Pub Date : 2024-09-02DOI: 10.1016/j.bbr.2024.115218
Huizi Tian , Zhifang Wang , Yao Meng , Lu Geng , Hao Lian , Zhifei Shi , Zhidong Zhuang , Wenpeng Cai , Mengyang He
Depression is associated with functional brain impairments, although comprehensive studies remain limited. This study reviews neural mechanisms underlying cognitive impairment in depression and identifies associated activation abnormalities in brain regions. The study also explores the underlying neural processes of cognitive benefits of exercise intervention for depression. Executive function impairments, including working memory, inhibitory control and cognitive flexibility are associated with frontal cortex and anterior cingulate areas, especially dorsolateral prefrontal cortex. Depression is associated with certain neural impairments of reward processing, especially orbitofrontal cortex, prefrontal cortex, nucleus accumbens and other striatal regions. Depressed patients exhibit decreased activity in the hippocampus during memory function. Physical exercise has been found to enhance memory function, executive function, and reward processing in depression patients by increasing functional brain regions and the brain-derived neurotrophic factor (BDNF) as a nutritional factor also plays a key role in exercise intervention. The study documents neurophysiological mechanisms behind exercise intervention's improved functions. In summary, the study provides insights into neural mechanisms underlying cognitive impairments in depression and the effectiveness of exercise as a treatment.
{"title":"Neural mechanisms underlying cognitive impairment in depression and cognitive benefits of exercise intervention","authors":"Huizi Tian , Zhifang Wang , Yao Meng , Lu Geng , Hao Lian , Zhifei Shi , Zhidong Zhuang , Wenpeng Cai , Mengyang He","doi":"10.1016/j.bbr.2024.115218","DOIUrl":"10.1016/j.bbr.2024.115218","url":null,"abstract":"<div><p>Depression is associated with functional brain impairments, although comprehensive studies remain limited. This study reviews neural mechanisms underlying cognitive impairment in depression and identifies associated activation abnormalities in brain regions. The study also explores the underlying neural processes of cognitive benefits of exercise intervention for depression. Executive function impairments, including working memory, inhibitory control and cognitive flexibility are associated with frontal cortex and anterior cingulate areas, especially dorsolateral prefrontal cortex. Depression is associated with certain neural impairments of reward processing, especially orbitofrontal cortex, prefrontal cortex, nucleus accumbens and other striatal regions. Depressed patients exhibit decreased activity in the hippocampus during memory function. Physical exercise has been found to enhance memory function, executive function, and reward processing in depression patients by increasing functional brain regions and the brain-derived neurotrophic factor (BDNF) as a nutritional factor also plays a key role in exercise intervention. The study documents neurophysiological mechanisms behind exercise intervention's improved functions. In summary, the study provides insights into neural mechanisms underlying cognitive impairments in depression and the effectiveness of exercise as a treatment.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"476 ","pages":"Article 115218"},"PeriodicalIF":2.6,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0166432824003747/pdfft?md5=f0e6217f69ae6878f85967c72082c1dc&pid=1-s2.0-S0166432824003747-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142054728","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 : 2024-09-02DOI: 10.1016/j.bbr.2024.115234
Kevin M. Moran, Leah Jarrell, Misheel Khashchuluun, Kurt R. Moran, Julia Rodriguez, Anna Tran, Yvon Delville
Social stress during adolescence results in long lasting weight gain, obesity, and enhanced food hoarding behavior in hamsters. We wanted to determine whether stress also enhanced conditioned place preference-like behavior (CPP-like) for food reward, as would be expected from studies with substances like cocaine. Our experimental animals were exposed daily to aggressive adults for two weeks in early puberty, while also trained to explore a V-shaped maze containing a food reward at one end. They were tested for CPP-like behavior on the last day of social stress. Our results showed that while stress enhanced weight gain, food intake, food efficiency, and body fat, it caused a reduction of Place Preference as compared to controls. In fact, the correlated relationship between Place Preference and body fat was inverted by stress exposure: while it was positively correlated in controls, it was mildly negatively correlated in stressed hamsters. These unexpected data illustrate the extent of adaptive behavior in foraging animals once a resource has become untrustworthy.
青春期的社会压力会导致仓鼠长期体重增加、肥胖和囤积食物行为增强。我们想确定压力是否也会增强对食物奖赏的条件性场所偏好行为(CPP-like),正如可卡因等物质的研究预期的那样。我们的实验动物在青春期早期每天接触具有攻击性的成年仓鼠两周,同时训练它们探索一个 V 形迷宫,迷宫的一端有食物奖励。在社会压力的最后一天,我们对它们进行了类似 CPP 行为的测试。我们的结果表明,与对照组相比,虽然压力会促进体重增加、食物摄入量、食物效率和体脂增加,但却会导致位置偏好降低。事实上,场所偏好与体脂之间的相关关系因压力暴露而颠倒:在对照组中呈正相关,而在压力仓鼠中则呈轻度负相关。这些出乎意料的数据说明,一旦资源变得不可信,觅食动物的适应行为程度会有多大。
{"title":"Blunted food conditioned place preference-like behavior in adolescent-stressed male hamsters","authors":"Kevin M. Moran, Leah Jarrell, Misheel Khashchuluun, Kurt R. Moran, Julia Rodriguez, Anna Tran, Yvon Delville","doi":"10.1016/j.bbr.2024.115234","DOIUrl":"10.1016/j.bbr.2024.115234","url":null,"abstract":"<div><p>Social stress during adolescence results in long lasting weight gain, obesity, and enhanced food hoarding behavior in hamsters. We wanted to determine whether stress also enhanced conditioned place preference-like behavior (CPP-like) for food reward, as would be expected from studies with substances like cocaine. Our experimental animals were exposed daily to aggressive adults for two weeks in early puberty, while also trained to explore a V-shaped maze containing a food reward at one end. They were tested for CPP-like behavior on the last day of social stress. Our results showed that while stress enhanced weight gain, food intake, food efficiency, and body fat, it caused a reduction of Place Preference as compared to controls. In fact, the correlated relationship between Place Preference and body fat was inverted by stress exposure: while it was positively correlated in controls, it was mildly negatively correlated in stressed hamsters. These unexpected data illustrate the extent of adaptive behavior in foraging animals once a resource has become untrustworthy.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"476 ","pages":"Article 115234"},"PeriodicalIF":2.6,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131724","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 : 2024-08-30DOI: 10.1016/j.bbr.2024.115231
Santiago Castro-Zaballa , Joaquín González , Matías Cavelli , Diego Mateos , Claudia Pascovich , Adriano Tort , Mark Jeremy Hunt , Pablo Torterolo
Ketamine is an NMDA receptor antagonist that has antidepressant and anesthetic properties. At subanesthetic doses, ketamine induces transient psychosis in humans, and is used to model psychosis in experimental animals. In rodents, subanesthetic doses of ketamine increase the power of high-frequency oscillations (HFO, > 100 Hz) in the electroencephalogram (EEG), a frequency band linked to cognitive functions. However, to date, the effects of ketamine in carnivores and primates have been poorly investigated. Here, we examined in the cat, cortical HFO during wakefulness, sleep, and after administering a sub-anesthetic dose of ketamine. Four cats were prepared with cortical electrodes for chronic polysomnographic recordings in head-restrained conditions. The cortical HFO power, connectivity, direction of the information flow using Granger Causality (GC) analysis, their relationships with respiratory activity, and the effect of auditory stimulation were analyzed. During wakefulness, but not during sleep, we found that HFO were coupled with the inspiratory phase of the respiration. After ketamine administration, HFO power was enhanced and remained associated with the inspiratory phase. GC analysis suggests that ketamine-enhanced HFO originate from the olfactory bulb (OB) and stream towards the prefrontal cortex (Pf). Accordingly, occluding the nostrils significantly reduced the power of the ketamine-enhanced HFO in both the OB and Pf. Finally, auditory stimulation did not affect HFO. In conclusion, the HFO are associated with respiration during wakefulness, but not during sleep. The enhancement of this rhythm by ketamine may disrupt cortical information processing, which could contribute to some of the neuropsychiatric effects associated with ketamine.
{"title":"Cortical high-frequency oscillations (≈ 110 Hz) in cats are state-dependent and enhanced by a subanesthetic dose of ketamine","authors":"Santiago Castro-Zaballa , Joaquín González , Matías Cavelli , Diego Mateos , Claudia Pascovich , Adriano Tort , Mark Jeremy Hunt , Pablo Torterolo","doi":"10.1016/j.bbr.2024.115231","DOIUrl":"10.1016/j.bbr.2024.115231","url":null,"abstract":"<div><p>Ketamine is an NMDA receptor antagonist that has antidepressant and anesthetic properties. At subanesthetic doses, ketamine induces transient psychosis in humans, and is used to model psychosis in experimental animals. In rodents, subanesthetic doses of ketamine increase the power of high-frequency oscillations (HFO, > 100 Hz) in the electroencephalogram (EEG), a frequency band linked to cognitive functions. However, to date, the effects of ketamine in carnivores and primates have been poorly investigated. Here, we examined in the cat, cortical HFO during wakefulness, sleep, and after administering a sub-anesthetic dose of ketamine. Four cats were prepared with cortical electrodes for chronic polysomnographic recordings in head-restrained conditions. The cortical HFO power, connectivity, direction of the information flow using Granger Causality (GC) analysis, their relationships with respiratory activity, and the effect of auditory stimulation were analyzed. During wakefulness, but not during sleep, we found that HFO were coupled with the inspiratory phase of the respiration. After ketamine administration, HFO power was enhanced and remained associated with the inspiratory phase. GC analysis suggests that ketamine-enhanced HFO originate from the olfactory bulb (OB) and stream towards the prefrontal cortex (Pf). Accordingly, occluding the nostrils significantly reduced the power of the ketamine-enhanced HFO in both the OB and Pf. Finally, auditory stimulation did not affect HFO. In conclusion, the HFO are associated with respiration during wakefulness, but not during sleep. The enhancement of this rhythm by ketamine may disrupt cortical information processing, which could contribute to some of the neuropsychiatric effects associated with ketamine.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"476 ","pages":"Article 115231"},"PeriodicalIF":2.6,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103953","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 : 2024-08-30DOI: 10.1016/j.bbr.2024.115221
Gabriela Corrêa Coelho , Luiz Gustavo Soares Carvalho Crespo , Maria de Fátima dos Santos Sampaio , Regina Claudia Barbosa Silva , Richard Ian Samuels , Robert J. Carey , Marinete Pinheiro Carrera
We report that environmental context can have a major impact on morphine locomotor behavior and ERK effects. We manipulated environmental context in terms of an environmental novelty/ familiarity dimension and measured morphine behavioral effects in both acute and chronic morphine treatment protocols. Wistar rats (n=7 per group) were injected with morphine 10 mg/kg or vehicle (s.c.), and immediately placed into an arena for 5 min, and locomotor activity was measured after one or 5 days. The morphine treatments were initiated either when the environment was novel or began after the rats had been familiarized with the arena by being given 5 daily nondrug tests in the arena. The results showed that acute and chronic morphine effects were strongly modified by whether the environment was novel or familiar. Acute morphine administered in a novel environment increased ERK activity more substantially in several brain areas, particularly in reward-associated areas such as the VTA in comparison to when morphine was given in a familiar environment. Repeated morphine treatments initiated in a novel environment induced a strong locomotor sensitization, whereas repeated morphine treatments initiated in a familiar environment did not induce a locomotor stimulant effect but rather a drug discriminative stimulus dis-habituation effect. The marked differential effects of environmental novelty/familiarity and ongoing dopamine activity on acute and chronic morphine treatments may be of potential clinical relevance for opioid drug addiction.
{"title":"Opioid-environment interaction: Contrasting effects of morphine administered in a novel versus familiar environment on acute and repeated morphine induced behavioral effects and on acute morphine ERK activation in reward associated brain areas","authors":"Gabriela Corrêa Coelho , Luiz Gustavo Soares Carvalho Crespo , Maria de Fátima dos Santos Sampaio , Regina Claudia Barbosa Silva , Richard Ian Samuels , Robert J. Carey , Marinete Pinheiro Carrera","doi":"10.1016/j.bbr.2024.115221","DOIUrl":"10.1016/j.bbr.2024.115221","url":null,"abstract":"<div><p>We report that environmental context can have a major impact on morphine locomotor behavior and ERK effects. We manipulated environmental context in terms of an environmental novelty/ familiarity dimension and measured morphine behavioral effects in both acute and chronic morphine treatment protocols. Wistar rats (n=7 per group) were injected with morphine 10 mg/kg or vehicle (s.c.), and immediately placed into an arena for 5 min, and locomotor activity was measured after one or 5 days. The morphine treatments were initiated either when the environment was novel or began after the rats had been familiarized with the arena by being given 5 daily nondrug tests in the arena. The results showed that acute and chronic morphine effects were strongly modified by whether the environment was novel or familiar. Acute morphine administered in a novel environment increased ERK activity more substantially in several brain areas, particularly in reward-associated areas such as the VTA in comparison to when morphine was given in a familiar environment. Repeated morphine treatments initiated in a novel environment induced a strong locomotor sensitization, whereas repeated morphine treatments initiated in a familiar environment did not induce a locomotor stimulant effect but rather a drug discriminative stimulus dis-habituation effect. The marked differential effects of environmental novelty/familiarity and ongoing dopamine activity on acute and chronic morphine treatments may be of potential clinical relevance for opioid drug addiction.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"476 ","pages":"Article 115221"},"PeriodicalIF":2.6,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103954","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}
Our comprehension of the interplay of cognition and the brain remains constrained. While functional imaging studies have identified cognitive brain regions, structural correlates of cognitive functions remain underexplored. Advanced methods like Diffusion Magnetic Resonance Imaging (DMRI) facilitate the exploration of brain connectivity and White Matter (WM) tract microstructure. Therefore, we conducted connectometry method on DMRI data, to reveal WM tracts associated with cognition.
Methods
125 healthy participants from the National Institute of Mental Health Intramural Healthy Volunteer Dataset were recruited. Multiple regression analyses were conducted between DMRI-derived Quantitative Anisotropy (QA) values within WM tracts and scores of participants in Flanker Inhibitory Control and Attention Test (attention), Dimensional Change Card Sort (executive function), Picture Sequence Memory Test (episodic memory), and List Sorting Working Memory Test (working memory) tasks from National Institute of Health toolbox. The significance level was set at False Discovery Rate (FDR)<0.05.
Results
We identified significant positive correlations between the QA of WM tracts within the left cerebellum and bilateral fornix with attention, executive functioning, and episodic memory (FDR=0.018, 0.0002, and 0.0002, respectively), and a negative correlation between QA of WM tracts within bilateral cerebellum with attention (FDR=0.028). Working memory demonstrated positive correlations with QA of left inferior longitudinal and left inferior fronto-occipital fasciculi (FDR=0.0009), while it showed a negative correlation with QA of right cerebellar tracts (FDR=0.0005).
Conclusion
Our results underscore the intricate link between cognitive performance and WM integrity in frontal, temporal, and cerebellar regions, offering insights into early detection and targeted interventions for cognitive disorders.
{"title":"White matter correlates of cognition: A diffusion magnetic resonance imaging study","authors":"Mohammadamin Parsaei , Gelayol Barahman , Parvaneh Hamian Roumiani , Ehsan Ranjbar , Sahar Ansari , Anahita Najafi , Hanie Karimi , Mohammad Hadi Aarabi , Hossein Sanjari Moghaddam","doi":"10.1016/j.bbr.2024.115222","DOIUrl":"10.1016/j.bbr.2024.115222","url":null,"abstract":"<div><h3>Background</h3><p>Our comprehension of the interplay of cognition and the brain remains constrained. While functional imaging studies have identified cognitive brain regions, structural correlates of cognitive functions remain underexplored. Advanced methods like Diffusion Magnetic Resonance Imaging (DMRI) facilitate the exploration of brain connectivity and White Matter (WM) tract microstructure. Therefore, we conducted connectometry method on DMRI data, to reveal WM tracts associated with cognition.</p></div><div><h3>Methods</h3><p>125 healthy participants from the National Institute of Mental Health Intramural Healthy Volunteer Dataset were recruited. Multiple regression analyses were conducted between DMRI-derived Quantitative Anisotropy (QA) values within WM tracts and scores of participants in Flanker Inhibitory Control and Attention Test (attention), Dimensional Change Card Sort (executive function), Picture Sequence Memory Test (episodic memory), and List Sorting Working Memory Test (working memory) tasks from National Institute of Health toolbox. The significance level was set at False Discovery Rate (FDR)<0.05.</p></div><div><h3>Results</h3><p>We identified significant positive correlations between the QA of WM tracts within the left cerebellum and bilateral fornix with attention, executive functioning, and episodic memory (FDR=0.018, 0.0002, and 0.0002, respectively), and a negative correlation between QA of WM tracts within bilateral cerebellum with attention (FDR=0.028). Working memory demonstrated positive correlations with QA of left inferior longitudinal and left inferior fronto-occipital fasciculi (FDR=0.0009), while it showed a negative correlation with QA of right cerebellar tracts (FDR=0.0005).</p></div><div><h3>Conclusion</h3><p>Our results underscore the intricate link between cognitive performance and WM integrity in frontal, temporal, and cerebellar regions, offering insights into early detection and targeted interventions for cognitive disorders.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"476 ","pages":"Article 115222"},"PeriodicalIF":2.6,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103955","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 : 2024-08-30DOI: 10.1016/j.bbr.2024.115219
Benjamín Zylberberg , Angela M. Suburo , M. Florencia Coronel , Graciela L. Mazzone
Our previous in vitro studies showed that excitotoxicity evoked by glutamate analogue kainate (KA) significantly decreased the number of rat spinal neurons and triggered high release of glutamate leading to locomotor network block. Our current objective was to assess the role of CREB as a predictive marker of damage following chemically-induced spinal cord injury by using in vivo and in vitro models. Thus, in vivo excitotoxicity in Balb/c adult mice was induced by KA intraspinal injection, while in vitro spinal cord excitotoxicity was produced by bath-applied KA. KA application evoked significant neuronal loss, deterioration in hindlimb motor coordination and thermal allodynia. In addition, immunohistochemical analysis showed that KA application resulted in decreased number of CREB positive nuclei in the ventral horn and in dorsal layers III-IV. Our data suggests that excitotoxic-induced neuronal loss may be potentially predicted by altered CREB nuclear translocation.
我们之前的体外研究表明,谷氨酸类似物凯恩酸盐(KA)诱发的兴奋毒性会显著减少大鼠脊髓神经元的数量,并引发谷氨酸的大量释放,导致运动网络阻滞。我们目前的目标是利用体内和体外模型评估 CREB 作为化学诱导脊髓损伤后损伤预测标志物的作用。因此,通过椎管内注射 KA 诱导 Balb/c 成年小鼠体内兴奋性中毒,而体外脊髓兴奋性中毒则是通过沐浴施加 KA 产生的。应用 KA 会诱发神经元大量缺失、后肢运动协调性恶化和热异感。此外,免疫组化分析表明,应用 KA 会导致腹侧角和背侧三至四层的 CREB 阳性核数目减少。我们的数据表明,兴奋毒性诱导的神经元损失可能是由 CREB 核转位的改变所预测的。
{"title":"Excitotoxic spinal damage induced by kainic acid impairs locomotion, alters nociception, and reduces CREB nuclear translocation","authors":"Benjamín Zylberberg , Angela M. Suburo , M. Florencia Coronel , Graciela L. Mazzone","doi":"10.1016/j.bbr.2024.115219","DOIUrl":"10.1016/j.bbr.2024.115219","url":null,"abstract":"<div><p>Our previous <em>in vitro</em> studies showed that excitotoxicity evoked by glutamate analogue kainate (KA) significantly decreased the number of rat spinal neurons and triggered high release of glutamate leading to locomotor network block. Our current objective was to assess the role of CREB as a predictive marker of damage following chemically-induced spinal cord injury by using <em>in vivo</em> and <em>in vitro</em> models. Thus, <em>in vivo</em> excitotoxicity in Balb/c adult mice was induced by KA intraspinal injection, while <em>in vitro</em> spinal cord excitotoxicity was produced by bath-applied KA. KA application evoked significant neuronal loss, deterioration in hindlimb motor coordination and thermal allodynia. In addition, immunohistochemical analysis showed that KA application resulted in decreased number of CREB positive nuclei in the ventral horn and in dorsal layers III-IV. Our data suggests that excitotoxic-induced neuronal loss may be potentially predicted by altered CREB nuclear translocation.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"475 ","pages":"Article 115219"},"PeriodicalIF":2.6,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142096986","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 : 2024-08-28DOI: 10.1016/j.bbr.2024.115223
Shanyong Yi , Bin Zhao , Lai Wei , Zhijun Yao , Bin Yang
Excessive stress can exceed the adjustment ability of body and cause injury and dysfunction, while elucidation of the mechanism and prevention measures of stress-related injury are still insufficient. The present study was to observe the effect of glucocorticoid (GC) on stress-induced hypothalamic nerve injury and elucidate the potential mechanism. The present study intended to establish a chronic restraint stress rat model for follow-up study. Open field test and elevated plus maze test were used to observe behavioral changes of stress rats; Enzyme-linked immunosorbent assay (ELISA) was used to detect changes in the levels of hypothalamus-pituitary-adrenal (HPA) axis-related hormones and inflammatory factors in hypothalamus; toluidine blue staining was used to observe pathological changes of hypothalamus. The results showed that stress rats showed obvious anxiety-like behaviors, the levels of HPA axis-related hormones and inflammatory factors showed abnormal fluctuations, and morphological results showed significant nerve injury in hypothalamus. Low-dose GC treatment significantly improved behavioral changes, alleviated hypothalamic nerve injury, and restored hypothalamic levels of inflammatory factors, serum levels of GC, corticotropin-releasing hormone (CRH), and adrenocorticotropic hormone (ACTH) and GC level in adrenal cortex of stressed rats, while GC receptor (GR) inhibitor, CRH receptor inhibitor, and adrenalectomy reversed the ameliorative effects of low-dose GC. Our study clarified that low-dose GC can restore stress coping ability by reshaping the homeostasis of the HPA axis, thus alleviating behavioral abnormalities and hypothalamic nerve injury in stressed rats.
{"title":"Glucocorticoid alleviates hypothalamic nerve injury via remodeling HPA axis homeostasis in stressed rats","authors":"Shanyong Yi , Bin Zhao , Lai Wei , Zhijun Yao , Bin Yang","doi":"10.1016/j.bbr.2024.115223","DOIUrl":"10.1016/j.bbr.2024.115223","url":null,"abstract":"<div><p>Excessive stress can exceed the adjustment ability of body and cause injury and dysfunction, while elucidation of the mechanism and prevention measures of stress-related injury are still insufficient. The present study was to observe the effect of glucocorticoid (GC) on stress-induced hypothalamic nerve injury and elucidate the potential mechanism. The present study intended to establish a chronic restraint stress rat model for follow-up study. Open field test and elevated plus maze test were used to observe behavioral changes of stress rats; Enzyme-linked immunosorbent assay (ELISA) was used to detect changes in the levels of hypothalamus-pituitary-adrenal (HPA) axis-related hormones and inflammatory factors in hypothalamus; toluidine blue staining was used to observe pathological changes of hypothalamus. The results showed that stress rats showed obvious anxiety-like behaviors, the levels of HPA axis-related hormones and inflammatory factors showed abnormal fluctuations, and morphological results showed significant nerve injury in hypothalamus. Low-dose GC treatment significantly improved behavioral changes, alleviated hypothalamic nerve injury, and restored hypothalamic levels of inflammatory factors, serum levels of GC, corticotropin-releasing hormone (CRH), and adrenocorticotropic hormone (ACTH) and GC level in adrenal cortex of stressed rats, while GC receptor (GR) inhibitor, CRH receptor inhibitor, and adrenalectomy reversed the ameliorative effects of low-dose GC. Our study clarified that low-dose GC can restore stress coping ability by reshaping the homeostasis of the HPA axis, thus alleviating behavioral abnormalities and hypothalamic nerve injury in stressed rats.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"475 ","pages":"Article 115223"},"PeriodicalIF":2.6,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142096988","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 : 2024-08-28DOI: 10.1016/j.bbr.2024.115220
Fa-yi Nie , Ru-yi Jin , Shan-shan Wu , Wei Yuan , Yu-wei Wu , Si-meng Xue , Xiao-hang Yang , Hai-fa Qiao
Background
The pathophysiology and molecular mechanisms of schizophrenia (SCZ) remain unclear, and the effective treatment resources are still limited. The goal of this study is to identify the expression of AQP4 in SCZ patients and explore whether AQP4 inhibition could ameliorate schizophrenia-like behaviors and its mechanisms.
Methods
Microarray datasets of PFC compared with healthy control were searched in the Gene Expression Omnibus (GEO) database, and differentially expressed genes (DEGs) were analyzed with the GEO2R online tool. The Venny online tool and metascape online software were used to identify common abnormally expressed genes and conduct cell type signature enrichment analysis. SCZ mouse models were induced with MK-801, an NMDA receptor antagonist (intraperitoneal injection, 0.1 mg/kg/day for 7 days), and C6 cell models were treated with 100 μM MK-801. RT-qPCR, Western Blotting, and immunofluorescence were employed to determine the expression of AQP4, proinflammatory cytokines, and GFAP. Open field tests and social interaction tests were performed to evaluate the schizophrenia-like behaviors.
Results
Bioinformatics analysis identified upregulation of AQP4 in the PFC of SCZ patients compared with healthy controls. Cell type signature enrichment analysis showed that all three DEGs lists were strongly enriched in the FAN EMBRYONIC CTX ASTROCYTE 2 category. Upregulation of AQP4 was also observed in MK-801-treated C6 cells and the PFC of MK-801-induced SCZ mouse model. Moreover, AQP4 inhibition with TGN-020 (an inhibitor of AQP4) improved anxiety-like behavior and social novelty preference defects in MK-801-treated mice. AQP4 inhibition also reduced the expression of IL-1β, IL-6, and TNF-α in MK-801-treated C6 cells and mouse model.
Conclusions
AQP4 is upregulated in the PFC of SCZ patients compared with healthy controls. AQP4 inhibition could alleviate the anxiety-like behavior and social novelty defects in MK-801-treated mice, this may be due to the role of AQP4 in the regulation of the expression of proinflammatory cytokines.
{"title":"AQP4 is upregulated in schizophrenia and Its inhibition attenuates MK-801-induced schizophrenia-like behaviors in mice","authors":"Fa-yi Nie , Ru-yi Jin , Shan-shan Wu , Wei Yuan , Yu-wei Wu , Si-meng Xue , Xiao-hang Yang , Hai-fa Qiao","doi":"10.1016/j.bbr.2024.115220","DOIUrl":"10.1016/j.bbr.2024.115220","url":null,"abstract":"<div><h3>Background</h3><p>The pathophysiology and molecular mechanisms of schizophrenia (SCZ) remain unclear, and the effective treatment resources are still limited. The goal of this study is to identify the expression of AQP4 in SCZ patients and explore whether AQP4 inhibition could ameliorate schizophrenia-like behaviors and its mechanisms.</p></div><div><h3>Methods</h3><p>Microarray datasets of PFC compared with healthy control were searched in the Gene Expression Omnibus (GEO) database, and differentially expressed genes (DEGs) were analyzed with the GEO2R online tool. The Venny online tool and metascape online software were used to identify common abnormally expressed genes and conduct cell type signature enrichment analysis. SCZ mouse models were induced with MK-801, an NMDA receptor antagonist (intraperitoneal injection, 0.1 mg/kg/day for 7 days), and C6 cell models were treated with 100 μM MK-801. RT-qPCR, Western Blotting, and immunofluorescence were employed to determine the expression of <em>AQP4,</em> proinflammatory cytokines, and GFAP. Open field tests and social interaction tests were performed to evaluate the schizophrenia-like behaviors.</p></div><div><h3>Results</h3><p>Bioinformatics analysis identified upregulation of AQP4 in the PFC of SCZ patients compared with healthy controls. Cell type signature enrichment analysis showed that all three DEGs lists were strongly enriched in the FAN EMBRYONIC CTX ASTROCYTE 2 category. Upregulation of <em>AQP4</em> was also observed in MK-801-treated C6 cells and the PFC of MK-801-induced SCZ mouse model. Moreover, AQP4 inhibition with TGN-020 (an inhibitor of AQP4) improved anxiety-like behavior and social novelty preference defects in MK-801-treated mice. AQP4 inhibition also reduced the expression of <em>IL-1β, IL-6,</em> and <em>TNF-α</em> in MK-801-treated C6 cells and mouse model.</p></div><div><h3>Conclusions</h3><p>AQP4 is upregulated in the PFC of SCZ patients compared with healthy controls. AQP4 inhibition could alleviate the anxiety-like behavior and social novelty defects in MK-801-treated mice, this may be due to the role of AQP4 in the regulation of the expression of proinflammatory cytokines.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"475 ","pages":"Article 115220"},"PeriodicalIF":2.6,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142096987","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 : 2024-08-28DOI: 10.1016/j.bbr.2024.115216
Brent Kelsen , Sophie Hsin-Yi Liang
Engaging in dialog requires interlocutors to coordinate sending and receiving linguistic signals to build a discourse based upon interpretations and perceptions interconnected with a range of emotions. Conversing in a foreign language may induce emotions such as anxiety which influence the quality communication. The neural processes underpinning these interactions are crucial to understanding foreign language anxiety (FLA). Electroencephalography (EEG) studies reveal that anxiety is often displayed via hemispheric frontal alpha asymmetry (FAA). To examine the neural mechanisms underlying FLA, we collected self-reported data on the listening and speaking sections of the Second language skill specific anxiety scale (L2AS) over behavioral, cognitive, and somatic domains and recorded EEG signals during participation in word chain turn-taking activities in first (L1, Chinese) and second (L2, English) languages. Regression analysis showed FAA for the L2 condition was a significant predictor primarily of the behavioral and somatic domains on the L2AS speaking section. The results are discussed along with implications for improving communication during L2 interactions.
{"title":"Frontal EEG alpha asymmetry predicts foreign language anxiety while speaking a foreign language","authors":"Brent Kelsen , Sophie Hsin-Yi Liang","doi":"10.1016/j.bbr.2024.115216","DOIUrl":"10.1016/j.bbr.2024.115216","url":null,"abstract":"<div><p>Engaging in dialog requires interlocutors to coordinate sending and receiving linguistic signals to build a discourse based upon interpretations and perceptions interconnected with a range of emotions. Conversing in a foreign language may induce emotions such as anxiety which influence the quality communication. The neural processes underpinning these interactions are crucial to understanding foreign language anxiety (FLA). Electroencephalography (EEG) studies reveal that anxiety is often displayed via hemispheric frontal alpha asymmetry (FAA). To examine the neural mechanisms underlying FLA, we collected self-reported data on the listening and speaking sections of the Second language skill specific anxiety scale (L2AS) over behavioral, cognitive, and somatic domains and recorded EEG signals during participation in word chain turn-taking activities in first (L1, Chinese) and second (L2, English) languages. Regression analysis showed FAA for the L2 condition was a significant predictor primarily of the behavioral and somatic domains on the L2AS speaking section. The results are discussed along with implications for improving communication during L2 interactions.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"475 ","pages":"Article 115216"},"PeriodicalIF":2.6,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0166432824003723/pdfft?md5=0be1218225e44981e880a35b7bc466d7&pid=1-s2.0-S0166432824003723-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142097040","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 : 2024-08-26DOI: 10.1016/j.bbr.2024.115211
Francisco José Lobato-Camacho , Juan Carlos López , Juan Pedro Vargas
This study explores the under-researched domain of long-term stimulant treatment in children and adolescents diagnosed with attention deficit hyperactivity disorder (ADHD). The necessity for extended treatment duration, often accompanied by safety concerns and side effects leading to treatment discontinuation, underscores the significance of this investigation. Concurrently, comparative studies have revealed adverse impacts on vulnerable regions within the hippocampal formation, accompanied by behavioral perturbations. We employed computerized tests and virtual reality to assess spatial memory, pattern separation, and object recognition memory in a cohort of children diagnosed with ADHD receiving stimulant treatment. We compared their performance to a group of neurotypical peers. Our findings indicate that the ADHD group exhibited a lower performance in spatial memory, pattern separation, and object recognition memory than ND group. Intriguingly, a positive relationship emerged between the duration of stimulant treatment and performance in these variables. Notably, this improvement was not immediate to MPH treatment but becomes significant after 24 months of treatment. In contrast to previous comparative investigations, our study did not reveal a detrimental impact on spatial navigation, object recognition memory, or pattern separation, despite the known interplay of these cognitive processes with the hippocampal formation. These results shed new light on the nuanced effects of stimulant treatment in ADHD, underscoring the need for a more comprehensive understanding of long-term treatment outcomes.
{"title":"Enhancing spatial memory and pattern separation: Long-term effects of stimulant treatment in individuals with ADHD","authors":"Francisco José Lobato-Camacho , Juan Carlos López , Juan Pedro Vargas","doi":"10.1016/j.bbr.2024.115211","DOIUrl":"10.1016/j.bbr.2024.115211","url":null,"abstract":"<div><p>This study explores the under-researched domain of long-term stimulant treatment in children and adolescents diagnosed with attention deficit hyperactivity disorder (ADHD). The necessity for extended treatment duration, often accompanied by safety concerns and side effects leading to treatment discontinuation, underscores the significance of this investigation. Concurrently, comparative studies have revealed adverse impacts on vulnerable regions within the hippocampal formation, accompanied by behavioral perturbations. We employed computerized tests and virtual reality to assess spatial memory, pattern separation, and object recognition memory in a cohort of children diagnosed with ADHD receiving stimulant treatment. We compared their performance to a group of neurotypical peers. Our findings indicate that the ADHD group exhibited a lower performance in spatial memory, pattern separation, and object recognition memory than ND group. Intriguingly, a positive relationship emerged between the duration of stimulant treatment and performance in these variables. Notably, this improvement was not immediate to MPH treatment but becomes significant after 24 months of treatment. In contrast to previous comparative investigations, our study did not reveal a detrimental impact on spatial navigation, object recognition memory, or pattern separation, despite the known interplay of these cognitive processes with the hippocampal formation. These results shed new light on the nuanced effects of stimulant treatment in ADHD, underscoring the need for a more comprehensive understanding of long-term treatment outcomes.</p></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"475 ","pages":"Article 115211"},"PeriodicalIF":2.6,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S016643282400367X/pdfft?md5=bf014b636bd64f145c503bd6057d865b&pid=1-s2.0-S016643282400367X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142054727","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}