Pub Date : 2025-02-28DOI: 10.1016/j.bbr.2025.115518
Amir Erfanparast, Esmaeal Tamaddonfard, Sina Tamaddonfard, Behzad Firooznia, Ali Hatami-Marandi
The hippocampus is well recognized for its significant contributions to learning, memory formation, and emotional regulation. In addition, it was approved by several studies that hippocampus plays a pivotal role in pain modulation; however, the exact mechanism has not yet been identified. In the current research, effects of microinjection of muscarinic M1 cholinergic agents into the CA1 region of the hippocampus in orofacial nociception evoked by formalin and corresponding memory impairment were investigated. Left and right sides of the hippocampus were implanted by guide cannulas. Orofacial nociception was elicited through subcutaneously injection of formalin (1.5 %) solution into the pad of vibrissa region. Evaluating memory was conducted with Morris water maze (MWM). Microinjections of McN-A-343 (a selective agonist of muscarinic M1 receptors) attenuated the both phases of orofacial nociceptive behavior, face rubbing. This effect of McN-A-343 was blocked by prior microinjection of pirenzepine (an antagonist of muscarinic receptors). On the other hand, McN-A-343 and pirenzepine increased and decreased traveled time as well as traveled distance in target zone of MWM, respectively. Additionally, McN-A-343 improved the memory deficits caused by orofacial nociception. Our results indicate that muscarinic acetylcholine receptors contribute significantly in the hippocampal modulation of orofacial nociception and related memory impairment.
{"title":"Muscarinic cholinergic system of the dorsal hippocampus involvement in the modulation of formalin-induced orofacial nociception and relevant memory impairment in rats","authors":"Amir Erfanparast, Esmaeal Tamaddonfard, Sina Tamaddonfard, Behzad Firooznia, Ali Hatami-Marandi","doi":"10.1016/j.bbr.2025.115518","DOIUrl":"10.1016/j.bbr.2025.115518","url":null,"abstract":"<div><div>The hippocampus is well recognized for its significant contributions to learning, memory formation, and emotional regulation. In addition, it was approved by several studies that hippocampus plays a pivotal role in pain modulation; however, the exact mechanism has not yet been identified. In the current research, effects of microinjection of muscarinic M<sub>1</sub> cholinergic agents into the CA1 region of the hippocampus in orofacial nociception evoked by formalin and corresponding memory impairment were investigated. Left and right sides of the hippocampus were implanted by guide cannulas. Orofacial nociception was elicited through subcutaneously injection of formalin (1.5 %) solution into the pad of vibrissa region. Evaluating memory was conducted with Morris water maze (MWM). Microinjections of McN-A-343 (a selective agonist of muscarinic M<sub>1</sub> receptors) attenuated the both phases of orofacial nociceptive behavior, face rubbing. This effect of McN-A-343 was blocked by prior microinjection of pirenzepine (an antagonist of muscarinic receptors). On the other hand, McN-A-343 and pirenzepine increased and decreased traveled time as well as traveled distance in target zone of MWM, respectively. Additionally, McN-A-343 improved the memory deficits caused by orofacial nociception. Our results indicate that muscarinic acetylcholine receptors contribute significantly in the hippocampal modulation of orofacial nociception and related memory impairment.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"484 ","pages":"Article 115518"},"PeriodicalIF":2.6,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143526744","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 : 2025-02-26DOI: 10.1016/j.bbr.2025.115495
Ruiling Li , Yuhui Zhang , Honghan Zhang , Chao Wang , Hao Duan , Siqi Sun , Dan Xiang , Zhongchun Liu
Major depressive disorder (MDD) is a prevalent psychiatric illness and a significant contributor to the global burden of disease. However, the molecular mechanisms underlying depression are complex and have yet to be fully elucidated. Previous studies demonstrated that collapsin response mediator protein 2 (CRMP2) involved in the onset of depression, but its role is unclear yet. To explore the mechanism of CRMP2 in depression and whether it ameliorates depressive-like behaviours by modulating synaptic functions, we manipulate the expression of CRMP2 by adeno-associated virus (AAV) injected into the hippocampal CA1 region and then induced depressive-like behaviour by subjecting the mice to chronic unpredictable mild stress (CUMS). Sucrose preference test (SPT), open field test (OFT), elevated plus maze test (EPM), forced swimming test (FST), and tail suspension test (TST) are utilized to detect behavioral changes. Golgi-Cox staining and electron microscopy were applied to examine alterations in the structure and morphology of neural synapses. Synaptophysin (SYP), synaptophysin 1 (SYN1), growth-associated protein 43 (GAP43), glutamate receptor 2 (GLUR2) and postsynaptic density protein 95 (PSD95) is tested for synaptic function. The proteins interacting with CRMP2 were comprehensively investigated utilizing Immunoprecipitation-Mass Spectrometry (IP-MS) analysis and the direct binding between CRMP2 and PSD95 was validated. In our study, we observed CRMP2 in the hippocampal CA1 region was downregulated following CUMS. Knockdown of CRMP2 resulted in impaired synaptic structure and decreased expression of synapse-associated proteins, accompanied by increased depressive-like behaviour, like anhedonia and hopelessness. Conversely, overexpression of CRMP2 significantly ameliorated behavioural deficits associated with depression and restore the compromised synaptic structure and function. Our findings suggest that CRMP2 exerts a crucial function in modulating depressive-like behaviours by influencing the synaptic structure and function, and it can directly interact with PSD95.
{"title":"CRMP2 in the hippocampus alleviates chronic stress-induced depressive-like behaviours in mice by affecting synaptic function","authors":"Ruiling Li , Yuhui Zhang , Honghan Zhang , Chao Wang , Hao Duan , Siqi Sun , Dan Xiang , Zhongchun Liu","doi":"10.1016/j.bbr.2025.115495","DOIUrl":"10.1016/j.bbr.2025.115495","url":null,"abstract":"<div><div>Major depressive disorder (MDD) is a prevalent psychiatric illness and a significant contributor to the global burden of disease. However, the molecular mechanisms underlying depression are complex and have yet to be fully elucidated. Previous studies demonstrated that collapsin response mediator protein 2 (CRMP2) involved in the onset of depression, but its role is unclear yet. To explore the mechanism of CRMP2 in depression and whether it ameliorates depressive-like behaviours by modulating synaptic functions, we manipulate the expression of CRMP2 by adeno-associated virus (AAV) injected into the hippocampal CA1 region and then induced depressive-like behaviour by subjecting the mice to chronic unpredictable mild stress (CUMS). Sucrose preference test (SPT), open field test (OFT), elevated plus maze test (EPM), forced swimming test (FST), and tail suspension test (TST) are utilized to detect behavioral changes. Golgi-Cox staining and electron microscopy were applied to examine alterations in the structure and morphology of neural synapses. Synaptophysin (SYP), synaptophysin 1 (SYN1), growth-associated protein 43 (GAP43), glutamate receptor 2 (GLUR2) and postsynaptic density protein 95 (PSD95) is tested for synaptic function. The proteins interacting with CRMP2 were comprehensively investigated utilizing Immunoprecipitation-Mass Spectrometry (IP-MS) analysis and the direct binding between CRMP2 and PSD95 was validated. In our study, we observed CRMP2 in the hippocampal CA1 region was downregulated following CUMS. Knockdown of CRMP2 resulted in impaired synaptic structure and decreased expression of synapse-associated proteins, accompanied by increased depressive-like behaviour, like anhedonia and hopelessness. Conversely, overexpression of CRMP2 significantly ameliorated behavioural deficits associated with depression and restore the compromised synaptic structure and function. Our findings suggest that CRMP2 exerts a crucial function in modulating depressive-like behaviours by influencing the synaptic structure and function, and it can directly interact with PSD95.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"484 ","pages":"Article 115495"},"PeriodicalIF":2.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143526745","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 : 2025-02-25DOI: 10.1016/j.bbr.2025.115494
Beenish Asrar, Mohammad Hassam, Sidra Rafi, Ikram Ullah, Judith R Homberg, Darakhshan Jabeen Haleem
Background: Chronic alcohol drinking changes central serotonin and dopamine levels, and thereby the functioning of brain circuits that support cognition and anxiety. Previously, it has been proven that Nigella sativa oil (NSO) improves cognition and reduces anxiety by regulating the neurotransmission but the underlying mechanisms are unknown.
Methods: To address the knowledge gap, an in vivo experiment was done to investigate effects of NSO on behavior and neurotransmission in alcohol (ethanol) drinking rats. Specifically, water control, water + NSO treated, ethanol control and ethanol + NSO treated rats were tested for changes in anxiety-like behavior, locomotor activity and learning and memory using the elevated plus-maze test (EPM) and light and dark box (L&D) test, open field test (OFT) and Morris water maze (MWM) test, respectively. Brain neurotransmitter concentrations were determined using HPLC-EC. To validate the in vivo findings, we assessed in silico the docking between NSO compounds and proteins using auto dock vina.
Key findings: Ethanol and NSO reduced weight in the ethanol and ethanol + NSO groups. Food intake, fluid consumption, calorie intake, and growth were similarly affected by ethanol and NSO. In the in vivo experiments, ethanol-treated rats spent less time in the open arms of the EPM and had fewer entries compared to controls, while ethanol + NSO also showed reduced entries. Similar patterns were observed in the OFT. No differences were found in the L&D box test. In the memory tests, ethanol + NSO increased latency in short-term memory, while ethanol increased latency in retention. Neurochemical analysis revealed that ethanol + NSO increased serotonin levels in the PFC and hippocampus while reducing dopamine levels in the PFC compared to all groups, and in the hippocampus compared to control and NSO groups. The in silico experiment revealed that NSO has nine main active compounds. By molecular docking, we found that all nine compounds showed good binding affinity with our target proteins but the best docking values were obtained with thymoquinone and dithymoquinone. The binding affinity estimations identified the superior binding affinity and efficiency of dithymoquinone over all nine NSO compounds for serotonin, dopamine receptors and MAO-enzymes.
Conclusions and significance: NSO partially modulated ethanol-induced neurobehavioral and neurochemical alterations, improving serotonin levels but not fully reversing behavioral deficits. Further studies are needed to explore its protective potential.
{"title":"Nigella sativa Oil Modulates Neurobehavioral and Neurochemical Alterations in Alcohol-Exposed Rats: An In Vivo and In Silico Study.","authors":"Beenish Asrar, Mohammad Hassam, Sidra Rafi, Ikram Ullah, Judith R Homberg, Darakhshan Jabeen Haleem","doi":"10.1016/j.bbr.2025.115494","DOIUrl":"https://doi.org/10.1016/j.bbr.2025.115494","url":null,"abstract":"<p><strong>Background: </strong>Chronic alcohol drinking changes central serotonin and dopamine levels, and thereby the functioning of brain circuits that support cognition and anxiety. Previously, it has been proven that Nigella sativa oil (NSO) improves cognition and reduces anxiety by regulating the neurotransmission but the underlying mechanisms are unknown.</p><p><strong>Methods: </strong>To address the knowledge gap, an in vivo experiment was done to investigate effects of NSO on behavior and neurotransmission in alcohol (ethanol) drinking rats. Specifically, water control, water + NSO treated, ethanol control and ethanol + NSO treated rats were tested for changes in anxiety-like behavior, locomotor activity and learning and memory using the elevated plus-maze test (EPM) and light and dark box (L&D) test, open field test (OFT) and Morris water maze (MWM) test, respectively. Brain neurotransmitter concentrations were determined using HPLC-EC. To validate the in vivo findings, we assessed in silico the docking between NSO compounds and proteins using auto dock vina.</p><p><strong>Key findings: </strong>Ethanol and NSO reduced weight in the ethanol and ethanol + NSO groups. Food intake, fluid consumption, calorie intake, and growth were similarly affected by ethanol and NSO. In the in vivo experiments, ethanol-treated rats spent less time in the open arms of the EPM and had fewer entries compared to controls, while ethanol + NSO also showed reduced entries. Similar patterns were observed in the OFT. No differences were found in the L&D box test. In the memory tests, ethanol + NSO increased latency in short-term memory, while ethanol increased latency in retention. Neurochemical analysis revealed that ethanol + NSO increased serotonin levels in the PFC and hippocampus while reducing dopamine levels in the PFC compared to all groups, and in the hippocampus compared to control and NSO groups. The in silico experiment revealed that NSO has nine main active compounds. By molecular docking, we found that all nine compounds showed good binding affinity with our target proteins but the best docking values were obtained with thymoquinone and dithymoquinone. The binding affinity estimations identified the superior binding affinity and efficiency of dithymoquinone over all nine NSO compounds for serotonin, dopamine receptors and MAO-enzymes.</p><p><strong>Conclusions and significance: </strong>NSO partially modulated ethanol-induced neurobehavioral and neurochemical alterations, improving serotonin levels but not fully reversing behavioral deficits. Further studies are needed to explore its protective potential.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"115494"},"PeriodicalIF":2.6,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522331","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 : 2025-02-25DOI: 10.1016/j.bbr.2025.115505
Vajinder Kaur, Aditya Sunkaria
Alzheimer's disease (AD) is a neurological disorder that affects cognition and behavior, accounting for 60–70 % of dementia cases. Its mechanisms involve amyloid aggregates, hyperphosphorylated tau tangles, and loss of neural connections. Current treatments have limited efficacy due to a lack of specific targets. Recently, microRNAs (miRNAs) have emerged as key modulators in AD, regulating gene expression through interactions with mRNA. Dysregulation of specific miRNAs contributes to disease progression by disrupting clearance pathways. Antisense oligonucleotide (ASO)-based therapies show promise for AD treatment, particularly when combined with miRNA mimics or antagonists, targeting complex regulatory networks. However, miRNAs can interact with each other, complicating cellular processes and potentially leading to side effects. Our review emphasizes the role of miRNAs in regulating amyloid-beta (Aβ) clearance and highlights their potential as therapeutic targets and early biomarkers for AD, underscoring the need for further research to enhance their efficacy and safety.
{"title":"Unlocking the therapeutic promise of miRNAs in promoting amyloid-β clearance for Alzheimer's disease","authors":"Vajinder Kaur, Aditya Sunkaria","doi":"10.1016/j.bbr.2025.115505","DOIUrl":"10.1016/j.bbr.2025.115505","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a neurological disorder that affects cognition and behavior, accounting for 60–70 % of dementia cases. Its mechanisms involve amyloid aggregates, hyperphosphorylated tau tangles, and loss of neural connections. Current treatments have limited efficacy due to a lack of specific targets. Recently, microRNAs (miRNAs) have emerged as key modulators in AD, regulating gene expression through interactions with mRNA. Dysregulation of specific miRNAs contributes to disease progression by disrupting clearance pathways. Antisense oligonucleotide (ASO)-based therapies show promise for AD treatment, particularly when combined with miRNA mimics or antagonists, targeting complex regulatory networks. However, miRNAs can interact with each other, complicating cellular processes and potentially leading to side effects. Our review emphasizes the role of miRNAs in regulating amyloid-beta (Aβ) clearance and highlights their potential as therapeutic targets and early biomarkers for AD, underscoring the need for further research to enhance their efficacy and safety.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"484 ","pages":"Article 115505"},"PeriodicalIF":2.6,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514482","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 : 2025-02-25DOI: 10.1016/j.bbr.2025.115515
Shuai Xu , Zi-Yu Zheng , Guang-Chao Zhao , Zhi-Hong Lu , Huang Nie , Xue-Jun Wang , Bin-Xiao Su , Cheng Jiang , Quan Li , Tao He , Tian-Yu Wei , Hao-Peng Zhang , Hai-Long Dong
The investigation of cognitive functions in response to high-altitude exposure has garnered increasing scientific interest. However, it remains unclear whether cognitive abilities are selectively impaired or what are the trends of the function. In this study, we examined the effects of acute exposure to 3800 m on cognition among 20 lowlanders (27.9 ± 3.08 years; 18 males) for 1 week. Cognitive functions, physiological parameters, various questionnaires, and electroencephalogram (EEG) data were assessed at 400 m (D0) and during the acute phase at 3800 m (D1, D2, D3, D5, D7). A control group consisting of 23 subjects (26.5 ± 3.17 years; 21 males) underwent identical assessments at 400 m. Our findings indicate that within two days following ascent to 3800 m, nearly all cognitive indicators exhibited impairment, but gradually improved from the 3rd day and largely recovered to the plain level on the 5th to 7th day. EEG frequency analysis also revealed significant alterations, relative power in the delta band decreased markedly by D7 compared with D0, while theta and alpha bands showed the opposite trends. Correlational analyses between EEG features and cognitive functions revealed that relative power in the delta band exhibited a negative correlation with most cognitive measures, while relative power in the theta and beta bands predominantly demonstrated positive correlations. We conclude that most cognitive functions exhibit a pattern characterized by initial decline followed by recovery at 3800 m—an observation closely linked to observed EEG changes. These findings provide valuable insights into cognitive function and EEG performance at high altitudes.
{"title":"The study on effects of acute exposure to high altitude hypoxia on cognitive function in lowlander","authors":"Shuai Xu , Zi-Yu Zheng , Guang-Chao Zhao , Zhi-Hong Lu , Huang Nie , Xue-Jun Wang , Bin-Xiao Su , Cheng Jiang , Quan Li , Tao He , Tian-Yu Wei , Hao-Peng Zhang , Hai-Long Dong","doi":"10.1016/j.bbr.2025.115515","DOIUrl":"10.1016/j.bbr.2025.115515","url":null,"abstract":"<div><div>The investigation of cognitive functions in response to high-altitude exposure has garnered increasing scientific interest. However, it remains unclear whether cognitive abilities are selectively impaired or what are the trends of the function. In this study, we examined the effects of acute exposure to 3800 m on cognition among 20 lowlanders (27.9 ± 3.08 years; 18 males) for 1 week. Cognitive functions, physiological parameters, various questionnaires, and electroencephalogram (EEG) data were assessed at 400 m (D0) and during the acute phase at 3800 m (D1, D2, D3, D5, D7). A control group consisting of 23 subjects (26.5 ± 3.17 years; 21 males) underwent identical assessments at 400 m. Our findings indicate that within two days following ascent to 3800 m, nearly all cognitive indicators exhibited impairment, but gradually improved from the 3rd day and largely recovered to the plain level on the 5th to 7th day. EEG frequency analysis also revealed significant alterations, relative power in the delta band decreased markedly by D7 compared with D0, while theta and alpha bands showed the opposite trends. Correlational analyses between EEG features and cognitive functions revealed that relative power in the delta band exhibited a negative correlation with most cognitive measures, while relative power in the theta and beta bands predominantly demonstrated positive correlations. We conclude that most cognitive functions exhibit a pattern characterized by initial decline followed by recovery at 3800 m—an observation closely linked to observed EEG changes. These findings provide valuable insights into cognitive function and EEG performance at high altitudes.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"484 ","pages":"Article 115515"},"PeriodicalIF":2.6,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514542","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 : 2025-02-25DOI: 10.1016/j.bbr.2025.115513
Ying Yang , Chen Yang , Changnan Guo , Li Mu
Sleep deprivation, both daily and occupational, has become a prevalent issue in modern society, significantly affecting individuals' attention functions. Traditionally, attention was viewed as a singular, unified system, but advances in neuroscience have revealed it as a network involving coordinated interactions across multiple brain regions. Posner and Petersen’s Attention Network Theory delineates three distinct subcomponents — alerting, orienting, and executive control — based on anatomical localization and neurobiochemical mechanisms. However, most studies on sleep deprivation often overlook these subcomponents, treating attention as a generalized process. This paper aims to address this gap by investigating the effects of total sleep deprivation (TSD) on these attentional subcomponents and their potential neural mechanisms focusing on both the general healthy population and specific occupational groups. Using the Attention Network Test (ANT) paradigm and its variants, the findings reveal that TSD differentially affects the three subcomponents of attentional networks, with occupation-specific differences. Notably, the impact of TSD on executive control exhibits greater variability. The state instability hypothesis and local sleep theory are proposed to explain these neural mechanisms, suggesting that TSD disrupts attentional networks through an interplay of top-down state instability and bottom-up local sleep processes. Future research should refine experimental paradigms related to attentional networks, integrate cognitive neuroscience methodologies and computational modeling approaches, and expand investigations into sleep restriction. Such advancements will provide a more comprehensive understanding of how TSD affects attentional networks and further elucidate the interplay between the state instability hypothesis and local sleep theory.
{"title":"The impact of total sleep deprivation on attentional networks and its neural mechanisms: Based on the Attention Network Test","authors":"Ying Yang , Chen Yang , Changnan Guo , Li Mu","doi":"10.1016/j.bbr.2025.115513","DOIUrl":"10.1016/j.bbr.2025.115513","url":null,"abstract":"<div><div>Sleep deprivation, both daily and occupational, has become a prevalent issue in modern society, significantly affecting individuals' attention functions. Traditionally, attention was viewed as a singular, unified system, but advances in neuroscience have revealed it as a network involving coordinated interactions across multiple brain regions. Posner and Petersen’s Attention Network Theory delineates three distinct subcomponents — alerting, orienting, and executive control — based on anatomical localization and neurobiochemical mechanisms. However, most studies on sleep deprivation often overlook these subcomponents, treating attention as a generalized process. This paper aims to address this gap by investigating the effects of total sleep deprivation (TSD) on these attentional subcomponents and their potential neural mechanisms focusing on both the general healthy population and specific occupational groups. Using the Attention Network Test (ANT) paradigm and its variants, the findings reveal that TSD differentially affects the three subcomponents of attentional networks, with occupation-specific differences. Notably, the impact of TSD on executive control exhibits greater variability. The state instability hypothesis and local sleep theory are proposed to explain these neural mechanisms, suggesting that TSD disrupts attentional networks through an interplay of top-down state instability and bottom-up local sleep processes. Future research should refine experimental paradigms related to attentional networks, integrate cognitive neuroscience methodologies and computational modeling approaches, and expand investigations into sleep restriction. Such advancements will provide a more comprehensive understanding of how TSD affects attentional networks and further elucidate the interplay between the state instability hypothesis and local sleep theory.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"484 ","pages":"Article 115513"},"PeriodicalIF":2.6,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522339","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 : 2025-02-24DOI: 10.1016/j.bbr.2025.115510
Megan de Lange, Vladyslava Yarosh, Kevin Farell, Caitlin McDonnell, Renee Patil, Isabel Hawthorn, Mok-Min Jung, Sophie Wenje, Joern R. Steinert
The prevalence of neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, is steadily increasing, thus posing significant challenges to global healthcare systems. Emerging evidence suggests that dietary habits, particularly consumption of high-fat diets, may play a pivotal role in the development and progression of neurodegenerative disorders. Moreover, several studies have shed light on the intricate communication between the gut and the brain, linking gut health with neuroinflammation and its involvement in neurodegenerative processes. This study aims to assess the effects of a high-fat dietary intake on various aspects of neuronal function during aging in a gender specific manner to help understand the potential contributions of diet to neuronal function. To investigate the effects of a high-fat diet, Drosophila melanogaster was used and exposed to a standard normal food diet (NF) and a high-fat diet (HF). Adults were grouped at 10 and 45 days of age in male and female flies reared under the same conditions starting the HF diet at 5 days of age with data showing differential gender- and HF diet-induced phenotypes. Malondialdehyde (MDA) levels were higher in males at 10 and 45 days (p < 0.05), caspase-3 expression increased at 45 days (p < 0.01) implicating apoptosis induction and a reduced climbing activity at 10 and 45 days was apparent in females only (p < 0.01). Adult lifespan under both dietary conditions was unchanged when reared at 18°C but odour-associated learning ability was reduced in larvae reared in a HF diet throughout their development (p < 0.05). This is the first study to characterise effects of a HF diet on neuronal phenotypes in an age- and gender-specific manner in a Drosophila model. Our findings suggest a HF diet induces differential effects of neuronal dysfunction with age and sex-specific outcomes, characterised by enhanced oxidative stress and cell death impacting on behaviour.
{"title":"High fat diet induces differential age- and gender-dependent changes in neuronal function in Drosophila linked to redox stress","authors":"Megan de Lange, Vladyslava Yarosh, Kevin Farell, Caitlin McDonnell, Renee Patil, Isabel Hawthorn, Mok-Min Jung, Sophie Wenje, Joern R. Steinert","doi":"10.1016/j.bbr.2025.115510","DOIUrl":"10.1016/j.bbr.2025.115510","url":null,"abstract":"<div><div>The prevalence of neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, is steadily increasing, thus posing significant challenges to global healthcare systems. Emerging evidence suggests that dietary habits, particularly consumption of high-fat diets, may play a pivotal role in the development and progression of neurodegenerative disorders. Moreover, several studies have shed light on the intricate communication between the gut and the brain, linking gut health with neuroinflammation and its involvement in neurodegenerative processes. This study aims to assess the effects of a high-fat dietary intake on various aspects of neuronal function during aging in a gender specific manner to help understand the potential contributions of diet to neuronal function. To investigate the effects of a high-fat diet, <em>Drosophila melanogaster</em> was used and exposed to a standard normal food diet (NF) and a high-fat diet (HF). Adults were grouped at 10 and 45 days of age in male and female flies reared under the same conditions starting the HF diet at 5 days of age with data showing differential gender- and HF diet-induced phenotypes. Malondialdehyde (MDA) levels were higher in males at 10 and 45 days (p < 0.05), caspase-3 expression increased at 45 days (p < 0.01) implicating apoptosis induction and a reduced climbing activity at 10 and 45 days was apparent in females only (p < 0.01). Adult lifespan under both dietary conditions was unchanged when reared at 18°C but odour-associated learning ability was reduced in larvae reared in a HF diet throughout their development (p < 0.05). This is the first study to characterise effects of a HF diet on neuronal phenotypes in an age- and gender-specific manner in a <em>Drosophila</em> model. Our findings suggest a HF diet induces differential effects of neuronal dysfunction with age and sex-specific outcomes, characterised by enhanced oxidative stress and cell death impacting on behaviour.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"484 ","pages":"Article 115510"},"PeriodicalIF":2.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514538","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 : 2025-02-24DOI: 10.1016/j.bbr.2025.115514
Marcus Heldmann , Louisa Müller-Miny , Tobias Wagner-Altendorf , Thomas F. Münte
The incentive sensitization theory suggests that repeated exposure to rewarding substances or food shapes neural circuits to create an attentional bias towards these stimuli. There is ongoing debate about whether attentional capture by such stimuli is an early automatic process or a later stage in the processing cascade. Event-related brain potentials (ERPs) provide a means to pinpoint the timing and location of attentional capture. ERPs were recorded from 28 normal weight healthy women as they attended to the left or right hemifield of a visual display while fixating a central point. Stimuli comprised bars presented left and right of the fixation point simultaneously with the task being to respond to slightly smaller bars on the attended side by button press. The bars appeared superimposed on task-irrelevant distractor stimuli (either food pictures or pictures of non-food objects). The bilateral stimuli elicited a positivity that was largest as posterior sites contralateral to the attended hemifield between 75 and 250 ms. Critically, this contralateral attention effect was enhanced by food distractors on the attended side and diminished by food distractors on the unattended side, demonstrating signs of attention capture by food stimuli as early as 80 ms poststimulus.
{"title":"Automatic attentional capture by food items in a visuospatial attention task – A study with event-related brain potentials","authors":"Marcus Heldmann , Louisa Müller-Miny , Tobias Wagner-Altendorf , Thomas F. Münte","doi":"10.1016/j.bbr.2025.115514","DOIUrl":"10.1016/j.bbr.2025.115514","url":null,"abstract":"<div><div>The incentive sensitization theory suggests that repeated exposure to rewarding substances or food shapes neural circuits to create an attentional bias towards these stimuli. There is ongoing debate about whether attentional capture by such stimuli is an early automatic process or a later stage in the processing cascade. Event-related brain potentials (ERPs) provide a means to pinpoint the timing and location of attentional capture. ERPs were recorded from 28 normal weight healthy women as they attended to the left or right hemifield of a visual display while fixating a central point. Stimuli comprised bars presented left and right of the fixation point simultaneously with the task being to respond to slightly smaller bars on the attended side by button press. The bars appeared superimposed on task-irrelevant distractor stimuli (either food pictures or pictures of non-food objects). The bilateral stimuli elicited a positivity that was largest as posterior sites contralateral to the attended hemifield between 75 and 250 ms. Critically, this contralateral attention effect was enhanced by food distractors on the attended side and diminished by food distractors on the unattended side, demonstrating signs of attention capture by food stimuli as early as 80 ms poststimulus.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"484 ","pages":"Article 115514"},"PeriodicalIF":2.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143510517","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 : 2025-02-23DOI: 10.1016/j.bbr.2025.115506
Yanqin Luo, Yiwen Zhang, Yongzhi Zhao, Fang Chen, Xueyan Li, Xinmin Liu, Muhammad Zulqarnain Shakir, Ning Jiang, Chunhui Shan
Chronic stress can affect brain function through various mechanisms, leading to the development of anxiety disorders. The chronic unpredictable mild stress (CUMS) is a classic model of chronic stress. This study evaluated the effects of different durations of CUMS on anxiety-like behavior, inflammation, and tryptophan metabolism in C57BL/6N mice. The results of behavioral assessments showed that after 3 and 4 weeks of CUMS exposure, the mice exhibited significant decreases in open arms ratio and time ratio in the elevated plus maze (EPM), prolonged latency in the novelty-suppressed feeding test (NSFT), and reduced transitions in the light/dark box (LDB), all indicative of anxiety-like behavior. The inflammatory factors expressions were quantified using qPCR, showing that pro-inflammatory and anti-inflammatory markers began to rise following 1-2 weeks of CUMS exposure. After 3 weeks of stress, TNF-α significantly increased, TGF-β levels started to decrease, and by 4 weeks of CUMS, Arg-1 expression also declined. In terms of tryptophan metabolism, 5-HT content in the hippocampus of the mice began to decrease after 3 weeks of CUMS, while the levels of neuroprotective kynurenic acid (KYNA) continued to rise. Concurrently, neurotoxic substances, including 3-hydroxykynurenine (3-HK) and quinolinic acid (QA), accumulated; after 4 weeks of CUMS, the KYNA content also started to decline. In conclusion, CUMS exposure for 3-4 weeks in male C57BL/6N mice induces anxiety-like behavior alongside the occurrence of inflammatory responses and disturbances in tryptophan metabolism. These findings highlight the complex interplay between stress, inflammation, and metabolic pathways in the etiology of anxiety-related behaviors.
{"title":"Chronic Unpredictable Mild Stress-Induced Anxiety is Linked to Inflammatory Responses and Disruptions in Tryptophan Metabolism in Male C57BL/6N Mice.","authors":"Yanqin Luo, Yiwen Zhang, Yongzhi Zhao, Fang Chen, Xueyan Li, Xinmin Liu, Muhammad Zulqarnain Shakir, Ning Jiang, Chunhui Shan","doi":"10.1016/j.bbr.2025.115506","DOIUrl":"https://doi.org/10.1016/j.bbr.2025.115506","url":null,"abstract":"<p><p>Chronic stress can affect brain function through various mechanisms, leading to the development of anxiety disorders. The chronic unpredictable mild stress (CUMS) is a classic model of chronic stress. This study evaluated the effects of different durations of CUMS on anxiety-like behavior, inflammation, and tryptophan metabolism in C57BL/6N mice. The results of behavioral assessments showed that after 3 and 4 weeks of CUMS exposure, the mice exhibited significant decreases in open arms ratio and time ratio in the elevated plus maze (EPM), prolonged latency in the novelty-suppressed feeding test (NSFT), and reduced transitions in the light/dark box (LDB), all indicative of anxiety-like behavior. The inflammatory factors expressions were quantified using qPCR, showing that pro-inflammatory and anti-inflammatory markers began to rise following 1-2 weeks of CUMS exposure. After 3 weeks of stress, TNF-α significantly increased, TGF-β levels started to decrease, and by 4 weeks of CUMS, Arg-1 expression also declined. In terms of tryptophan metabolism, 5-HT content in the hippocampus of the mice began to decrease after 3 weeks of CUMS, while the levels of neuroprotective kynurenic acid (KYNA) continued to rise. Concurrently, neurotoxic substances, including 3-hydroxykynurenine (3-HK) and quinolinic acid (QA), accumulated; after 4 weeks of CUMS, the KYNA content also started to decline. In conclusion, CUMS exposure for 3-4 weeks in male C57BL/6N mice induces anxiety-like behavior alongside the occurrence of inflammatory responses and disturbances in tryptophan metabolism. These findings highlight the complex interplay between stress, inflammation, and metabolic pathways in the etiology of anxiety-related behaviors.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"115506"},"PeriodicalIF":2.6,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143498229","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}
Despite significant strides in reducing smoking prevalence globally, tobacco use remains a leading contributor to ill health and premature death worldwide. While the detrimental impacts of smoking on various organs are well-established, its specific effects on nervous system function remain an area of ongoing investigation. This systematic review delves into the neurobiological effects of smoking, particularly through the lens of resting-state electroencephalography (EEG). A systematic search was conducted in May 2024 in PubMed, Embase, and Web of Science databases, and all available evidence comparing resting-state EEG findings between smokers and non-smokers was assessed. The 13 included studies investigated a total of 684 participants, with a median female percentage of of 25 % (range: 0–100), and the age of participants ranged from 18 to approximately 73 years. Alterations in the alpha band were the most prevalent findings observed in the EEG of smokers compared to non-smokers, observed in 8 studies, suggesting changes in the attention and cognitive functions of smokers. However, findings regarding the specific direction and location of changes were not consistent. Additionally, changes in delta, theta, and beta bands were identified on a less frequent basis. There was evidence suggesting that the observed neural oscillation changes are influenced by various factors, including the number of cigarettes used, pack years of smoking, age of smoking initiation, and smoking cessation status. These findings underscore the multifaceted nature of the impact of smoking on brain activity, especially on cognition and the attentional system.
{"title":"Chronic effects of tobacco smoking on electrical brain activity: A systematic review on electroencephalography studies","authors":"Morvarid Taebi , Fateme Taghavizanjani , Mohammadamin Parsaei , Mohamadjavad Ershadmanesh , Alireza Beikmarzehei , OmidReza Gorjestani , Zahra Rezaei , Alireza Hasanzadeh , Hossein Sanjari Moghaddam","doi":"10.1016/j.bbr.2025.115479","DOIUrl":"10.1016/j.bbr.2025.115479","url":null,"abstract":"<div><div>Despite significant strides in reducing smoking prevalence globally, tobacco use remains a leading contributor to ill health and premature death worldwide. While the detrimental impacts of smoking on various organs are well-established, its specific effects on nervous system function remain an area of ongoing investigation. This systematic review delves into the neurobiological effects of smoking, particularly through the lens of resting-state electroencephalography (EEG). A systematic search was conducted in May 2024 in PubMed, Embase, and Web of Science databases, and all available evidence comparing resting-state EEG findings between smokers and non-smokers was assessed. The 13 included studies investigated a total of 684 participants, with a median female percentage of of 25 % (range: 0–100), and the age of participants ranged from 18 to approximately 73 years. Alterations in the alpha band were the most prevalent findings observed in the EEG of smokers compared to non-smokers, observed in 8 studies, suggesting changes in the attention and cognitive functions of smokers. However, findings regarding the specific direction and location of changes were not consistent. Additionally, changes in delta, theta, and beta bands were identified on a less frequent basis. There was evidence suggesting that the observed neural oscillation changes are influenced by various factors, including the number of cigarettes used, pack years of smoking, age of smoking initiation, and smoking cessation status. These findings underscore the multifaceted nature of the impact of smoking on brain activity, especially on cognition and the attentional system.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"484 ","pages":"Article 115479"},"PeriodicalIF":2.6,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487704","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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