Pub Date : 2026-02-02DOI: 10.1016/j.physbeh.2026.115247
Chenkun Jiang, William Lampman, Juliana Base, Lucas Pineiro, Kai Chen, Edmundo Salvatier-Alvarez, Aubrey Qian, Zaina Barakat, Anthony Hernandez, Jordan Peters, Theodore Garland
Sleep deprivation negatively impacts both physical and psychological health in both humans and animal models. Exercise, on the other hand, can have beneficial effects on various aspects of physical and mental health. However, little is known about the ways in which sleep deprivation and exercise may interact, especially for exceptionally high levels of exercise. We studied High Runner (HR) mice from a long-term artificial selection experiment to investigate how genetically high exercise level could impact the response to sleep deprivation. A total of 192 adult mice from four replicate HR and four non-selected Control lines (balanced for sex) completed six days of baseline wheel access, followed by three days with or without 6 h/day of total sleep deprivation (TSD) via gentle handling. As expected, HR mice ran farther and faster compared to Controls during days 1-6. TSD reduced the running distance and duration in mice from Control lines, while HR increased running speed and maintained distance (treatment × linetype interaction). TSD-induced changes in body mass differed between linetypes (treatment × linetype interaction): Controls tended to gain mass, whereas HRs lost mass. During the three days prior to TSD, HR mice consistently exhibited more active and fewer maintenance behaviors than Controls. TSD increased resting and decreased wheel activity in Controls but not HRs (treatment × linetype effects significant for both categories). These results demonstrate that genetically based high voluntary activity levels are associated with altered responses to TSD.
{"title":"Mice from lines selectively bred for innately high activity levels have altered behavioral and energetic responses to repeated sleep deprivation.","authors":"Chenkun Jiang, William Lampman, Juliana Base, Lucas Pineiro, Kai Chen, Edmundo Salvatier-Alvarez, Aubrey Qian, Zaina Barakat, Anthony Hernandez, Jordan Peters, Theodore Garland","doi":"10.1016/j.physbeh.2026.115247","DOIUrl":"https://doi.org/10.1016/j.physbeh.2026.115247","url":null,"abstract":"<p><p>Sleep deprivation negatively impacts both physical and psychological health in both humans and animal models. Exercise, on the other hand, can have beneficial effects on various aspects of physical and mental health. However, little is known about the ways in which sleep deprivation and exercise may interact, especially for exceptionally high levels of exercise. We studied High Runner (HR) mice from a long-term artificial selection experiment to investigate how genetically high exercise level could impact the response to sleep deprivation. A total of 192 adult mice from four replicate HR and four non-selected Control lines (balanced for sex) completed six days of baseline wheel access, followed by three days with or without 6 h/day of total sleep deprivation (TSD) via gentle handling. As expected, HR mice ran farther and faster compared to Controls during days 1-6. TSD reduced the running distance and duration in mice from Control lines, while HR increased running speed and maintained distance (treatment × linetype interaction). TSD-induced changes in body mass differed between linetypes (treatment × linetype interaction): Controls tended to gain mass, whereas HRs lost mass. During the three days prior to TSD, HR mice consistently exhibited more active and fewer maintenance behaviors than Controls. TSD increased resting and decreased wheel activity in Controls but not HRs (treatment × linetype effects significant for both categories). These results demonstrate that genetically based high voluntary activity levels are associated with altered responses to TSD.</p>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":" ","pages":"115247"},"PeriodicalIF":2.5,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146120006","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 : 2026-01-31DOI: 10.1016/j.physbeh.2026.115245
Yimei Fan , Hui Luo , Nana Zheng , Longyan Li , Jihui Zhang , Biao Li , Hongliang Feng
The circadian clock genes Per1 and Per2 play a crucial role in regulating circadian rhythms. However, the consequences of their deficiency on motor function and age-related behavioral changes remain poorly understood. This study aimed to investigate the age-dependent effects of Per1/Per2 double knockout (DKO) on motor function in mice. Using wheel-running assays under a 12-hour light/12-hour dark cycle, we compared circadian entrainment between 2-month-old and 9-month-old DKO and wild-type (WT) mice. Motor function was assessed via the pole test and rotarod test, while exploratory behavior was evaluated using the open field test. We further analyzed the main and interaction effects of genotype and age on both circadian and motor parameters. Results showed that Per1/Per2 DKO markedly disrupted light-entrained behavioral rhythms in both age groups. While DKO mice aged from showing no motor deficits at 2 months to pronounced declines in balance and exploration by 9 months. Interaction analysis revealed a significant main effect of Per1/Per2 deficiency on balance and coordination, whereas age alone had no significant effect. Both factors affected exploration, with the genetic effect worsening with age. Notably, severe circadian disruption was present in young mice before motor deficits appeared. In conclusion, Per1/Per2 deficiency exacerbates age-related motor decline. Our finding that circadian disruption precedes motor deficits demonstrates that these clock genes are indispensable for preserving motor function and behavioral organization during aging.
{"title":"Circadian clock genes Per1/Per2 deficiency induces premature age-related motor function decline in mice","authors":"Yimei Fan , Hui Luo , Nana Zheng , Longyan Li , Jihui Zhang , Biao Li , Hongliang Feng","doi":"10.1016/j.physbeh.2026.115245","DOIUrl":"10.1016/j.physbeh.2026.115245","url":null,"abstract":"<div><div>The circadian clock genes <em>Per1</em> and <em>Per2</em> play a crucial role in regulating circadian rhythms. However, the consequences of their deficiency on motor function and age-related behavioral changes remain poorly understood. This study aimed to investigate the age-dependent effects of <em>Per1/Per2</em> double knockout (DKO) on motor function in mice. Using wheel-running assays under a 12-hour light/12-hour dark cycle, we compared circadian entrainment between 2-month-old and 9-month-old DKO and wild-type (WT) mice. Motor function was assessed via the pole test and rotarod test, while exploratory behavior was evaluated using the open field test. We further analyzed the main and interaction effects of genotype and age on both circadian and motor parameters. Results showed that <em>Per1/Per2</em> DKO markedly disrupted light-entrained behavioral rhythms in both age groups. While DKO mice aged from showing no motor deficits at 2 months to pronounced declines in balance and exploration by 9 months. Interaction analysis revealed a significant main effect of <em>Per1/Per2</em> deficiency on balance and coordination, whereas age alone had no significant effect. Both factors affected exploration, with the genetic effect worsening with age. Notably, severe circadian disruption was present in young mice before motor deficits appeared. In conclusion, <em>Per1/Per2</em> deficiency exacerbates age-related motor decline. Our finding that circadian disruption precedes motor deficits demonstrates that these clock genes are indispensable for preserving motor function and behavioral organization during aging.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"308 ","pages":"Article 115245"},"PeriodicalIF":2.5,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146106689","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 : 2026-01-31DOI: 10.1016/j.physbeh.2026.115246
Anna F. Radford, Conner J. Whitten, Ashley N. Wells, Mackenzie K. Hooker, Matthew A. Cooper
The development of dominance relationships generates experience-dependent plasticity in cortical circuits controlling social behavior and responses to stress. Perineuronal nets (PNN) are specialized extracellular structures that surround cortical neurons and contribute to experience-dependent neural plasticity. Using a Syrian hamster model, we investigated whether the development of dominance relationships altered the expression of PNNs in the infralimbic (IL) and prelimbic (PL) regions of the ventral medial prefrontal cortex, as well as the basolateral amygdala (BLA). We also tested whether PNN expression predicted agonistic behavior during the early or late phases of dominance interactions. Male and female hamsters were paired with same-sex partners and exposed to daily dominance interactions for two weeks. In Study 1, brains from male hamsters were collected for PNN staining 60 mins or 1–3 days following the final dominance interaction. We found that dominant males had more IL neurons surrounded by PNNs compared to subordinate males, and all hamsters showed greater PNN expression in caudal, compared to rostral, regions of the IL and PL. In Study 2, we included both males and females and collected brains 60 mins after the final dominance interaction. In Study 2, we found that subordinate females had more PL neurons surrounded by PNNs compared to dominants and social exposure controls. The rate of attacks during the late phase of dominance interactions predicted the number of PNN+ cells in the PL in dominant males, which is consistent with neural plasticity in PL neurons leading to elevated aggression in dominant males. Overall, the neural plasticity in the PL and IL induced by the formation of dominance relationships may contribute to sex differences in responses to social challenges.
{"title":"Effects of social dominance on perineuronal nets in medial prefrontal cortex and basolateral amygdala","authors":"Anna F. Radford, Conner J. Whitten, Ashley N. Wells, Mackenzie K. Hooker, Matthew A. Cooper","doi":"10.1016/j.physbeh.2026.115246","DOIUrl":"10.1016/j.physbeh.2026.115246","url":null,"abstract":"<div><div>The development of dominance relationships generates experience-dependent plasticity in cortical circuits controlling social behavior and responses to stress. Perineuronal nets (PNN) are specialized extracellular structures that surround cortical neurons and contribute to experience-dependent neural plasticity. Using a Syrian hamster model, we investigated whether the development of dominance relationships altered the expression of PNNs in the infralimbic (IL) and prelimbic (PL) regions of the ventral medial prefrontal cortex, as well as the basolateral amygdala (BLA). We also tested whether PNN expression predicted agonistic behavior during the early or late phases of dominance interactions. Male and female hamsters were paired with same-sex partners and exposed to daily dominance interactions for two weeks. In Study 1, brains from male hamsters were collected for PNN staining 60 mins or 1–3 days following the final dominance interaction. We found that dominant males had more IL neurons surrounded by PNNs compared to subordinate males, and all hamsters showed greater PNN expression in caudal, compared to rostral, regions of the IL and PL. In Study 2, we included both males and females and collected brains 60 mins after the final dominance interaction. In Study 2, we found that subordinate females had more PL neurons surrounded by PNNs compared to dominants and social exposure controls. The rate of attacks during the late phase of dominance interactions predicted the number of PNN+ cells in the PL in dominant males, which is consistent with neural plasticity in PL neurons leading to elevated aggression in dominant males. Overall, the neural plasticity in the PL and IL induced by the formation of dominance relationships may contribute to sex differences in responses to social challenges.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"308 ","pages":"Article 115246"},"PeriodicalIF":2.5,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146106869","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 : 2026-01-29DOI: 10.1016/j.physbeh.2026.115243
Sarah Farooq, Angela Inglis, Falah Almohanna, Jennifer Thiam, Samiyah Al-Khaldi, Rayanah Barnawi, Hazem Ghebeh, Monther Al-Alwan
Fascin 1 is an actin-bundling protein with limited expression in normal tissues, such as the brain and spleen. Fascin knockout mice exhibit enlarged lateral ventricles and impaired neuronal extension in the posterior region of the anterior commissure. Despite these observations, the effect of fascin loss on animal behavior and cognitive function has not been previously assessed. In the present study, fascin knockout (fascin-/-) and wild-type (fascin+/+) female mice were compared on a number of standard behavioral tests, including open-field, object recognition, elevated plus maze, light-dark transition, sociability, and Morris water maze tests. Fascin-/- mice exhibited reduced locomotor activity during the open-field test and spent more time in the dark zone during the light-dark transition tests. Furthermore, fascin-/- mice showed comparable social interactions and exhibited altered early exploratory behavior during Morris water maze tests. This study concluded that whole-body fascin loss modestly affects animal behavior, particularly locomotor and exploratory activities. The whole-body knockout experimental findings highlight the regulatory role of fascin on these behavioral domains and emphasize the importance of considering these effects in future studies using this animal model.
{"title":"Effect of fascin loss on animal behavior using a knockout mouse model.","authors":"Sarah Farooq, Angela Inglis, Falah Almohanna, Jennifer Thiam, Samiyah Al-Khaldi, Rayanah Barnawi, Hazem Ghebeh, Monther Al-Alwan","doi":"10.1016/j.physbeh.2026.115243","DOIUrl":"10.1016/j.physbeh.2026.115243","url":null,"abstract":"<p><p>Fascin 1 is an actin-bundling protein with limited expression in normal tissues, such as the brain and spleen. Fascin knockout mice exhibit enlarged lateral ventricles and impaired neuronal extension in the posterior region of the anterior commissure. Despite these observations, the effect of fascin loss on animal behavior and cognitive function has not been previously assessed. In the present study, fascin knockout (fascin<sup>-/-</sup>) and wild-type (fascin<sup>+/+</sup>) female mice were compared on a number of standard behavioral tests, including open-field, object recognition, elevated plus maze, light-dark transition, sociability, and Morris water maze tests. Fascin<sup>-/-</sup> mice exhibited reduced locomotor activity during the open-field test and spent more time in the dark zone during the light-dark transition tests. Furthermore, fascin<sup>-/-</sup> mice showed comparable social interactions and exhibited altered early exploratory behavior during Morris water maze tests. This study concluded that whole-body fascin loss modestly affects animal behavior, particularly locomotor and exploratory activities. The whole-body knockout experimental findings highlight the regulatory role of fascin on these behavioral domains and emphasize the importance of considering these effects in future studies using this animal model.</p>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":" ","pages":"115243"},"PeriodicalIF":2.5,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146096925","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 : 2026-01-27DOI: 10.1016/j.physbeh.2026.115242
Alexey Sarapultsev, Maria Komelkova, Evgenii Gusev, Desheng Hu, Vladimir Naumenko
Background: Social context modulates stress physiology and resilience, yet preclinical rat paradigms vary widely in stressor type, timing of social exposure, contact modality, and endpoint definitions. We synthesized rat studies to quantify directional and, where feasible, standardized effect-size evidence for social buffering and to outline translational implications.
Methods: PubMed, Scopus, and Web of Science were searched (2008-2025) for in vivo rat studies comparing conspecific (pair/group housing or conspecific presence) versus solitary conditions across validated stress and PTSD-like paradigms (e.g., fear conditioning/extinction, CUS/CMS, social defeat, predator threat). Data extraction and reporting followed PRISMA 2020 and SYRCLE guidance. Synthesis followed a two-tier approach: (i) all eligible contrasts were direction-coded as beneficial, neutral/mixed, or detrimental under conspecific conditions based strictly on reported statistical contrasts; and (ii) for domains with sufficient coded contrasts, the proportion of beneficial comparisons was estimated with exact binomial tests and 95% confidence intervals. Standardized mean-difference meta-analysis (Hedges' g; random-effects REML) was conducted only for predefined outcomes with adequate numerical reporting.
Results: Forty studies met inclusion criteria, yielding 89 extracted comparisons. Overall, 69/89 comparisons (≈78%) favored conspecific conditions. Domain-level directional syntheses supported predominance of beneficial outcomes for hormonal (0.72; 95% CI 0.50-1.00; p = 0.048) and neurotrophic/plasticity markers (0.89; 95% CI 0.57-1.00; p = 0.020), whereas inflammatory/oxidative outcomes were more variable (0.71; 95% CI 0.39-0.94; p = 0.227). For predefined behavioral endpoints with sufficient data, effect-size pooling showed a large reduction in conditioned fear (Hedges' g = -1.22 [-1.53; -0.91], p < 0.0001).
Conclusions: Social buffering is robust at behavioral and neuroendocrine levels and often aligns with neurotrophic/plasticity markers, while peripheral immune/redox readouts are more context-dependent.
背景：社会环境调节应激生理和恢复力，然而临床前大鼠范式在应激源类型、社会暴露时间、接触方式和终点定义方面差异很大。我们综合了大鼠研究，以量化定向的，在可行的情况下，标准化的社会缓冲效应证据，并概述翻译意义。方法：检索PubMed、Scopus和Web of Science（2008-2025）的体内大鼠研究，比较同种（配对/群体居住或同种存在）与孤独条件下的有效应激和类ptsd范式（如恐惧条件反射/灭绝、CUS/CMS、社会失败、捕食者威胁）。数据提取和报告遵循PRISMA 2020和cycle指南。综合采用两层方法：(i)严格根据报告的统计对比，在相同条件下，所有符合条件的对比被方向编码为有益、中性/混合或有害；（ii）对于具有足够编码对比的域，使用精确的二项检验和95%置信区间估计有益比较的比例。标准化均差荟萃分析（Hedges' g；随机效应REML）仅对预定义结果进行了充分的数值报告。结果：40项研究符合纳入标准，产生89项提取比较。总体而言，69/89比较（≈78%）倾向于同特定条件。领域水平的定向合成支持激素（0.72;95% CI 0.50-1.00; p=0.048）和神经营养/可塑性标志物（0.89;95% CI 0.57-1.00; p=0.020）的有利结果占主导地位，而炎症/氧化结果则更为可变（0.71;95% CI 0.39-0.94; p=0.227）。对于具有足够数据的预定义行为终点，效应大小池显示条件恐惧的大幅减少（Hedges' g=-1.22[-1.53; -0.91]）。结论：社会缓冲在行为和神经内分泌水平上是强大的，并且通常与神经营养/可塑性标记一致，而外周免疫/氧化还原读数更多地依赖于环境。
{"title":"Social buffering of stress in rats: a multisystem meta-analysis and translational framework for stress resilience.","authors":"Alexey Sarapultsev, Maria Komelkova, Evgenii Gusev, Desheng Hu, Vladimir Naumenko","doi":"10.1016/j.physbeh.2026.115242","DOIUrl":"10.1016/j.physbeh.2026.115242","url":null,"abstract":"<p><strong>Background: </strong>Social context modulates stress physiology and resilience, yet preclinical rat paradigms vary widely in stressor type, timing of social exposure, contact modality, and endpoint definitions. We synthesized rat studies to quantify directional and, where feasible, standardized effect-size evidence for social buffering and to outline translational implications.</p><p><strong>Methods: </strong>PubMed, Scopus, and Web of Science were searched (2008-2025) for in vivo rat studies comparing conspecific (pair/group housing or conspecific presence) versus solitary conditions across validated stress and PTSD-like paradigms (e.g., fear conditioning/extinction, CUS/CMS, social defeat, predator threat). Data extraction and reporting followed PRISMA 2020 and SYRCLE guidance. Synthesis followed a two-tier approach: (i) all eligible contrasts were direction-coded as beneficial, neutral/mixed, or detrimental under conspecific conditions based strictly on reported statistical contrasts; and (ii) for domains with sufficient coded contrasts, the proportion of beneficial comparisons was estimated with exact binomial tests and 95% confidence intervals. Standardized mean-difference meta-analysis (Hedges' g; random-effects REML) was conducted only for predefined outcomes with adequate numerical reporting.</p><p><strong>Results: </strong>Forty studies met inclusion criteria, yielding 89 extracted comparisons. Overall, 69/89 comparisons (≈78%) favored conspecific conditions. Domain-level directional syntheses supported predominance of beneficial outcomes for hormonal (0.72; 95% CI 0.50-1.00; p = 0.048) and neurotrophic/plasticity markers (0.89; 95% CI 0.57-1.00; p = 0.020), whereas inflammatory/oxidative outcomes were more variable (0.71; 95% CI 0.39-0.94; p = 0.227). For predefined behavioral endpoints with sufficient data, effect-size pooling showed a large reduction in conditioned fear (Hedges' g = -1.22 [-1.53; -0.91], p < 0.0001).</p><p><strong>Conclusions: </strong>Social buffering is robust at behavioral and neuroendocrine levels and often aligns with neurotrophic/plasticity markers, while peripheral immune/redox readouts are more context-dependent.</p>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":" ","pages":"115242"},"PeriodicalIF":2.5,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146087078","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 : 2026-01-23DOI: 10.1016/j.physbeh.2026.115241
Beatriz Nunes Petribu, Karina Possa Abrahao, Maria Lucia Oliveira Souza-Formigoni
The co-consumption of alcohol (ethanol) and caffeine, commonly found in alcoholic beverages mixed with energy drinks (AmED), has been linked to increased alcohol intake and heightened risk-taking behaviors. However, the effects of this combination under voluntary drinking conditions in animal models remain poorly understood. The present study investigated whether caffeine modulates ethanol intake in Swiss male mice, an outbred strain with inherent low ethanol preference. Mice were exposed to a two-bottle choice Intermittent Overnight Drinking (IOD) protocol for 12 sessions. Each mouse had access to water and either ethanol (10%), caffeine (0.75 mg/mL), or a combination of both. Using lickometer devices, we analyzed drinking microstructure, including total intake, latency to first lick and bout, and temporal licking patterns. Caffeine and water were consumed in similar amounts and followed comparable circadian patterns, whereas both ethanol and ethanol + caffeine solutions were consistently avoided. Thus, in Swiss male mice, caffeine did not modify ethanol intake. These findings emphasize the importance of strain-specific studies for a better understanding of the behavioral interaction between alcohol and caffeine.
{"title":"Does caffeine alter preference or patterns of voluntary ethanol consumption in Swiss male mice?","authors":"Beatriz Nunes Petribu, Karina Possa Abrahao, Maria Lucia Oliveira Souza-Formigoni","doi":"10.1016/j.physbeh.2026.115241","DOIUrl":"10.1016/j.physbeh.2026.115241","url":null,"abstract":"<p><p>The co-consumption of alcohol (ethanol) and caffeine, commonly found in alcoholic beverages mixed with energy drinks (AmED), has been linked to increased alcohol intake and heightened risk-taking behaviors. However, the effects of this combination under voluntary drinking conditions in animal models remain poorly understood. The present study investigated whether caffeine modulates ethanol intake in Swiss male mice, an outbred strain with inherent low ethanol preference. Mice were exposed to a two-bottle choice Intermittent Overnight Drinking (IOD) protocol for 12 sessions. Each mouse had access to water and either ethanol (10%), caffeine (0.75 mg/mL), or a combination of both. Using lickometer devices, we analyzed drinking microstructure, including total intake, latency to first lick and bout, and temporal licking patterns. Caffeine and water were consumed in similar amounts and followed comparable circadian patterns, whereas both ethanol and ethanol + caffeine solutions were consistently avoided. Thus, in Swiss male mice, caffeine did not modify ethanol intake. These findings emphasize the importance of strain-specific studies for a better understanding of the behavioral interaction between alcohol and caffeine.</p>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":" ","pages":"115241"},"PeriodicalIF":2.5,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047108","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 : 2026-01-23DOI: 10.1016/j.physbeh.2026.115240
Samantha M. Stead , Phoebe Edwards , Rudy Boonstra , Rupert Palme , Edward Mujjuzi , Julie A. Teichroeb
Glucocorticoids (GCs) are hormones that are secreted in response to energetic demands, allowing animals to cope with internal and external challenges. We investigated the factors impacting fecal GC metabolite (FGM) concentrations (a proxy of blood GC concentrations) in a population of Rwenzori Angolan colobus monkeys (Colobus angolensis ruwenzorii) in Uganda. These monkeys live in a multi-level society with three tiers of non-random association: the core unit (individuals that feed, rest, and travel together), the clan (core units that associate preferentially), and the band (core units that share a home range). We used linear mixed-effect models to assess the impact of reproductive state, fruit availability, and core unit composition on FGM concentrations of reproductive females. We found that FGM concentrations increased over the course of pregnancy and decreased over the course of lactation. There was a quadratic relationship between FGM concentrations and core unit size, with FGM concentrations being lower for mothers living in intermediate-sized core units compared to those living in smaller and larger core units. This aligns with previous work on this population showing that individuals living in intermediate-sized core units expend the least energy travelling. Future work should investigate the impact of FGM concentrations on infant growth and development in this subspecies.
{"title":"Impacts of reproductive state and social environment on glucocorticoid concentrations in female Rwenzori Angolan colobus monkeys (Colobus angolensis ruwenzorii)","authors":"Samantha M. Stead , Phoebe Edwards , Rudy Boonstra , Rupert Palme , Edward Mujjuzi , Julie A. Teichroeb","doi":"10.1016/j.physbeh.2026.115240","DOIUrl":"10.1016/j.physbeh.2026.115240","url":null,"abstract":"<div><div>Glucocorticoids (GCs) are hormones that are secreted in response to energetic demands, allowing animals to cope with internal and external challenges. We investigated the factors impacting fecal GC metabolite (FGM) concentrations (a proxy of blood GC concentrations) in a population of Rwenzori Angolan colobus monkeys (<em>Colobus angolensis ruwenzorii</em>) in Uganda. These monkeys live in a multi-level society with three tiers of non-random association: the core unit (individuals that feed, rest, and travel together), the clan (core units that associate preferentially), and the band (core units that share a home range). We used linear mixed-effect models to assess the impact of reproductive state, fruit availability, and core unit composition on FGM concentrations of reproductive females. We found that FGM concentrations increased over the course of pregnancy and decreased over the course of lactation. There was a quadratic relationship between FGM concentrations and core unit size, with FGM concentrations being lower for mothers living in intermediate-sized core units compared to those living in smaller and larger core units. This aligns with previous work on this population showing that individuals living in intermediate-sized core units expend the least energy travelling. Future work should investigate the impact of FGM concentrations on infant growth and development in this subspecies.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"307 ","pages":"Article 115240"},"PeriodicalIF":2.5,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047159","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}
<div><h3>Objective</h3><div>Desulfovibrio is a genus of sulfate-reducing bacteria residing in the gut, and growing evidence has implicated it in the pathogenesis of depression. However, the exact association and intrinsic mechanisms between the two remain unelucidated. This study aims to investigate whether Desulfovibrio induces depression-like behaviors in mice via the Microbiota-Gut-Brain Axis and to preliminarily elucidate the underlying mechanisms.</div></div><div><h3>Methods</h3><div>A two-week Desulfovibrio-induced mouse model of depression was established in this study. Based on preliminary experimental results, a Desulfovibrio bacterial suspension concentration of 1 × 10^8 CFU/ml, which demonstrated a more pronounced impact on depression-like behaviors in mice, was selected to investigate the intervention effect of Desulfovibrio on depression and its underlying mechanisms. Behavioral changes in mice were assessed using the sucrose preference test (SPT), open field test (OFT), tail suspension test (TST), and forced swim test (FST) to evaluate the antidepressant effects. The abundance of Desulfovibrio in mouse intestines was quantified using quantitative polymerase chain reaction (q-PCR). Targeted metabolomic analysis of short-chain fatty acids (SCFAs) in mice was performed using GC–MS. Targeted metabolomic analysis of arachidonic acid (AA) in mice was conducted using LC-MS. Additionally, histopathological changes in mouse colon tissue were observed via HE staining.</div></div><div><h3>Results</h3><div>Q-PCR analysis revealed a significant increase in the abundance of Desulfovibrio in the intestinal tract of mice in the model group, indicating successful colonization of Desulfovibrio in these animals. Behavioral results indicated that intervention with Desulfovibrio significantly induced behavioral phenotypes of anhedonia, reduced spontaneous activity, and behavioral despair in mice, demonstrating its direct role in promoting depression-like phenotypes. Histological findings revealed disordered colonic gland structures, epithelial damage, and increased inflammatory cell infiltration in the model group, suggesting impaired intestinal barrier function. Metabolomic analysis showed that Desulfovibrio intervention reshaped the serum short-chain fatty acid profile, with butyrate decreased and propionate increased. Concurrently, arachidonic acid metabolism shifted toward a pro-inflammatory state, evidenced by elevated levels of pro-inflammatory mediators such as Prostaglandin E2 (PGE2) and Leukotriene B4 (LTB4), while the anti-inflammatory substance Docosahexaenoic Acid (DHA) was reduced.</div></div><div><h3>Conclusion</h3><div>Desulfovibrio trigger depression-like behaviors in mice by disrupting the colonic barrier structure, perturbing the short-chain fatty acid metabolic profile, and activating the pro-inflammatory arachidonic acid metabolic pathway. To further explore the relationship between gut microbiota and the onset of depression, depress
{"title":"Desulfovibrio vulgaris trigger depression-like behavior in mice through dual disruption of colonic homeostasis and fatty acid metabolism","authors":"Linlu Peng , Xuguang Zhang , Jiaojiao Tian , Jiangfeng Wen , Ruijuan Qiu , Yiwei Zheng , Chunlin Chen , Hao Ma","doi":"10.1016/j.physbeh.2026.115232","DOIUrl":"10.1016/j.physbeh.2026.115232","url":null,"abstract":"<div><h3>Objective</h3><div>Desulfovibrio is a genus of sulfate-reducing bacteria residing in the gut, and growing evidence has implicated it in the pathogenesis of depression. However, the exact association and intrinsic mechanisms between the two remain unelucidated. This study aims to investigate whether Desulfovibrio induces depression-like behaviors in mice via the Microbiota-Gut-Brain Axis and to preliminarily elucidate the underlying mechanisms.</div></div><div><h3>Methods</h3><div>A two-week Desulfovibrio-induced mouse model of depression was established in this study. Based on preliminary experimental results, a Desulfovibrio bacterial suspension concentration of 1 × 10^8 CFU/ml, which demonstrated a more pronounced impact on depression-like behaviors in mice, was selected to investigate the intervention effect of Desulfovibrio on depression and its underlying mechanisms. Behavioral changes in mice were assessed using the sucrose preference test (SPT), open field test (OFT), tail suspension test (TST), and forced swim test (FST) to evaluate the antidepressant effects. The abundance of Desulfovibrio in mouse intestines was quantified using quantitative polymerase chain reaction (q-PCR). Targeted metabolomic analysis of short-chain fatty acids (SCFAs) in mice was performed using GC–MS. Targeted metabolomic analysis of arachidonic acid (AA) in mice was conducted using LC-MS. Additionally, histopathological changes in mouse colon tissue were observed via HE staining.</div></div><div><h3>Results</h3><div>Q-PCR analysis revealed a significant increase in the abundance of Desulfovibrio in the intestinal tract of mice in the model group, indicating successful colonization of Desulfovibrio in these animals. Behavioral results indicated that intervention with Desulfovibrio significantly induced behavioral phenotypes of anhedonia, reduced spontaneous activity, and behavioral despair in mice, demonstrating its direct role in promoting depression-like phenotypes. Histological findings revealed disordered colonic gland structures, epithelial damage, and increased inflammatory cell infiltration in the model group, suggesting impaired intestinal barrier function. Metabolomic analysis showed that Desulfovibrio intervention reshaped the serum short-chain fatty acid profile, with butyrate decreased and propionate increased. Concurrently, arachidonic acid metabolism shifted toward a pro-inflammatory state, evidenced by elevated levels of pro-inflammatory mediators such as Prostaglandin E2 (PGE2) and Leukotriene B4 (LTB4), while the anti-inflammatory substance Docosahexaenoic Acid (DHA) was reduced.</div></div><div><h3>Conclusion</h3><div>Desulfovibrio trigger depression-like behaviors in mice by disrupting the colonic barrier structure, perturbing the short-chain fatty acid metabolic profile, and activating the pro-inflammatory arachidonic acid metabolic pathway. To further explore the relationship between gut microbiota and the onset of depression, depress","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"307 ","pages":"Article 115232"},"PeriodicalIF":2.5,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145998867","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 : 2026-01-15DOI: 10.1016/j.physbeh.2026.115231
Spencer E. Fields , Arul Elango , Elif Ece Akgun , Adrianna M. Sweeney , Eileen Carry , Ariane Vasilatis , Emma Bernstein , James E. Simon , Qingli Wu , Nicholas T. Bello
Kratom (Mitragyna speciosa) has been marketed and used for a variety of health-promoting applications. Kratom contains an expansive bioactive alkaloid profile with mitragynine (MTG) as the most abundant. Individual responses to kratom have been reported, but the role of obesity as a factor influencing the effects of kratom has not been studied. First, we used a standardized kratom extract (KE) to determine the cardiopulmonary differences with KE (290, 500 mg/kg) and matched MTG (18 mg/kg) in high-fat diet (HFD; 45% Fat) induced obese male C57Bl/6 J mice. As measured by whole-body plethysmography, acute oral dosing revealed an approximate 15% reduction in the respiratory rate with all doses of KE and MTG. Unlike a well-known respiratory depressant, alprazolam, KE and MTG did not reduce minute ventilation (MvB; ml/min). As measured by volume-pressure recordings, KE 500 mg/kg produced an approximate 12% reduction in heart rate in normal weight mice. Second, we determined whether daily oral dosing KE (50, 150 mg/kg) prevented HFD-induced weight gain. Daily 150 mg/kg resulted in an increase in body weight gain (∼1 g) in the last week after 21 days of dosing. After 4 days following kratom cessation, there was reduced distance traveled in the KE 150 mg/kg compared with the KE 50 mg/kg group in an elevated plus maze test. These findings demonstrate a dose-dependent-increase in weight gain with KE, suggesting further investigation is needed to delineate kratom alkaloid effects on metabolism and body weight control.
{"title":"Kratom (Mitragyna speciosa) alkaloids influence on cardiopulmonary measures and high-fat diet-induced weight gain in mice","authors":"Spencer E. Fields , Arul Elango , Elif Ece Akgun , Adrianna M. Sweeney , Eileen Carry , Ariane Vasilatis , Emma Bernstein , James E. Simon , Qingli Wu , Nicholas T. Bello","doi":"10.1016/j.physbeh.2026.115231","DOIUrl":"10.1016/j.physbeh.2026.115231","url":null,"abstract":"<div><div>Kratom (<em>Mitragyna speciosa</em>) has been marketed and used for a variety of health-promoting applications. Kratom contains an expansive bioactive alkaloid profile with mitragynine (MTG) as the most abundant. Individual responses to kratom have been reported, but the role of obesity as a factor influencing the effects of kratom has not been studied. First, we used a standardized kratom extract (KE) to determine the cardiopulmonary differences with KE (290, 500 mg/kg) and matched MTG (18 mg/kg) in high-fat diet (HFD; 45% Fat) induced obese male C57Bl/6 J mice. As measured by whole-body plethysmography, acute oral dosing revealed an approximate 15% reduction in the respiratory rate with all doses of KE and MTG. Unlike a well-known respiratory depressant, alprazolam, KE and MTG did not reduce minute ventilation (MvB; ml/min). As measured by volume-pressure recordings, KE 500 mg/kg produced an approximate 12% reduction in heart rate in normal weight mice. Second, we determined whether daily oral dosing KE (50, 150 mg/kg) prevented HFD-induced weight gain. Daily 150 mg/kg resulted in an increase in body weight gain (∼1 g) in the last week after 21 days of dosing. After 4 days following kratom cessation, there was reduced distance traveled in the KE 150 mg/kg compared with the KE 50 mg/kg group in an elevated plus maze test. These findings demonstrate a dose-dependent-increase in weight gain with KE, suggesting further investigation is needed to delineate kratom alkaloid effects on metabolism and body weight control.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"307 ","pages":"Article 115231"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994466","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 : 2026-01-14DOI: 10.1016/j.physbeh.2026.115228
Zequn Li , Kairi Hayashi , Gen Tanabe , Hiroshi Churei , Toshiaki Ueno , Kenji Fueki
Hyposalivation affects cognitive function. However, its impact on hippocampus-dependent memory remains unclear. Saliva contains brain-derived neurotrophic factor (BDNF), which is also synthesized in the hippocampus and can pass through the blood-brain barrier (BBB) to influence hippocampal plasticity. Therefore, we hypothesized that hyposalivation reduces peripheral BDNF availability, leading to decreased hippocampal BDNF levels and cognitive impairment. In this study, this relationship was investigated using an in vivo model of sialadenectomy-induced hyposalivation. A total of 24 8-week-old male ddY mice were divided into control and extraction (EXT) groups. The EXT group underwent submandibular and sublingual salivary gland extractions, whereas the control group underwent a sham operation. Saliva was collected at baseline (0 weeks) and at 2- and 3-weeks postoperatively. Cognitive function was assessed using the Y-maze, fear conditioning (FC), novel object recognition (NOR), and object location tests (OLT). Anxiety-like behavior was evaluated using the open field test (OFT) and elevated plus-maze (EPM) tests. Hippocampi were collected at 3 weeks post-operation for BDNF quantification using enzyme-linked immunosorbent assay, and its concentration in subregions of the hippocampus was determined by semi-quantitative analysis. Hyposalivation significantly impaired spatial working memory in the Y-maze test and contextual fear memory in the FC, both of which are hippocampus-dependent. NOR showed only a transient deficit at 24 h during the 2-week period (no significant difference in 3-week post-operation), whereas long-term spatial memory measured by the OLT exhibited a persistent 24-h impairment at both 2 and 3 weeks, indicating reduced long-term spatial memory rather than accelerated decay. No significant differences were observed in anxiety-like behavior. Although sialoadenectomy significantly reduced salivary secretion and total salivary BDNF output, the concentration of BDNF in saliva in both groups remained unchanged at 2- and 3-weeks post-operation. However, hippocampal BDNF levels were significantly lower in the EXT group than in the control group. These findings suggest that hyposalivation may selectively impair hippocampus-related spatial memory without affecting recognition memory or anxiety-related behaviors.
{"title":"Hyposalivation induced by salivary gland extraction impairs cognitive function in mice","authors":"Zequn Li , Kairi Hayashi , Gen Tanabe , Hiroshi Churei , Toshiaki Ueno , Kenji Fueki","doi":"10.1016/j.physbeh.2026.115228","DOIUrl":"10.1016/j.physbeh.2026.115228","url":null,"abstract":"<div><div>Hyposalivation affects cognitive function. However, its impact on hippocampus-dependent memory remains unclear. Saliva contains brain-derived neurotrophic factor (BDNF), which is also synthesized in the hippocampus and can pass through the blood-brain barrier (BBB) to influence hippocampal plasticity. Therefore, we hypothesized that hyposalivation reduces peripheral BDNF availability, leading to decreased hippocampal BDNF levels and cognitive impairment. In this study, this relationship was investigated using an in vivo model of sialadenectomy-induced hyposalivation. A total of 24 8-week-old male ddY mice were divided into control and extraction (EXT) groups. The EXT group underwent submandibular and sublingual salivary gland extractions, whereas the control group underwent a sham operation. Saliva was collected at baseline (0 weeks) and at 2- and 3-weeks postoperatively. Cognitive function was assessed using the Y-maze, fear conditioning (FC), novel object recognition (NOR), and object location tests (OLT). Anxiety-like behavior was evaluated using the open field test (OFT) and elevated plus-maze (EPM) tests. Hippocampi were collected at 3 weeks post-operation for BDNF quantification using enzyme-linked immunosorbent assay, and its concentration in subregions of the hippocampus was determined by semi-quantitative analysis. Hyposalivation significantly impaired spatial working memory in the Y-maze test and contextual fear memory in the FC, both of which are hippocampus-dependent. NOR showed only a transient deficit at 24 h during the 2-week period (no significant difference in 3-week post-operation), whereas long-term spatial memory measured by the OLT exhibited a persistent 24-h impairment at both 2 and 3 weeks, indicating reduced long-term spatial memory rather than accelerated decay. No significant differences were observed in anxiety-like behavior. Although sialoadenectomy significantly reduced salivary secretion and total salivary BDNF output, the concentration of BDNF in saliva in both groups remained unchanged at 2- and 3-weeks post-operation. However, hippocampal BDNF levels were significantly lower in the EXT group than in the control group. These findings suggest that hyposalivation may selectively impair hippocampus-related spatial memory without affecting recognition memory or anxiety-related behaviors.</div></div>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":"307 ","pages":"Article 115228"},"PeriodicalIF":2.5,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990305","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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