Pub Date : 2026-02-04DOI: 10.1016/j.physbeh.2026.115248
Anna Laura Amato, Paola Gualtieri, Michela Cirillo, Giada La Placa, Giulia Frank, Rossella Cianci, Laura Di Renzo
Food addiction (FA) is a complex clinical condition that refers to addiction to highly palatable foods, represented by compulsive eating behavior and an incapacity to control food consumption, similar to other forms of addiction. This review examines the literature on FA and its impact on eating disorders and obesity. Using databases such as PubMed, Cochrane Library and Google Scholar, recent studies were analyzed to show how FA may reduce treatment effectiveness, increase symptom severity, promote resistance to nutritional or pharmacological interventions, and elevate the risk of relapse. The search strategy used the keywords food addiction, obesity, eating disorders, psychotherapy, and dietary therapy, limiting the reference period to studies published in the last five years. In reviewing the available articles, several nuances emerged that are fundamental to understanding FA, including neurobiological mechanisms, psychiatric comorbidities, environmental determinants, alterations in the gut microbiota, and the pervasive influence of ultra-processed foods. Taken together, the data indicate that FA not only intensifies symptom manifestation but also contributes to worse outcomes, with reduced compliance to standard treatments and an increased likelihood of relapse. These observations underscore the importance of recognizing FA as a critical component in clinical practice; neglecting its role and symptom may compromise therapeutic efficacy. Further research is needed to establish integrative treatment models that include FA as a fundamental component of clinical patient care.
{"title":"The Impact of Food Addiction on the Treatment of Eating Disorders and Obesity: A Systematic Review.","authors":"Anna Laura Amato, Paola Gualtieri, Michela Cirillo, Giada La Placa, Giulia Frank, Rossella Cianci, Laura Di Renzo","doi":"10.1016/j.physbeh.2026.115248","DOIUrl":"https://doi.org/10.1016/j.physbeh.2026.115248","url":null,"abstract":"<p><p>Food addiction (FA) is a complex clinical condition that refers to addiction to highly palatable foods, represented by compulsive eating behavior and an incapacity to control food consumption, similar to other forms of addiction. This review examines the literature on FA and its impact on eating disorders and obesity. Using databases such as PubMed, Cochrane Library and Google Scholar, recent studies were analyzed to show how FA may reduce treatment effectiveness, increase symptom severity, promote resistance to nutritional or pharmacological interventions, and elevate the risk of relapse. The search strategy used the keywords food addiction, obesity, eating disorders, psychotherapy, and dietary therapy, limiting the reference period to studies published in the last five years. In reviewing the available articles, several nuances emerged that are fundamental to understanding FA, including neurobiological mechanisms, psychiatric comorbidities, environmental determinants, alterations in the gut microbiota, and the pervasive influence of ultra-processed foods. Taken together, the data indicate that FA not only intensifies symptom manifestation but also contributes to worse outcomes, with reduced compliance to standard treatments and an increased likelihood of relapse. These observations underscore the importance of recognizing FA as a critical component in clinical practice; neglecting its role and symptom may compromise therapeutic efficacy. Further research is needed to establish integrative treatment models that include FA as a fundamental component of clinical patient care.</p>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":" ","pages":"115248"},"PeriodicalIF":2.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146132836","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 : 2026-02-04DOI: 10.1016/j.physbeh.2026.115250
Lingfeng Wu, Renlai Zhou
It remains unclear whether acute aerobic exercise can effectively mitigate the inhibitory control deficits caused by test anxiety. This study investigated the effects of 30 min of moderate-intensity acute aerobic exercise on inhibitory control and related neural activities in individuals with high test anxiety. Forty participants were randomly assigned to an aerobic exercise group or a seated-reading control group, completing pre- and post-intervention assessments spaced one week apart. Statistical analyses using a series of repeated-measures ANOVAs revealed that, compared to the control group, the exercise group showed a significant reduction in self-reported test anxiety. Behaviorally, exercise led to significantly faster reaction times across both congruent and incongruent trials, coupled with a specific reduction in the Flanker conflict effect (RT difference between conditions), indicating enhanced interference control. Electrophysiologically, analysis of event-related potentials demonstrated that acute exercise modulated key cognitive components: N2 amplitude was significantly reduced and P3 amplitude was significantly enhanced in both task conditions following exercise, with no comparable changes in the control group. These findings suggest that acute aerobic exercise can enhance inhibitory control and alleviate test anxiety in university students.
{"title":"Acute aerobic exercise improves inhibitory control in individuals with test anxiety: evidence from event-related potentials.","authors":"Lingfeng Wu, Renlai Zhou","doi":"10.1016/j.physbeh.2026.115250","DOIUrl":"10.1016/j.physbeh.2026.115250","url":null,"abstract":"<p><p>It remains unclear whether acute aerobic exercise can effectively mitigate the inhibitory control deficits caused by test anxiety. This study investigated the effects of 30 min of moderate-intensity acute aerobic exercise on inhibitory control and related neural activities in individuals with high test anxiety. Forty participants were randomly assigned to an aerobic exercise group or a seated-reading control group, completing pre- and post-intervention assessments spaced one week apart. Statistical analyses using a series of repeated-measures ANOVAs revealed that, compared to the control group, the exercise group showed a significant reduction in self-reported test anxiety. Behaviorally, exercise led to significantly faster reaction times across both congruent and incongruent trials, coupled with a specific reduction in the Flanker conflict effect (RT difference between conditions), indicating enhanced interference control. Electrophysiologically, analysis of event-related potentials demonstrated that acute exercise modulated key cognitive components: N2 amplitude was significantly reduced and P3 amplitude was significantly enhanced in both task conditions following exercise, with no comparable changes in the control group. These findings suggest that acute aerobic exercise can enhance inhibitory control and alleviate test anxiety in university students.</p>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":" ","pages":"115250"},"PeriodicalIF":2.5,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146132838","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 : 2026-02-03DOI: 10.1016/j.physbeh.2026.115249
Ailyn Luna-Hernández, Raymundo Domínguez-Ordóñez, Marcos García-Juárez, José Luis Encarnación Sánchez, José Luis Tlachi-López, James G Pfaus, Oscar González-Flores
The present study aimed to determine whether apelin-13 facilitates lordosis behavior through the activation of specific hypothalamic kinases and to identify which signaling pathways mediate this response. Because lordosis is a well-established neuroendocrine indicator of female sexual receptivity, it served as an appropriate behavioral model to detect peptide-induced facilitation. Thus, we examined the role of protein kinase A (PKA), protein kinase C (PKC), mitogen activated protein kinase (MAPK), or Src kinase (Src), in the facilitation of lordosis behavior following bilateral intrahypothalamic injection of 0.75 μg of apelin-13 to ovariectomized-estradiol benzoate (OVX-EB) primed rats. Apelin-13 consistently induced lordosis at 30, 120, and 240 minutes post-infusion. To explore the role of these kinases, various inhibitors or their vehicles were administered bilaterally into the ventromedial hypothalamus (VMH) of OVX-EB-primed rats 30 min before the infusion of apelin-13. The inhibitors used were Rp-cAMPS for PKA, bisindolilmaleimide (BIS) for PKC, PD98059 for MAPK, and PP2 for Src. The VMH injection of Rp-cAMPS failed to reverse the facilitation of lordosis at the different times tested, while BIS or PP2 decreased the lordosis quotient (LQ) significantly only at 240 min without any statistical effect on the lordosis score (LS). However, PD98059 significantly reduced both the LQ and LS at 120 and 240 min. These data indicate that apelin-13 exerts its facilitatory effects on lordosis through MAPK, PKC, and/or Src, but not PKA pathways.
{"title":"Apelin-13 induces lordosis behavior in estradiol-primed ovariectomized rats via the activation of multiple protein kinases in the ventromedial hypothalamus.","authors":"Ailyn Luna-Hernández, Raymundo Domínguez-Ordóñez, Marcos García-Juárez, José Luis Encarnación Sánchez, José Luis Tlachi-López, James G Pfaus, Oscar González-Flores","doi":"10.1016/j.physbeh.2026.115249","DOIUrl":"https://doi.org/10.1016/j.physbeh.2026.115249","url":null,"abstract":"<p><p>The present study aimed to determine whether apelin-13 facilitates lordosis behavior through the activation of specific hypothalamic kinases and to identify which signaling pathways mediate this response. Because lordosis is a well-established neuroendocrine indicator of female sexual receptivity, it served as an appropriate behavioral model to detect peptide-induced facilitation. Thus, we examined the role of protein kinase A (PKA), protein kinase C (PKC), mitogen activated protein kinase (MAPK), or Src kinase (Src), in the facilitation of lordosis behavior following bilateral intrahypothalamic injection of 0.75 μg of apelin-13 to ovariectomized-estradiol benzoate (OVX-EB) primed rats. Apelin-13 consistently induced lordosis at 30, 120, and 240 minutes post-infusion. To explore the role of these kinases, various inhibitors or their vehicles were administered bilaterally into the ventromedial hypothalamus (VMH) of OVX-EB-primed rats 30 min before the infusion of apelin-13. The inhibitors used were Rp-cAMPS for PKA, bisindolilmaleimide (BIS) for PKC, PD98059 for MAPK, and PP2 for Src. The VMH injection of Rp-cAMPS failed to reverse the facilitation of lordosis at the different times tested, while BIS or PP2 decreased the lordosis quotient (LQ) significantly only at 240 min without any statistical effect on the lordosis score (LS). However, PD98059 significantly reduced both the LQ and LS at 120 and 240 min. These data indicate that apelin-13 exerts its facilitatory effects on lordosis through MAPK, PKC, and/or Src, but not PKA pathways.</p>","PeriodicalId":20201,"journal":{"name":"Physiology & Behavior","volume":" ","pages":"115249"},"PeriodicalIF":2.5,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146126200","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 : 2026-02-02DOI: 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 : 2026-01-23DOI: 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}