Pub Date : 2024-12-18DOI: 10.1016/j.bbr.2024.115403
Juan Balcazar , Joseph M. Orr
Cognitive flexibility, the brain’s ability to adjust to changes in the environment, is a critical component of executive functioning. Previous literature shows a robust relationship between reward dynamics and flexibility: flexibility is highest when reward changes, while flexibility decreases when reward remains stable. The purpose of this study was to examine the role of uncertain reward in a voluntary task switching paradigm on behavior, pupillometry, and eye gaze. We used pupil dilation as a neuropsychological correlate of arousal and accumulated fixations on a region (i.e. dwell time) to measure oculomotor attention capture. Results during the cue phase showed that pupil dilation under a deterministic, but not a stochastic reinforcement schedule tracked arousal from the magnitude of reward. In addition, dwell time was increased for the eventual choice and dwell-time was reduced under high reward. Taken together, results show that arousal and attentional capture by reward depends to some extent on reward certainty. Turning to reward outcome, pupil dilation was highest (and average dwell time was lowest) following Error feedback compared to correct rewarded feedback. Overall results show that uncertain reward cues may alter pupil-linked arousal and attention as compared to certain reward, highlighting the role of uncertainty as an important modulator affecting attention and reward processing in environments that demand cognitive flexibility.
{"title":"The role of uncertain reward in voluntary task-switching as revealed by pupillometry and gaze","authors":"Juan Balcazar , Joseph M. Orr","doi":"10.1016/j.bbr.2024.115403","DOIUrl":"10.1016/j.bbr.2024.115403","url":null,"abstract":"<div><div>Cognitive flexibility, the brain’s ability to adjust to changes in the environment, is a critical component of executive functioning. Previous literature shows a robust relationship between reward dynamics and flexibility: flexibility is highest when reward changes, while flexibility decreases when reward remains stable. The purpose of this study was to examine the role of uncertain reward in a voluntary task switching paradigm on behavior, pupillometry, and eye gaze. We used pupil dilation as a neuropsychological correlate of arousal and accumulated fixations on a region (i.e. dwell time) to measure oculomotor attention capture. Results during the cue phase showed that pupil dilation under a deterministic, but not a stochastic reinforcement schedule tracked arousal from the magnitude of reward. In addition, dwell time was increased for the eventual choice and dwell-time was reduced under high reward. Taken together, results show that arousal and attentional capture by reward depends to some extent on reward certainty. Turning to reward outcome, pupil dilation was highest (and average dwell time was lowest) following Error feedback compared to correct rewarded feedback. Overall results show that uncertain reward cues may alter pupil-linked arousal and attention as compared to certain reward, highlighting the role of uncertainty as an important modulator affecting attention and reward processing in environments that demand cognitive flexibility.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115403"},"PeriodicalIF":2.6,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The mechanisms governing food intake and appetite regulation in the brain are intricate and vary across different animal species. Dopamine and cholecystokinin (CCK) are recognized as two critical neurotransmitters involved in the control of food intake; however, the potential interactions between these neurotransmitters remain poorly understood. Consequently, this study aimed to investigate the interactions between central CCK and the dopaminergic system in the feeding behavior of layer-type chickens. In this experiment, birds were administered intracerebroventricular (ICV) injections of CCK4, CCK8, and CCK8s at doses of 0.25, 0.5, and 1 nmol, respectively. Additionally, various compounds were injected ICV, including L-DOPA (a dopamine precursor), 6-OHDA (a dopamine synthesis inhibitor), SCH 23390 (a D1 receptor antagonist), AMI-193 (a D2 receptor antagonist), NGB 2904 (a D3 receptor antagonist), and L-741,742 (a D4 receptor antagonist), either alone or in combination with CCK8s (1 nmol). The cumulative feed consumption was measured at 30, 60, and 120 minutes following the injections. The results indicated that ICV administration of CCK4 and CCK8 did not significantly influence feeding behavior (P ≥ 0.05). In contrast, CCK8s at a dose of 1 nmol resulted in a dose-dependent reduction in feed consumption (P < 0.05). Furthermore, SCH 23390 (5 nmol) and 6-OHDA (150 nmol) mitigated the inhibitory effect of CCK8s on feed consumption (P < 0.05), whereas NGB2904 (6.4 nmol), AMI-193 (5 nmol), and L-741,742 (6 nmol) did not exhibit significant effects (P ≥ 0.05). This study substantiates the involvement of D1 receptors in the hypophagic response induced by CCK8s in layer-type chickens.
{"title":"Interaction between central cholecystokinin and dopaminergic system in layer-type chickens' food intake","authors":"Mahshid Ebrahimnejad , Morteza Zendehdel , Vahab Babapour , Bita Vazir , Alireza Jahandideh","doi":"10.1016/j.bbr.2024.115383","DOIUrl":"10.1016/j.bbr.2024.115383","url":null,"abstract":"<div><div>The mechanisms governing food intake and appetite regulation in the brain are intricate and vary across different animal species. Dopamine and cholecystokinin (CCK) are recognized as two critical neurotransmitters involved in the control of food intake; however, the potential interactions between these neurotransmitters remain poorly understood. Consequently, this study aimed to investigate the interactions between central CCK and the dopaminergic system in the feeding behavior of layer-type chickens. In this experiment, birds were administered intracerebroventricular (ICV) injections of CCK4, CCK8, and CCK8s at doses of 0.25, 0.5, and 1 nmol, respectively. Additionally, various compounds were injected ICV, including L-DOPA (a dopamine precursor), 6-OHDA (a dopamine synthesis inhibitor), SCH 23390 (a D1 receptor antagonist), AMI-193 (a D2 receptor antagonist), NGB 2904 (a D3 receptor antagonist), and L-741,742 (a D4 receptor antagonist), either alone or in combination with CCK8s (1 nmol). The cumulative feed consumption was measured at 30, 60, and 120 minutes following the injections. The results indicated that ICV administration of CCK4 and CCK8 did not significantly influence feeding behavior (P ≥ 0.05). In contrast, CCK8s at a dose of 1 nmol resulted in a dose-dependent reduction in feed consumption (P < 0.05). Furthermore, SCH 23390 (5 nmol) and 6-OHDA (150 nmol) mitigated the inhibitory effect of CCK8s on feed consumption (P < 0.05), whereas NGB2904 (6.4 nmol), AMI-193 (5 nmol), and L-741,742 (6 nmol) did not exhibit significant effects (P ≥ 0.05). This study substantiates the involvement of D1 receptors in the hypophagic response induced by CCK8s in layer-type chickens.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115383"},"PeriodicalIF":2.6,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Antimuscarinic administration and food intake cause convulsions in mice and rats after fasting for 48 h or less. Increased M1 and M2 muscarinic receptor expression in brain regions during fasting, and reversal of changes by refeeding may contribute to these seizures. Since receptor expression is regulated in response to agonist stimulation, this study investigated effects of nonselective muscarinic receptor agonist oxotremorine on convulsions in fasted animals. Mice deprived of food for 24 h were given oxotremorine during (0.1 mg/kg, twice daily, s.c.) or after (0.05 or 0.1 mg/kg, i.p.) fasting. Fasted animals were treated with saline or scopolamine (i.p.) and observed for 30 min for the convulsions after being allowed to eat ad libitum. Oxotremorine administration during fasting produced no significant effect on convulsion development. Incidence and onset of convulsions, and seizure stages were indifferent between the scopolamine and oxotremorine - scopolamine groups. However, oxotremorine (0.1 mg/kg) administration after fasting reduced incidence of convulsions. Resulting from an agonist-antagonist interaction at M1 and/or M2 muscarinic receptors, oxotremorine administered after fasting exhibited an anticonvulsant activity. Oxotremorine administration during fasting was expected to suppress seizure development via inhibition of receptor expression. Results did not confirm this expectation and suggested that muscarinic receptor expression was either not affected or not related to the convulsions. Food intake after fasting, and food deprivation have been shown to induce cholinergic hyperexcitability. Although contrary to our hypothesis, future research may investigate whether increased expression of muscarinic receptors mediate or contribute to an increase in cholinergic activity.
{"title":"Effects of oxotremorine on convulsions in mice induced by scopolamine and food intake after fasting","authors":"Berna Midilli , Asiye Nurten , Başak Gürtekin , Nurhan Enginar","doi":"10.1016/j.bbr.2024.115402","DOIUrl":"10.1016/j.bbr.2024.115402","url":null,"abstract":"<div><div>Antimuscarinic administration and food intake cause convulsions in mice and rats after fasting for 48 h or less. Increased M<sub>1</sub> and M<sub>2</sub> muscarinic receptor expression in brain regions during fasting, and reversal of changes by refeeding may contribute to these seizures. Since receptor expression is regulated in response to agonist stimulation, this study investigated effects of nonselective muscarinic receptor agonist oxotremorine on convulsions in fasted animals. Mice deprived of food for 24 h were given oxotremorine during (0.1 mg/kg, twice daily, s.c.) or after (0.05 or 0.1 mg/kg, i.p.) fasting. Fasted animals were treated with saline or scopolamine (i.p.) and observed for 30 min for the convulsions after being allowed to eat <em>ad libitum</em>. Oxotremorine administration during fasting produced no significant effect on convulsion development. Incidence and onset of convulsions, and seizure stages were indifferent between the scopolamine and oxotremorine - scopolamine groups. However, oxotremorine (0.1 mg/kg) administration after fasting reduced incidence of convulsions. Resulting from an agonist-antagonist interaction at M<sub>1</sub> and/or M<sub>2</sub> muscarinic receptors, oxotremorine administered after fasting exhibited an anticonvulsant activity. Oxotremorine administration during fasting was expected to suppress seizure development via inhibition of receptor expression. Results did not confirm this expectation and suggested that muscarinic receptor expression was either not affected or not related to the convulsions. Food intake after fasting, and food deprivation have been shown to induce cholinergic hyperexcitability. Although contrary to our hypothesis, future research may investigate whether increased expression of muscarinic receptors mediate or contribute to an increase in cholinergic activity.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115402"},"PeriodicalIF":2.6,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142852305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-15DOI: 10.1016/j.bbr.2024.115396
Ruth Albert-Lyons, Stephanie S. Desrochers, Catherine Fengler, Katherine M. Nautiyal
Adolescence is a developmental period characterized by changes in the brain and behavior, including heightened reward seeking, increased impulsivity, and elevated risk-taking behavior. It is also a sensitive period for the development of a number of behavioral and psychiatric disorders associated with pathological phenotypes of reward processing and impulsivity. Landmark human studies are charting the development of impulsivity and other reward-related phenotypes to identify the facets and timecourse of the adolescent phenotype. Collecting similar data from mice is important to enable molecular, cellular, and circuit-level interrogation of adolescent maturation of reward, motivation, and impulsive behavior. These complex phenotypes have traditionally been difficult to assay in adolescent mice. Here, using a combination of approaches including homecage testing, we tested a number of facets of reward seeking, impulsivity, motivation, and incentive salience attribution during adolescent development. We found that adolescent mice show increased reward seeking, impulsive action, and motivation. Interestingly, we found no effect of adolescence on impulsive choice, sign-tracking, reward-learning, or conditioned reinforcement. Overall, our studies set the stage for approaches to study multi-faceted phenotypes related to impulsivity and other reward-related behaviors in adolescent mice to examine the developmental trajectories of brain and behavior.
{"title":"Fractionating impulsivity and reward-related phenotypes in adolescent mice","authors":"Ruth Albert-Lyons, Stephanie S. Desrochers, Catherine Fengler, Katherine M. Nautiyal","doi":"10.1016/j.bbr.2024.115396","DOIUrl":"10.1016/j.bbr.2024.115396","url":null,"abstract":"<div><div>Adolescence is a developmental period characterized by changes in the brain and behavior, including heightened reward seeking, increased impulsivity, and elevated risk-taking behavior. It is also a sensitive period for the development of a number of behavioral and psychiatric disorders associated with pathological phenotypes of reward processing and impulsivity. Landmark human studies are charting the development of impulsivity and other reward-related phenotypes to identify the facets and timecourse of the adolescent phenotype. Collecting similar data from mice is important to enable molecular, cellular, and circuit-level interrogation of adolescent maturation of reward, motivation, and impulsive behavior. These complex phenotypes have traditionally been difficult to assay in adolescent mice. Here, using a combination of approaches including homecage testing, we tested a number of facets of reward seeking, impulsivity, motivation, and incentive salience attribution during adolescent development. We found that adolescent mice show increased reward seeking, impulsive action, and motivation. Interestingly, we found no effect of adolescence on impulsive choice, sign-tracking, reward-learning, or conditioned reinforcement. Overall, our studies set the stage for approaches to study multi-faceted phenotypes related to impulsivity and other reward-related behaviors in adolescent mice to examine the developmental trajectories of brain and behavior.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115396"},"PeriodicalIF":2.6,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-15DOI: 10.1016/j.bbr.2024.115401
Myrela Ribeiro Teixeira , Tamara Silva , Rafaela de Freitas Martins Felício , Patrícia Torres Bozza , Verônica Marques Zembrzuski , Cicero Brasileiro de Mello Neto , Ana Carolina Proença da Fonseca , Fabiana Barzotto Kohlrausch , Kaio Cezar Rodrigues Salum
Obesity is a widespread global health concern that affects a significant portion of the population and is associated with reduced quality of life, morbidity, and mortality. It is considered a pandemic, with its prevalence constantly rising in Western countries. As a result, numerous studies have focused on understanding the elements that contribute to obesity. Researchers have focused on neurotransmitters in the brain to develop weight management drugs that regulate food intake. This review explores the literature on genetic influences on dopaminergic processes to determine whether genetic variation has an association with obesity in reward-responsive regions, including mesolimbic efferent and mesocortical areas. Various neurotransmitters play an essential role in regulating food intake, such as dopamine which controls through mesolimbic circuits in the brain that modulate food reward. Appetite stimulation, including primary reinforcers such as food, leads to an increase in dopamine release in the reward centers of the brain. This release is related to motivation and reinforcement, which determines the motivational weighting of the reinforcer. Changes in dopamine expression can lead to hedonic eating behaviors and contribute to the development of obesity. Genetic polymorphisms have been investigated due to their potential role in modulating the risk of obesity and eating behaviors. Therefore, it is crucial to assess the impact of genetic alterations that disrupt this pathway on the obesity phenotype.
{"title":"Exploring the genetic contribution in obesity: An overview of dopaminergic system genes","authors":"Myrela Ribeiro Teixeira , Tamara Silva , Rafaela de Freitas Martins Felício , Patrícia Torres Bozza , Verônica Marques Zembrzuski , Cicero Brasileiro de Mello Neto , Ana Carolina Proença da Fonseca , Fabiana Barzotto Kohlrausch , Kaio Cezar Rodrigues Salum","doi":"10.1016/j.bbr.2024.115401","DOIUrl":"10.1016/j.bbr.2024.115401","url":null,"abstract":"<div><div>Obesity is a widespread global health concern that affects a significant portion of the population and is associated with reduced quality of life, morbidity, and mortality. It is considered a pandemic, with its prevalence constantly rising in Western countries. As a result, numerous studies have focused on understanding the elements that contribute to obesity. Researchers have focused on neurotransmitters in the brain to develop weight management drugs that regulate food intake. This review explores the literature on genetic influences on dopaminergic processes to determine whether genetic variation has an association with obesity in reward-responsive regions, including mesolimbic efferent and mesocortical areas. Various neurotransmitters play an essential role in regulating food intake, such as dopamine which controls through mesolimbic circuits in the brain that modulate food reward. Appetite stimulation, including primary reinforcers such as food, leads to an increase in dopamine release in the reward centers of the brain. This release is related to motivation and reinforcement, which determines the motivational weighting of the reinforcer. Changes in dopamine expression can lead to hedonic eating behaviors and contribute to the development of obesity. Genetic polymorphisms have been investigated due to their potential role in modulating the risk of obesity and eating behaviors. Therefore, it is crucial to assess the impact of genetic alterations that disrupt this pathway on the obesity phenotype.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115401"},"PeriodicalIF":2.6,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-15DOI: 10.1016/j.bbr.2024.115400
Yichen Zhang , Yong’An Jiang , Hengyi Fan , Raorao Yuan , Jianhui Cai , Bo Zhong , Qian Qin , Zile Zhang , Yan Zhang , Shiqi Cheng
Background
An epidemiological association between anxiety and stroke is well-established; however, the role of shared genetic factors remain unclear. This study aimed to investigate the shared genetic architecture between anxiety and stroke.
Methods
Using public genome-wide association study (GWAS) summary statistics of anxiety and stroke, we performed linkage disequilibrium score regression and super genetic covariance analyzer for global and local genetic correlation studies. Risk single nucleotide polymorphisms (SNPs) were identified through genome-wide association meta-analysis, multi-trait analysis of GWAS and PLINK, followed by functional mapping and annotation. Additionally, we conducted transcriptome-wide association studies to explore the relationship between genes and associated disease risk.
Results
Our analysis revealed a significant genome-wide genetic correlation between anxiety and stroke. We also identified one previously unreported significant SNP (rs62099231), one risk loci, as well as identified three shared risk genes for anxiety and stroke (WDR6, CCDC71, NCKIPSD).
Conclusion
Our study demonstrated a shared genetic structure between anxiety and stroke, enhancing our understanding of their pathogenesis and highlighting potential therapeutic targets.
{"title":"Investigating the shared genetic architecture between anxiety and stroke","authors":"Yichen Zhang , Yong’An Jiang , Hengyi Fan , Raorao Yuan , Jianhui Cai , Bo Zhong , Qian Qin , Zile Zhang , Yan Zhang , Shiqi Cheng","doi":"10.1016/j.bbr.2024.115400","DOIUrl":"10.1016/j.bbr.2024.115400","url":null,"abstract":"<div><h3>Background</h3><div>An epidemiological association between anxiety and stroke is well-established; however, the role of shared genetic factors remain unclear. This study aimed to investigate the shared genetic architecture between anxiety and stroke.</div></div><div><h3>Methods</h3><div>Using public genome-wide association study (GWAS) summary statistics of anxiety and stroke, we performed linkage disequilibrium score regression and super genetic covariance analyzer for global and local genetic correlation studies. Risk single nucleotide polymorphisms (SNPs) were identified through genome-wide association meta-analysis, multi-trait analysis of GWAS and PLINK, followed by functional mapping and annotation. Additionally, we conducted transcriptome-wide association studies to explore the relationship between genes and associated disease risk.</div></div><div><h3>Results</h3><div>Our analysis revealed a significant genome-wide genetic correlation between anxiety and stroke. We also identified one previously unreported significant SNP (rs62099231), one risk loci, as well as identified three shared risk genes for anxiety and stroke (<em>WDR6, CCDC71, NCKIPSD</em>).</div></div><div><h3>Conclusion</h3><div>Our study demonstrated a shared genetic structure between anxiety and stroke, enhancing our understanding of their pathogenesis and highlighting potential therapeutic targets.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115400"},"PeriodicalIF":2.6,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-13DOI: 10.1016/j.bbr.2024.115399
Shakiba Salarvandian , Hadi Digaleh , Fariba Khodagholi , Pegah Javadpour , Sareh Asadi , Amir Ali Orang Zaman , Leila Dargahi
In recent years, glutamate has attracted significant attention for its roles in various brain processes. However, one of its key regulators, glutamate dehydrogenase (GDH), remains understudied despite its pivotal role in several biochemical pathways. Dysfunction or dysregulation of GDH has been implicated in aging and various neurological disorders, such as Alzheimer's disease and Parkinson's disease. In this review, the impact of GDH on aging, cognitive impairment, and neurodegenerative conditions, as exemplars of the phenomena that may affected by neuroplasticity, has been reviewed. Despite extensive research on synaptic plasticity, the precise influence of GDH on brain structure and function remains undiscovered. This review of existing literature on GDH and neuroplasticity reveals diverse and occasionally conflicting effects. Future research endeavors should aim to describe the precise mechanisms by which GDH influences neuroplasticity (eg. synaptic plasticity and neurogenesis), particularly in the context of human aging and disease progression. Studies on GDH activity have been limited by factors such as insufficient sample sizes and varying experimental conditions. Researchers should focus on investigating the molecular mechanisms by which GDH modulates neuroplasticity, utilizing various animal strains and species, ages, sexes, GDH isoforms, brain regions, and cell types. Understanding GDH's role in neuroplasticity may offer innovative therapeutic strategies for neurodegenerative and psychiatric diseases, potentially slowing the aging process and promoting brain regeneration.
{"title":"Harmonic activity of glutamate dehydrogenase and neuroplasticity: The impact on aging, cognitive dysfunction, and neurodegeneration","authors":"Shakiba Salarvandian , Hadi Digaleh , Fariba Khodagholi , Pegah Javadpour , Sareh Asadi , Amir Ali Orang Zaman , Leila Dargahi","doi":"10.1016/j.bbr.2024.115399","DOIUrl":"10.1016/j.bbr.2024.115399","url":null,"abstract":"<div><div>In recent years, glutamate has attracted significant attention for its roles in various brain processes. However, one of its key regulators, glutamate dehydrogenase (GDH), remains understudied despite its pivotal role in several biochemical pathways. Dysfunction or dysregulation of GDH has been implicated in aging and various neurological disorders, such as Alzheimer's disease and Parkinson's disease. In this review, the impact of GDH on aging, cognitive impairment, and neurodegenerative conditions, as exemplars of the phenomena that may affected by neuroplasticity, has been reviewed. Despite extensive research on synaptic plasticity, the precise influence of GDH on brain structure and function remains undiscovered. This review of existing literature on GDH and neuroplasticity reveals diverse and occasionally conflicting effects. Future research endeavors should aim to describe the precise mechanisms by which GDH influences neuroplasticity (eg. synaptic plasticity and neurogenesis), particularly in the context of human aging and disease progression. Studies on GDH activity have been limited by factors such as insufficient sample sizes and varying experimental conditions. Researchers should focus on investigating the molecular mechanisms by which GDH modulates neuroplasticity, utilizing various animal strains and species, ages, sexes, GDH isoforms, brain regions, and cell types. Understanding GDH's role in neuroplasticity may offer innovative therapeutic strategies for neurodegenerative and psychiatric diseases, potentially slowing the aging process and promoting brain regeneration.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115399"},"PeriodicalIF":2.6,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-12DOI: 10.1016/j.bbr.2024.115397
Jackson E. Onuelu , Benneth Ben-Azu , Olusegun G. Adebayo , Aliance R. Fokoua , Miracle K. Nekabari , Esther O. Ozah , Prosper Iwhiwhu , Abayomi M. Ajayi , Obukohwo M. Oyovwi , Itiviere A. Omogbiy , Anthony T. Eduviere , Matthew O. Ojezele
Reducing antioxidant levels exacerbates the generation of reactive oxygen/nitrogen species, leading to alpha-synuclein aggregation and the degeneration of dopaminergic neurons. These play a key role in the onset of Parkinson’s disease (PD), for which effective treatment remains elusive. This study examined the neuroprotective effects of taurine, an essential β-amino acid with antioxidant and antiinflammation properties, in Swiss male mice exposed to rotenone-induced PD. Mice (20–25 g) were grouped into seven groups (n = 9) and treated with taurine alone (5, 10 and 20 mg/kg, p.o) or levodopa (10 mg/kg, p.o) for 28 consecutive days following intraperitoneal co-administration of rotenone (1.5 mg/kg, in 5 % dimethylsulfoxide) for 14 alternate days. Open-field, rota-rod and hanging-wire motor performance and coordination tests were conducted on days 26–28. Oxidative stress and neuroinflammatory markers; levels of acetylcholinesterase enzyme activity, dopamine, and alpha-synuclein were assayed in the striatal and prefrontal-cortical regions alongside histological examinations. Rotenone significantly reduced latency to fall and akinesia-like behavior with several slip/error relative to vehicle groups. Taurine increased the latency to fall, notably improving motor coordination, locomotor deficit, and neuromuscular competence. Also, rotenone significantly increased malondialdehyde and nitrite; while decreasing acetylcholinesterase activity, glutathione, catalase, superoxide-dismutase, and glutathione-S-transferase levels in the striatum and prefrontal-cortex respectively, which were attenuated by taurine. Taurine increased dopamine levels in the striatum and prefrontal cortex dose-independently. Like carbidopa, taurine decreased alpha-synuclein, tumor-necrosis factor-α and interleukin-6 levels in the striatum and prefrontal-cortex. Additionally, taurine-reversed rotenone-induced neurodegeneration in the striatum and prefrontal cortex indicates neuroprotective function. Conclusively, taurine attenuates rotenone-induced PD-like behavior by enhancing the brain's antioxidant system, inhibiting pro-inflammatory cytokine release, reducing α-synuclein formation, and augmenting dopaminergic release in mice's brains.
{"title":"Taurine, an essential amino acid, attenuates rotenone-induced Parkinson’s disease in rats by inhibiting alpha-synuclein aggregation and augmenting dopamine release","authors":"Jackson E. Onuelu , Benneth Ben-Azu , Olusegun G. Adebayo , Aliance R. Fokoua , Miracle K. Nekabari , Esther O. Ozah , Prosper Iwhiwhu , Abayomi M. Ajayi , Obukohwo M. Oyovwi , Itiviere A. Omogbiy , Anthony T. Eduviere , Matthew O. Ojezele","doi":"10.1016/j.bbr.2024.115397","DOIUrl":"10.1016/j.bbr.2024.115397","url":null,"abstract":"<div><div>Reducing antioxidant levels exacerbates the generation of reactive oxygen/nitrogen species, leading to alpha-synuclein aggregation and the degeneration of dopaminergic neurons. These play a key role in the onset of Parkinson’s disease (PD), for which effective treatment remains elusive. This study examined the neuroprotective effects of taurine, an essential β-amino acid with antioxidant and antiinflammation properties, in Swiss male mice exposed to rotenone-induced PD. Mice (20–25 g) were grouped into seven groups (n = 9) and treated with taurine alone (5, 10 and 20 mg/kg, <em>p.o</em>) or levodopa (10 mg/kg, <em>p.o</em>) for 28 consecutive days following intraperitoneal co-administration of rotenone (1.5 mg/kg, in 5 % dimethylsulfoxide) for 14 alternate days. Open-field, rota-rod and hanging-wire motor performance and coordination tests were conducted on days 26–28. Oxidative stress and neuroinflammatory markers; levels of acetylcholinesterase enzyme activity, dopamine, and alpha-synuclein were assayed in the striatal and prefrontal-cortical regions alongside histological examinations. Rotenone significantly reduced latency to fall and akinesia-like behavior with several slip/error relative to vehicle groups. Taurine increased the latency to fall, notably improving motor coordination, locomotor deficit, and neuromuscular competence. Also, rotenone significantly increased malondialdehyde and nitrite; while decreasing acetylcholinesterase activity, glutathione, catalase, superoxide-dismutase, and glutathione-S-transferase levels in the striatum and prefrontal-cortex respectively, which were attenuated by taurine. Taurine increased dopamine levels in the striatum and prefrontal cortex dose-independently. Like carbidopa, taurine decreased alpha-synuclein, tumor-necrosis factor-α and interleukin-6 levels in the striatum and prefrontal-cortex. Additionally, taurine-reversed rotenone-induced neurodegeneration in the striatum and prefrontal cortex indicates neuroprotective function. Conclusively, taurine attenuates rotenone-induced PD-like behavior by enhancing the brain's antioxidant system, inhibiting pro-inflammatory cytokine release, reducing α-synuclein formation, and augmenting dopaminergic release in mice's brains.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115397"},"PeriodicalIF":2.6,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Visual stimulation to the embodied virtual body could modulate human perception, however the associated neurophysiological mechanisms have not elucidated yet. The present study aimed to reveal the underlying neurophysiological mechanisms from a neurophysiological viewpoint. Fifteen healthy participants were subjected to three visual conditions (i.e., fire, water, and non-visual effect conditions) and psychological pain stimulation (thermal grill stimulation). Oscillatory neural activities during stimulation were measured with electroencephalogram. The association between accessory visual stimulation applied to the embodied virtual body, induced by virtual reality, and perception was examined through neuronal oscillatory analysis using electroencephalogram data. Regression analysis was performed to obtain data on brain regions contributing to sensory modulation with body illusion. The results of subjective measures under the fire and water conditions showed that thermal perception were modulated by a visual stimulus to the virtual hand. Furthermore, we found that the insula was commonly associated with thermal perception under the fire and water conditions. This result indicate that the insula may control sensory information as a gatekeeper as well as facilitate the access to human attention and cognition as a hub, suggesting the influence on perception and cognition.
{"title":"Modulation of thermal perception by VR-based visual stimulation to the embodied virtual body","authors":"Yuhi Takeo , Masayuki Hara , Naofumi Otsuru , Takeru Taihei , Ryushin Kawasoe , Hisato Sugata","doi":"10.1016/j.bbr.2024.115395","DOIUrl":"10.1016/j.bbr.2024.115395","url":null,"abstract":"<div><div>Visual stimulation to the embodied virtual body could modulate human perception, however the associated neurophysiological mechanisms have not elucidated yet. The present study aimed to reveal the underlying neurophysiological mechanisms from a neurophysiological viewpoint. Fifteen healthy participants were subjected to three visual conditions (i.e., fire, water, and non-visual effect conditions) and psychological pain stimulation (thermal grill stimulation). Oscillatory neural activities during stimulation were measured with electroencephalogram. The association between accessory visual stimulation applied to the embodied virtual body, induced by virtual reality, and perception was examined through neuronal oscillatory analysis using electroencephalogram data. Regression analysis was performed to obtain data on brain regions contributing to sensory modulation with body illusion. The results of subjective measures under the fire and water conditions showed that thermal perception were modulated by a visual stimulus to the virtual hand. Furthermore, we found that the insula was commonly associated with thermal perception under the fire and water conditions. This result indicate that the insula may control sensory information as a gatekeeper as well as facilitate the access to human attention and cognition as a hub, suggesting the influence on perception and cognition.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115395"},"PeriodicalIF":2.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-10DOI: 10.1016/j.bbr.2024.115393
Fabio Pilato , Davide Norata , Maria Grazia Rossi , Vincenzo Di Lazzaro , Rosalinda Calandrelli
In patients with chronic kidney disease, particularly those in end-stage kidney failure and undergoing dialysis treatment, brain complications may arise, and their potential reversibility mainly hinges on timely diagnosis and intervention. Neurological symptoms may be non-specific ranging from slight or pronounced consciousness disturbance till coma, and imaging is the main tool to guide diagnosis and may reveal the underlying pathophysiological mechanism. Kidney impairment, causing a surge in blood pressure, increases the risk of Posterior Reversible Encephalopathy Syndrome and, leads to neurochemical alterations that result in uremic encephalopathy. In end-stage kidney failure patients, Posterior Reversible Encephalopathy Syndrome predominantly occurs in atypical locations, often involving the bilateral basal ganglia, and exhibit larger volumes compared to patients without kidney dysfunction. Uremic encephalopathy may involve the basal ganglia, white matter, and cortical or subcortical regions; in the latter case, imaging features resemble the typical location of Posterior Reversible Encephalopathy Syndrome. Dialysis Disequilibrium Syndrome, Osmotic Demyelination Syndrome, and Wernicke’s encephalopathy are uncommon complications associated with dialysis. Each syndrome manifests distinct imaging patterns: Dialysis Disequilibrium Syndrome shows bilateral, patchy, diffuse white matter alterations; Osmotic Demyelination Syndrome causes central pontine and less often extrapontine lesions (involving bilateral basal ganglia, thalamus, and cerebral peduncles); Wernicke’s encephalopathy determines symmetrical abnormalities in the thalamus, mammillary bodies, periaqueductal gray matter, midbrain tectal plate but the nature of brain edema associated with these complications remains controversial. Besides, in rare cases, overlapping imaging features may occur, and only the accurate patient's clinical history reconstruction along with laboratory examination results can lead to a better evaluation of MRI findings and underlying causes allowing prompt therapy.
{"title":"Consciousness disturbance in patients with chronic kidney disease: Rare but potentially treatable complication. Clinical and neuroradiological review","authors":"Fabio Pilato , Davide Norata , Maria Grazia Rossi , Vincenzo Di Lazzaro , Rosalinda Calandrelli","doi":"10.1016/j.bbr.2024.115393","DOIUrl":"10.1016/j.bbr.2024.115393","url":null,"abstract":"<div><div>In patients with chronic kidney disease, particularly those in end-stage kidney failure and undergoing dialysis treatment, brain complications may arise, and their potential reversibility mainly hinges on timely diagnosis and intervention. Neurological symptoms may be non-specific ranging from slight or pronounced consciousness disturbance till coma, and imaging is the main tool to guide diagnosis and may reveal the underlying pathophysiological mechanism. Kidney impairment, causing a surge in blood pressure, increases the risk of Posterior Reversible Encephalopathy Syndrome and, leads to neurochemical alterations that result in uremic encephalopathy. In end-stage kidney failure patients, Posterior Reversible Encephalopathy Syndrome predominantly occurs in atypical locations, often involving the bilateral basal ganglia, and exhibit larger volumes compared to patients without kidney dysfunction. Uremic encephalopathy may involve the basal ganglia, white matter, and cortical or subcortical regions; in the latter case, imaging features resemble the typical location of Posterior Reversible Encephalopathy Syndrome. Dialysis Disequilibrium Syndrome, Osmotic Demyelination Syndrome, and Wernicke’s encephalopathy are uncommon complications associated with dialysis. Each syndrome manifests distinct imaging patterns: Dialysis Disequilibrium Syndrome shows bilateral, patchy, diffuse white matter alterations; Osmotic Demyelination Syndrome causes central pontine and less often extrapontine lesions (involving bilateral basal ganglia, thalamus, and cerebral peduncles); Wernicke’s encephalopathy determines symmetrical abnormalities in the thalamus, mammillary bodies, periaqueductal gray matter, midbrain tectal plate but the nature of brain edema associated with these complications remains controversial. Besides, in rare cases, overlapping imaging features may occur, and only the accurate patient's clinical history reconstruction along with laboratory examination results can lead to a better evaluation of MRI findings and underlying causes allowing prompt therapy.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"480 ","pages":"Article 115393"},"PeriodicalIF":2.6,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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