Pub Date : 2026-01-13DOI: 10.1016/j.physbeh.2026.115229
Liujing Yang , Tongtong Guo , Yubin Wei , Zheng Zhang , Yan Sun , Ning Yan , Songtao Ding , Lin Jiang , Handeng Liu
Previous studies have shown that Lactobacillus acidophilus (LA) improves gut microbiota, which is believed to play a role in Parkinson's disease pathogenesis by modulating neuroinflammation. Therefore, we investigated the role of LA in mice with PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). To explore microbial-based interventions for Parkinson's disease (PD), we examined whether Lactobacillus acidophilus (LA) protects against neurodegeneration via the gut-brain axis. In MPTP-induced PD mice, LA treatment improved motor function, increased TH+ neurons, and suppressed neuroinflammation. Crucially, LA restored gut microbiota ecology and enhanced the gut-brain signaling pathway, evidenced by increased colonic GLP-1/FFAR2/FFAR3 and brain GLP-1 receptor levels, alongside improved gut barrier integrity. Our findings demonstrate that LA alleviates PD pathology by concurrently targeting the gut microbiota and the GLP-1 receptor pathway, underscoring a viable gut-brain axis strategy for neuroprotection.
{"title":"Lactobacillus acidophilus exerts neuroprotective effects in MPTP mice: potential links to the gut microbiota and GLP-1","authors":"Liujing Yang , Tongtong Guo , Yubin Wei , Zheng Zhang , Yan Sun , Ning Yan , Songtao Ding , Lin Jiang , Handeng Liu","doi":"10.1016/j.physbeh.2026.115229","DOIUrl":"10.1016/j.physbeh.2026.115229","url":null,"abstract":"<div><div>Previous studies have shown that Lactobacillus acidophilus (LA) improves gut microbiota, which is believed to play a role in Parkinson's disease pathogenesis by modulating neuroinflammation. Therefore, we investigated the role of LA in mice with PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). To explore microbial-based interventions for Parkinson's disease (PD), we examined whether Lactobacillus acidophilus (LA) protects against neurodegeneration via the gut-brain axis. In MPTP-induced PD mice, LA treatment improved motor function, increased TH+ neurons, and suppressed neuroinflammation. Crucially, LA restored gut microbiota ecology and enhanced the gut-brain signaling pathway, evidenced by increased colonic GLP-1/FFAR2/FFAR3 and brain GLP-1 receptor levels, alongside improved gut barrier integrity. Our findings demonstrate that LA alleviates PD pathology by concurrently targeting the gut microbiota and the GLP-1 receptor pathway, underscoring a viable gut-brain axis strategy for neuroprotection.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"307 ","pages":"Article 115229"},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-10DOI: 10.1016/j.physbeh.2026.115227
Xiang Chen , Bo Wang , Yu-Hui Tang , Yi-Li Yi , Wei Zou , Xiao-Qing Tang , San-Qiao Yang
Background
Depression remains a major global health challenge, and current treatments are suboptimal. Hydrogen sulfide (H₂S), an endogenous gasotransmitter, has antidepressant potential; however, its mechanisms remain incompletely understood. Understanding the mechanisms underlying the antidepressant-like role of H₂S is essential for developing H₂S as a therapeutic candidate for treating depression.
Methods
Depressive-like behaviors were assessed via the open field test (OFT), novelty-suppressed feeding test (NSFT), sucrose preference test (SPT), tail suspension test (TST), and forced swim test (FST). Western blotting was used to analyze the protein expression levels. Cytokines (TNF-α, IL-1β, IL-4, IL-6, and IL-10) were quantified via ELISA. Kynurenine-pathway (KP) metabolites were assayed by selective reaction/multiple reaction monitoring technology.
Results
Chronic unpredictable mild stress (CUMS) reduced hippocampal growth differentiation factor 11 (GDF11) expression. H₂S significantly increased the expression of GDF11 and the ratio of p-Smad2/3/Smad2/3, a downstream effector of TGFBR1, indicating that H2S enhances the activation of GDF11/TGFBR1 pathway in the hippocampus of CUMS-exposed rats. Furthermore, hippocampal GDF11 knockdown and pharmacological blockade of TGFBR1 with SB525334, which disrupts H₂S-induced activation of the GDF11/TGFBR1 pathway, reversed the molecular effects of H₂S in CUMS-exposed rats, including suppression of necroptosis, attenuation of neuroinflammation, and normalization of kynurenine-pathway enzymes and metabolites, as well as abolished the antidepressant-like effects of H₂S.
Conclusion
The hippocampal GDF11/TGFBR1 pathway mediates the antidepressant-like effects of H₂S by restraining the cascade of hippocampal necroptosis–neuroinflammation–KP disorder, suggesting that the GDF11/TGFBR1 pathway is a promising therapeutic target for depression.
{"title":"GDF11/TGFBR1 activation is essential for the antidepressant-like effect of H₂S: Role of suppressing the hippocampal cascade of necroptosis-neuroinflammation-Kynurenine pathway disorder","authors":"Xiang Chen , Bo Wang , Yu-Hui Tang , Yi-Li Yi , Wei Zou , Xiao-Qing Tang , San-Qiao Yang","doi":"10.1016/j.physbeh.2026.115227","DOIUrl":"10.1016/j.physbeh.2026.115227","url":null,"abstract":"<div><h3>Background</h3><div>Depression remains a major global health challenge, and current treatments are suboptimal. Hydrogen sulfide (H₂S), an endogenous gasotransmitter, has antidepressant potential; however, its mechanisms remain incompletely understood. Understanding the mechanisms underlying the antidepressant-like role of H₂S is essential for developing H₂S as a therapeutic candidate for treating depression.</div></div><div><h3>Methods</h3><div>Depressive-like behaviors were assessed via the open field test (OFT), novelty-suppressed feeding test (NSFT), sucrose preference test (SPT), tail suspension test (TST), and forced swim test (FST). Western blotting was used to analyze the protein expression levels. Cytokines (TNF-α, IL-1β, IL-4, IL-6, and IL-10) were quantified via ELISA. Kynurenine-pathway (KP) metabolites were assayed by selective reaction/multiple reaction monitoring technology.</div></div><div><h3>Results</h3><div>Chronic unpredictable mild stress (CUMS) reduced hippocampal growth differentiation factor 11 (GDF11) expression. H₂S significantly increased the expression of GDF11 and the ratio of p-Smad2/3/Smad2/3, a downstream effector of TGFBR1, indicating that H<sub>2</sub>S enhances the activation of GDF11/TGFBR1 pathway in the hippocampus of CUMS-exposed rats. Furthermore, hippocampal GDF11 knockdown and pharmacological blockade of TGFBR1 with SB525334, which disrupts H₂S-induced activation of the GDF11/TGFBR1 pathway, reversed the molecular effects of H₂S in CUMS-exposed rats, including suppression of necroptosis, attenuation of neuroinflammation, and normalization of kynurenine-pathway enzymes and metabolites, as well as abolished the antidepressant-like effects of H₂S.</div></div><div><h3>Conclusion</h3><div>The hippocampal GDF11/TGFBR1 pathway mediates the antidepressant-like effects of H₂S by restraining the cascade of hippocampal necroptosis–neuroinflammation–KP disorder, suggesting that the GDF11/TGFBR1 pathway is a promising therapeutic target for depression.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"306 ","pages":"Article 115227"},"PeriodicalIF":2.5,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145952863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-08DOI: 10.1016/j.physbeh.2026.115226
Ivanka Rainer , Leah Hershberger , Megan Pedicini , Madison Davis , Yvonne M. Ulrich-Lai
Many individuals eat highly palatable foods to cope with stress, and this so-called ‘comfort’ feeding occurs to a greater extent in people who are overweight and obese. To study this relationship, we previously characterized a limited sucrose intake (LSI) paradigm that reduces hypothalamic-pituitary-adrenocortical (HPA) axis stress responses in normal weight rats, but not in those with Western diet-induced obesity (DIO). The present work tests the hypothesis that a larger volume of sucrose drink recovers effective HPA blunting during obesity. Time-limited sucrose access, in which sucrose was offered in an unlimited volume for 30 min twice-daily to chow-fed lean and Western DIO rats for 2 weeks, resulted in greater sucrose drink intake than that allowed in the LSI paradigm (4 ml/twice-daily session) and reduced post-stress plasma corticosterone relative to water controls in both lean and DIO rats. Likewise, when given volume-limited access to a larger sucrose volume (6 ml vs. the standard 4 ml per twice-daily session) the 6 ml volume reduced post-stress plasma corticosterone relative to water controls, in both lean and DIO rats, whereas the 4 ml volume was only effective in lean rats. These data replicate that the typical LSI sucrose volume does not produce effective stress-blunting during Western DIO, and extend this to show that larger sucrose volumes, given via either time- or volume-limited access paradigms, recovers this effect. This suggests that stress-related eaters with obesity may require larger amounts of palatable foods to maintain adequate stress relief.
{"title":"A larger amount of palatable food is needed to provide stress relief during Western diet-induced obesity","authors":"Ivanka Rainer , Leah Hershberger , Megan Pedicini , Madison Davis , Yvonne M. Ulrich-Lai","doi":"10.1016/j.physbeh.2026.115226","DOIUrl":"10.1016/j.physbeh.2026.115226","url":null,"abstract":"<div><div>Many individuals eat highly palatable foods to cope with stress, and this so-called ‘comfort’ feeding occurs to a greater extent in people who are overweight and obese. To study this relationship, we previously characterized a limited sucrose intake (LSI) paradigm that reduces hypothalamic-pituitary-adrenocortical (HPA) axis stress responses in normal weight rats, but not in those with Western diet-induced obesity (DIO). The present work tests the hypothesis that a larger volume of sucrose drink recovers effective HPA blunting during obesity. Time-limited sucrose access, in which sucrose was offered in an unlimited volume for 30 min twice-daily to chow-fed lean and Western DIO rats for 2 weeks, resulted in greater sucrose drink intake than that allowed in the LSI paradigm (4 ml/twice-daily session) and reduced post-stress plasma corticosterone relative to water controls in both lean and DIO rats. Likewise, when given volume-limited access to a larger sucrose volume (6 ml vs. the standard 4 ml per twice-daily session) the 6 ml volume reduced post-stress plasma corticosterone relative to water controls, in both lean and DIO rats, whereas the 4 ml volume was only effective in lean rats. These data replicate that the typical LSI sucrose volume does not produce effective stress-blunting during Western DIO, and extend this to show that larger sucrose volumes, given via either time- or volume-limited access paradigms, recovers this effect. This suggests that stress-related eaters with obesity may require larger amounts of palatable foods to maintain adequate stress relief.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"307 ","pages":"Article 115226"},"PeriodicalIF":2.5,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic insomnia can negatively influence physical health and mental health, including symptoms of anxiety and depression, which have a bidirectional association with insomnia. In separate studies, exercise has elicited significant improvements in insomnia and reductions in anxiety and depressed mood. The objective of this systematic review and meta-analysis was to evaluate the effects of exercise on symptoms of anxiety and depression as primary outcomes in patients with insomnia. Secondary outcomes were improvements in sleep. A systematic literature review was based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The search was conducted in Embase, Scopus, Web of Science, CINAHL, PsycINFO, CENTRAL, MEDLINE and SPORTDiscus databases. Six randomized controlled trials (RCT) and one Quasi-RCT, published between 2010 and 2022 (with a total of 336 participants), were selected. The results showed that exercise interventions significantly improved anxiety (SMD -0.44, 95% CI = -0.72 to -0.15), depressed mood (SMD -0.53, 95% CI = -0,78 to -0.29), the Insomnia Severity Index (SMD -0.62, 95% CI = -0.87 to -0.37) and the Pittsburg Sleep Quality Index (MD -2.94, 95% CI = -3.85 to -2.03). In actigraphic assessments, a significant reduction in wake after sleep onset was found (MD -8.67, 95% CI = -16.17 to -1.17). The meta-analysis results indicate that exercise in patients with insomnia significantly improved anxiety and depression, reduced insomnia severity, increased sleep quality, and decreased wake after sleep onset (PROSPERO, CRD42022374853).
慢性失眠会对身体健康和精神健康产生负面影响，包括焦虑和抑郁症状，这些症状与失眠有双向关联。在不同的研究中，运动可以显著改善失眠，减少焦虑和抑郁情绪。本系统综述和荟萃分析的目的是评估运动对失眠患者焦虑和抑郁症状的影响。次要结果是睡眠改善。系统文献综述基于系统评价和荟萃分析的首选报告项目（PRISMA）。在Embase、Scopus、Web of Science、CINAHL、PsycINFO、CENTRAL、MEDLINE和SPORTDiscus数据库中进行检索。选取2010年至2022年间发表的6项随机对照试验（RCT）和1项准RCT (Quasi-RCT)（共336名受试者）。结果显示，运动干预显著改善了焦虑（SMD -0.44, 95% CI -0.72至- 0.15;I²=0%）、抑郁情绪（SMD -0.53, CI 95% -0,78至-0.29;I² = 3%）、失眠严重程度指数（SMD -0.62, 95% CI -0.87至-0.37;I²=0%）和匹兹堡睡眠质量指数[MD = -2.94；95% ci (-3.85; -2.03)；P < 0.00001]。在活动图评估中，发现睡眠开始后清醒显著减少[MD = -8.67；95% ci (-16.17; -1.17)；p = 0.02]。荟萃分析结果表明，失眠患者的运动可显著改善焦虑和抑郁，减轻失眠严重程度，提高睡眠质量，减少睡眠后醒来（PROSPERO, CRD42022374853）。
{"title":"Effects of exercise on anxiety and depression in patients with insomnia: a systematic review and meta-analysis","authors":"Daniela Pantaleão Ferreira , Giselle Soares Passos , Shawn D. Youngstedt , Marcos Gonçalves Santana","doi":"10.1016/j.physbeh.2026.115225","DOIUrl":"10.1016/j.physbeh.2026.115225","url":null,"abstract":"<div><div>Chronic insomnia can negatively influence physical health and mental health, including symptoms of anxiety and depression, which have a bidirectional association with insomnia. In separate studies, exercise has elicited significant improvements in insomnia and reductions in anxiety and depressed mood. The objective of this systematic review and meta-analysis was to evaluate the effects of exercise on symptoms of anxiety and depression as primary outcomes in patients with insomnia. Secondary outcomes were improvements in sleep. A systematic literature review was based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The search was conducted in Embase, Scopus, Web of Science, CINAHL, PsycINFO, CENTRAL, MEDLINE and SPORTDiscus databases. Six randomized controlled trials (RCT) and one Quasi-RCT, published between 2010 and 2022 (with a total of 336 participants), were selected. The results showed that exercise interventions significantly improved anxiety (SMD -0.44, 95% CI = -0.72 to -0.15), depressed mood (SMD -0.53, 95% CI = -0,78 to -0.29), the Insomnia Severity Index (SMD -0.62, 95% CI = -0.87 to -0.37) and the Pittsburg Sleep Quality Index (MD -2.94, 95% CI = -3.85 to -2.03). In actigraphic assessments, a significant reduction in wake after sleep onset was found (MD -8.67, 95% CI = -16.17 to -1.17). The meta-analysis results indicate that exercise in patients with insomnia significantly improved anxiety and depression, reduced insomnia severity, increased sleep quality, and decreased wake after sleep onset (PROSPERO, CRD42022374853).</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"306 ","pages":"Article 115225"},"PeriodicalIF":2.5,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-07DOI: 10.1016/j.physbeh.2026.115224
Phong K.T. Chau, Fred Haugen
This study aimed to explore the daily rhythmicity of mechanical sensitivity in a mouse model of induced subcutaneous inflammation, with the broader goal of understanding circadian oscillations that may influence pain conditions. Mice received unilateral injections of Complete Freund’s Adjuvant (CFA) in one hind paw to induce localized inflammation; the contralateral paw received saline as a control. On days 3 post injection (acute stage) and 5 (persistent stage), mechanical sensitivity was assessed by paw withdrawal behaviour using calibrated monofilaments to apply defined force at three time points: ZT4 (early light phase), ZT12 (end of light phase), and ZT20 (dark phase). RNA was extracted from dorsal root ganglia (DRG) on days 4 and 6 for RNA-seq and droplet digital PCR (ddPCR).
CFA-induced responsiveness to light mechanical force (0.16 g and 0.4 g) shifted from being time-of-day independent in the acute phase to time-of-day dependent in the persistent phase. The opposite pattern was observed with higher force (0.6 g), showing time-of-day dependency in the acute phase. Substance P transcription was upregulated at ZT4 relative to ZT12 on day 4 but not on day 6. Transcripts of two core clock components (Bmal1 and Per1) in the DRG were not significantly influenced by CFA-injection. Additional RNA-seq analysis identified differentially expressed genes at ZT4 as CFA-responsive independent of time-of-day.
These findings reveal a circadian modulation of CFA-induced mechanical hypersensitivity to light mechanical force during the persistent stages of pain, which is associated with alterations in gene expression within the dorsal root ganglion (DRG).
{"title":"Temporal dynamics of mechanical hypersensitivity and dorsal root ganglion transcription in a bilateral CFA-Induced inflammation model in mice","authors":"Phong K.T. Chau, Fred Haugen","doi":"10.1016/j.physbeh.2026.115224","DOIUrl":"10.1016/j.physbeh.2026.115224","url":null,"abstract":"<div><div>This study aimed to explore the daily rhythmicity of mechanical sensitivity in a mouse model of induced subcutaneous inflammation, with the broader goal of understanding circadian oscillations that may influence pain conditions. Mice received unilateral injections of Complete Freund’s Adjuvant (CFA) in one hind paw to induce localized inflammation; the contralateral paw received saline as a control. On days 3 post injection (acute stage) and 5 (persistent stage), mechanical sensitivity was assessed by paw withdrawal behaviour using calibrated monofilaments to apply defined force at three time points: ZT4 (early light phase), ZT12 (end of light phase), and ZT20 (dark phase). RNA was extracted from dorsal root ganglia (DRG) on days 4 and 6 for RNA-seq and droplet digital PCR (ddPCR).</div><div>CFA-induced responsiveness to light mechanical force (0.16 g and 0.4 g) shifted from being time-of-day independent in the acute phase to time-of-day dependent in the persistent phase. The opposite pattern was observed with higher force (0.6 g), showing time-of-day dependency in the acute phase. Substance P transcription was upregulated at ZT4 relative to ZT12 on day 4 but not on day 6. Transcripts of two core clock components (<em>Bmal1</em> and <em>Per1</em>) in the DRG were not significantly influenced by CFA-injection. Additional RNA-seq analysis identified differentially expressed genes at ZT4 as CFA-responsive independent of time-of-day.</div><div>These findings reveal a circadian modulation of CFA-induced mechanical hypersensitivity to light mechanical force during the persistent stages of pain, which is associated with alterations in gene expression within the dorsal root ganglion (DRG).</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"306 ","pages":"Article 115224"},"PeriodicalIF":2.5,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145940251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-05DOI: 10.1016/j.physbeh.2026.115217
Bosong Wang , Asim Ahmed , Kartikeya Murari , Ning Cheng
Fragile X Syndrome (FXS), the most common monogenic cause of autism spectrum disorder, exhibits sex differences in prevalence and phenotypic severity. Electroencephalography provides translational insights into its pathophysiology, yet prior research focuses predominantly on males. In C57BL/6J mice, male Fmr1 knockout models show increased absolute gamma power across developmental stages, while female phenotypes, particularly in juveniles, remain uncharacterized. This study addresses this gap by comparing juvenile female Fmr1 knockout and wild-type mice. Frontal-parietal differential electroencephalography was recorded in home cage, light-dark test, and open field test. Analyses included absolute/relative power, peak alpha frequency, theta-beta ratio, phase-amplitude coupling, amplitude-amplitude coupling, and multiscale entropy. Knockout mice exhibited reduced absolute theta, alpha, and beta power across all conditions. Relative power analysis revealed decreased alpha and increased gamma activity. Phase-amplitude coupling showed diminished alpha-gamma coordination, while amplitude-amplitude coupling displayed state-dependent alterations. Peak alpha frequency and theta-beta ratio were reduced or unchanged depending on condition. Signal complexity remained comparable between genotypes. Behaviorally, knockout mice demonstrated hyper-exploration in the open field test. No robust correlations emerged between electroencephalography power and behavior. Our results demonstrate that juvenile female Fmr1 KO mice on a B6 background exhibit EEG alterations highly consistent with those reported in FXS patients, particularly increased gamma and reduced alpha power. The increase in gamma activity represents a conserved biomarker of potential cortical hyperexcitability, while alpha power reductions and decreased peak alpha frequency implicate thalamocortical network involvement. Together, these findings highlight the translational value of this model for studying core circuit dysfunctions in FXS.
{"title":"Alterations in electroencephalography signals in female fragile X syndrome mouse model on a C57BL/6J background","authors":"Bosong Wang , Asim Ahmed , Kartikeya Murari , Ning Cheng","doi":"10.1016/j.physbeh.2026.115217","DOIUrl":"10.1016/j.physbeh.2026.115217","url":null,"abstract":"<div><div>Fragile X Syndrome (FXS), the most common monogenic cause of autism spectrum disorder, exhibits sex differences in prevalence and phenotypic severity. Electroencephalography provides translational insights into its pathophysiology, yet prior research focuses predominantly on males. In C57BL/6J mice, male <em>Fmr1</em> knockout models show increased absolute gamma power across developmental stages, while female phenotypes, particularly in juveniles, remain uncharacterized. This study addresses this gap by comparing juvenile female <em>Fmr1</em> knockout and wild-type mice. Frontal-parietal differential electroencephalography was recorded in home cage, light-dark test, and open field test. Analyses included absolute/relative power, peak alpha frequency, theta-beta ratio, phase-amplitude coupling, amplitude-amplitude coupling, and multiscale entropy. Knockout mice exhibited reduced absolute theta, alpha, and beta power across all conditions. Relative power analysis revealed decreased alpha and increased gamma activity. Phase-amplitude coupling showed diminished alpha-gamma coordination, while amplitude-amplitude coupling displayed state-dependent alterations. Peak alpha frequency and theta-beta ratio were reduced or unchanged depending on condition. Signal complexity remained comparable between genotypes. Behaviorally, knockout mice demonstrated hyper-exploration in the open field test. No robust correlations emerged between electroencephalography power and behavior. Our results demonstrate that juvenile female <em>Fmr1</em> KO mice on a B6 background exhibit EEG alterations highly consistent with those reported in FXS patients, particularly increased gamma and reduced alpha power. The increase in gamma activity represents a conserved biomarker of potential cortical hyperexcitability, while alpha power reductions and decreased peak alpha frequency implicate thalamocortical network involvement. Together, these findings highlight the translational value of this model for studying core circuit dysfunctions in FXS.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"306 ","pages":"Article 115217"},"PeriodicalIF":2.5,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145918306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-30DOI: 10.1016/j.physbeh.2025.115216
Alexander W. Johnson , Kelly L. Klump , Kristen M. Culbert , Jenna Lee-Tanner , Cheryl L. Sisk
Binge eating is a key feeding behavior that is a core symptom of most major eating disorders, with disruptions in the neurotransmitter dopamine gaining significant interest as a potential risk factor. In the current study we sought to examine functional and molecular changes that may underlie alterations in the dopamine system in female rats prone to binge eating. Rats received six feeding tests with intermittent access to palatable food (PF), which was used to identify binge eating resistant (BER) and prone (BEP) phenotypes based on examining tertiles across the feeding tests. Subsequently, rats received separate additional feeding tests following administration of either: the D1R agonist SKF 38393 (1.0, 3 mg/kg); D1R antagonist SCH 23390 (0.1, 0.3 mg/kg); D2/3R agonist quinpirole (0.03, 0.1 mg/kg); or the D2R antagonist, raclopride (0,1, 0.2 mg/kg). Stimulation of D1R reduced both PF and chow intake in BEP but not BER rats. Similarly, inhibition of D1R disrupted intake selectively in BEP rats, however these effects were restricted to PF intake. Alternatively, D2/3R stimulation inhibited PF intake in both groups of rats, although the suppression of PF intake was more prolonged in BEP rats. Blockade of D2Rs failed to impact feeding behavior in either group of rats. This general pattern of heightened responsivity to D1R manipulation was consistent with qPCR findings, which revealed in BEP compared to BER rats, a downregulation in the ventral tegmental area, and an upregulation in nucleus accumbens of D1R gene expression. Collectively these findings show that BEP rats overeat PF, which may be due to altered mesolimbic expression of D1R and corresponding heightened sensitivity to the rewarding properties of PF.
{"title":"Increased responsivity to pharmacological manipulations of dopamine D1 receptors in binge eating prone rats","authors":"Alexander W. Johnson , Kelly L. Klump , Kristen M. Culbert , Jenna Lee-Tanner , Cheryl L. Sisk","doi":"10.1016/j.physbeh.2025.115216","DOIUrl":"10.1016/j.physbeh.2025.115216","url":null,"abstract":"<div><div>Binge eating is a key feeding behavior that is a core symptom of most major eating disorders, with disruptions in the neurotransmitter dopamine gaining significant interest as a potential risk factor. In the current study we sought to examine functional and molecular changes that may underlie alterations in the dopamine system in female rats prone to binge eating. Rats received six feeding tests with intermittent access to palatable food (PF), which was used to identify binge eating resistant (BER) and prone (BEP) phenotypes based on examining tertiles across the feeding tests. Subsequently, rats received separate additional feeding tests following administration of either: the D1R agonist SKF 38393 (1.0, 3 mg/kg); D1R antagonist SCH 23390 (0.1, 0.3 mg/kg); D2/3R agonist quinpirole (0.03, 0.1 mg/kg); or the D2R antagonist, raclopride (0,1, 0.2 mg/kg). Stimulation of D1R reduced both PF and chow intake in BEP but not BER rats. Similarly, inhibition of D1R disrupted intake selectively in BEP rats, however these effects were restricted to PF intake. Alternatively, D2/3R stimulation inhibited PF intake in both groups of rats, although the suppression of PF intake was more prolonged in BEP rats. Blockade of D2Rs failed to impact feeding behavior in either group of rats. This general pattern of heightened responsivity to D1R manipulation was consistent with qPCR findings, which revealed in BEP compared to BER rats, a downregulation in the ventral tegmental area, and an upregulation in nucleus accumbens of D1R gene expression. Collectively these findings show that BEP rats overeat PF, which may be due to altered mesolimbic expression of D1R and corresponding heightened sensitivity to the rewarding properties of PF.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"306 ","pages":"Article 115216"},"PeriodicalIF":2.5,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-30DOI: 10.1016/j.physbeh.2025.115215
Mateus Torres-Cruz, Gilberto Fernando Xavier
The covert orienting of attention task allows investigating the effects of spatial cues on the accuracy and speed of detection of targets. It has been extensively used in humans to investigate both attention triggered by anticipation of sensory events relying on memories of past experiences, i.e., endogenous, and attention generated by the occurrence of salient conspicuous sensory inputs, i.e., exogenous. Although this task has an analogue for rats - the three-hole nose-poke task - it has an important limitation: it uses peripheral visual cues; as these cues may engage both exogenous and endogenous attention simultaneously, it may confound phenomena associated with them. In the present study, a modified version of the task was employed, using bilateral auditory cues, which only engage endogenous orienting via a non-spatial property - pitch. Our results show that rats responded faster and more accurately when the auditory cues were informative of target location, compared to when they were not. This suggests that the task allows investigating endogenous attention in rats without confounding effects from exogenous attention. Further, this is the first unequivocal demonstration that rats can orient attention endogenously. Future studies on the neurobiology of attention may find this task useful for assessing how learned associations contribute for endogenous orienting of spatial attention in rats.
{"title":"Endogenous orienting of attention in rats","authors":"Mateus Torres-Cruz, Gilberto Fernando Xavier","doi":"10.1016/j.physbeh.2025.115215","DOIUrl":"10.1016/j.physbeh.2025.115215","url":null,"abstract":"<div><div>The covert orienting of attention task allows investigating the effects of spatial cues on the accuracy and speed of detection of targets. It has been extensively used in humans to investigate both attention triggered by anticipation of sensory events relying on memories of past experiences, i.e., endogenous, and attention generated by the occurrence of salient conspicuous sensory inputs, i.e., exogenous. Although this task has an analogue for rats - the three-hole nose-poke task - it has an important limitation: it uses peripheral visual cues; as these cues may engage both exogenous and endogenous attention simultaneously, it may confound phenomena associated with them. In the present study, a modified version of the task was employed, using bilateral auditory cues, which only engage endogenous orienting via a non-spatial property - pitch. Our results show that rats responded faster and more accurately when the auditory cues were informative of target location, compared to when they were not. This suggests that the task allows investigating endogenous attention in rats without confounding effects from exogenous attention. Further, this is the first unequivocal demonstration that rats can orient attention endogenously. Future studies on the neurobiology of attention may find this task useful for assessing how learned associations contribute for endogenous orienting of spatial attention in rats.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"306 ","pages":"Article 115215"},"PeriodicalIF":2.5,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-24DOI: 10.1016/j.physbeh.2025.115214
Yuri A. Freire , Rodrigo A.V. Browne , Ludmila L.P. Cabral , Tiago V. Barreira , Eduardo C. Costa
To investigate the moderating role of physical activity intensity and sedentary break patterns on the association between sedentary time (ST) and cardiometabolic risk in older adults.
Methods
This cross-sectional study included 248 community-dwelling older adults without major cardiovascular diseases (66.0 ± 4.6 years; 78% female). Physical activity and ST were measured using a hip-worn accelerometer over seven consecutive days. Cardiometabolic disease risk was assessed using a sex-specific continuous metabolic syndrome score (cMetS). ST was entered as the explanatory variable for cMetS, while moderate-to-vigorous physical activity (MVPA), light physical activity (LPA), and the number of short (1–5 min) and long (>5 min) sedentary breaks were tested as moderators. All analyses were adjusted for traditional cardiometabolic risk factors and accelerometer wear time.
Results
MVPA (β = -0.005, p = 0.046), LPA (β = -0.030, p = 0.050), short (β = -0.003, p = 0.070) and long (β = -0.010, p = 0.011) sedentary breaks moderated the association between ST and cMetS. The Johnson-Neyman technique revealed that the association between ST and cMetS became non-significant (p ≥ 0.05) at thresholds of MVPA ≥ 19 min/day, LPA ≥ 5.9 h/day, short breaks ≥ 87/day, and long breaks ≥ 10/day.
Conclusion
Our findings suggest that specific thresholds of MVPA and LPA, as well as short and long sedentary breaks may offset the deleterious association between ST and cardiometabolic risk in older adults.
{"title":"Moderating effects of physical activity intensity and sedentary break patterns on the association between sedentary time and cardiometabolic risk in older adults","authors":"Yuri A. Freire , Rodrigo A.V. Browne , Ludmila L.P. Cabral , Tiago V. Barreira , Eduardo C. Costa","doi":"10.1016/j.physbeh.2025.115214","DOIUrl":"10.1016/j.physbeh.2025.115214","url":null,"abstract":"<div><div>To investigate the moderating role of physical activity intensity and sedentary break patterns on the association between sedentary time (ST) and cardiometabolic risk in older adults.</div></div><div><h3>Methods</h3><div>This cross-sectional study included 248 community-dwelling older adults without major cardiovascular diseases (66.0 ± 4.6 years; 78% female). Physical activity and ST were measured using a hip-worn accelerometer over seven consecutive days. Cardiometabolic disease risk was assessed using a sex-specific continuous metabolic syndrome score (cMetS). ST was entered as the explanatory variable for cMetS, while moderate-to-vigorous physical activity (MVPA), light physical activity (LPA), and the number of short (1–5 min) and long (>5 min) sedentary breaks were tested as moderators. All analyses were adjusted for traditional cardiometabolic risk factors and accelerometer wear time.</div></div><div><h3>Results</h3><div>MVPA (β = -0.005, <em>p</em> = 0.046), LPA (β = -0.030, <em>p</em> = 0.050), short (β = -0.003, <em>p</em> = 0.070) and long (β = -0.010, <em>p</em> = 0.011) sedentary breaks moderated the association between ST and cMetS. The Johnson-Neyman technique revealed that the association between ST and cMetS became non-significant (<em>p</em> ≥ 0.05) at thresholds of MVPA ≥ 19 min/day, LPA ≥ 5.9 h/day, short breaks ≥ 87/day, and long breaks ≥ 10/day.</div></div><div><h3>Conclusion</h3><div>Our findings suggest that specific thresholds of MVPA and LPA, as well as short and long sedentary breaks may offset the deleterious association between ST and cardiometabolic risk in older adults.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"306 ","pages":"Article 115214"},"PeriodicalIF":2.5,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145844092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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