fiber density (TH + terminals) in the striatum. These findings indicated that AR improved motor symptoms by promoting neurogenesis and synaptic transmission in the nigrostriatal pathway in PD rats.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"281 ","pages":"Article 110687"},"PeriodicalIF":4.6,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080354","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":"Corrigendum to “Chronic psilocybin administration increases sociability and alters the gut microbiome in male wild-type mice but not in a preclinical model of obsessive-compulsive disorder” [Neuropharmacology 279 (2025) 110648]","authors":"James J. Gattuso ,&nbsp;Geraldine Kong ,&nbsp;Bilgenur Bezcioglu ,&nbsp;Da Lu ,&nbsp;Millicent N. Ekwudo ,&nbsp;Carey Wilson ,&nbsp;Carolina Gubert ,&nbsp;Anthony J. Hannan ,&nbsp;Thibault Renoir","doi":"10.1016/j.neuropharm.2025.110679","DOIUrl":"10.1016/j.neuropharm.2025.110679","url":null,"abstract":"","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"280 ","pages":"Article 110679"},"PeriodicalIF":4.6,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145054867","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}