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How do lateral septum projections to the ventral CA1 influence sociability?

neural Regeneration Research 2024年第8期19卷 1789-1801页

作者： Dan Wang Di Zhao Wentao Wang Fengai Hu Minghu Cui Jing Liu Fantao Meng Cuilan Liu Changyun Qiu Dunjiang Liu Zhicheng Xu Yameng Wang Yu Zhang Wei Li Chen Li Department of Rehabilitation Medicine Binzhou Medical University HospitalBinzhouShandong ProvinceChina Medical Research Center Binzhou Medical University HospitalBinzhouShandong ProvinceChina Institute for Metabolic&Neuropsychiatric Disorders Binzhou Medical University HospitalBinzhouShandong ProvinceChina Department of Psychology Binzhou Medical University HospitalBinzhouShandong ProvinceChina College of Nursing Binzhou Medical UniversityBinzhouShandong ProvinceChina

Social dysfunction is a risk factor for several neuropsychiatric illnesses.Previous studies have shown that the lateral septum(LS)-related pathway plays a critical role in mediating social behaviors.Howeve r,the role of the connections between the LS and its downstream brain regions in social behavio rs remains unclea r.In this study,we conducted a three-chamber test using electrophysiological and chemogenetic approaches in mice to determine how LS projections to ventral CA1(vCA1)influence sociability.Our res ults showed that gamma-aminobutyric acid(GABA)-e rgic neuro ns were activated following social experience,and that social behavio rs were enhanced by chemogenetic modulation of these neurons.Moreover,LS GABAergic neurons extended their functional neural connections via vCA1 glutamatergic pyramidal neurons,and regulating LSGABA→vCA1Gluneural projections affected social behaviors,which were impeded by suppressing LSprojecting vCA1 neuronal activity or inhibiting GABAAreceptors in vCA1.These findings support the hypothesis that LS inputs to the vCA1 can control social prefe rences and social novelty behaviors.These findings provide new insights rega rding the neural circuits that regulate sociability.

关键词： chemogenetics GABA receptor GABAergic neurons glutamatergic neurons lateral septum neural excitability neural projection social novelty social preference ventral CA1

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Soleus arthrogenic muscle inhibition following acute lateral ankle sprain correlates with symptoms and ankle disability but not with postural control

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Journal of Sport and Health Science 2024年第4期13卷 559-568,F0003页

作者： Kyung-Min Kim Joo-Sung Kim Alan R.Needle Department of Sport Science Sungkyunkwan UniversitySuwon-si 16419Republic of Korea Department of Health and Human Performance Texas State UniversitySan MarcosTX 78666USA Department of Public Health&Exercise Science Appalachian State UniversityBooneNC 28608USA Department of Rehabilitation Science Appalachian State UniversityBooneNC 28608USA

Background:Acute lateral ankle sprains(ALAS)are associated with long-term impairments and instability tied to altered neural excitability.Arthrogenic muscle inhibition(AMI)has been observed in this population;however,relationships with injury-related impairments are unclear,potentially due to the resting,prone position in which AMI is typically measured.Assessing AMI during bipedal stance may provide a better understanding of this relationship.Methods:AMI was assessed in 38 young adults(19 ALAS within 72 h of injury:10 males,21.4±2.7 years;19 healthy controls:10 males,21.9±2.2 years;mean±SD)using the Hoffmann reflex(H-reflex)during bipedal stance.Electrical stimulation was administered to identify the _(max)imal H-reflex(H_(max))and _(max)imal motor response(M_(max))from the soleus,fibularis longus,and tibialis anterior muscles.The primary outcome measure was the H_(max)/M_(max) ratio.Secondary outcomes included acute symptoms(pain and swelling),postural control during bipedal stance,and self-reported function.Results:No significant group-by-limb interactions were observed for any muscle.However,a significant group main effect was observed in the soleus muscle(F(1,35)=6.82,p=0.013),indicating significantly lower H_(max)/M_(max) ratios following ALAS(0.38±0.20)compared to healthy controls(0.53±0.16).Furthermore,lower H_(max)/M_(max) ratios in the soleus significantly correlated with acute symptoms and self-reported function but not with postural control.Conclusion:This study supports previous evidence of AMI in patients with ALAS,providing insight into neurophysiologic impacts of musculoskeletal injury.Our results suggest that assessing AMI in a standing position following acute injury may provide valuable insight into how AMI develops and guide potential therapeutic options to curb and offset the formation of joint instability.

关键词： Acute injuries Balance Hoffmann reflex neural excitability Patient-reported outcomes

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Inhibition of intracellular proton-sensitive Ca^(2+)-permeable TRPV3 channels protects against ischemic brain injury

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Acta Pharmaceutica Sinica B 2022年第5期12卷 2330-2347页

作者： Xiaoling Chen Jingliang Zhang KeWei Wang Department of Molecular and Cellular Pharmacology State Key Laboratory of Natural and Biomimetic DrugsSchool of Pharmaceutical SciencesPeking UniversityBeijing 100191China Department of Pharmacology Qingdao University School of PharmacyQingdao 266021China

Ischemic brain stroke is pathologically characterized by tissue acidosis, sustained calcium entry and progressive cell death. Previous studies focusing on antagonizing N-methyl-D-aspartate(NMDA) receptors have failed to translate any clinical benefits, suggesting a non-NMDA mechanism involved in the sustained injury after stroke. Here, we report that inhibition of intracellular proton-sensitive Ca^(2+)-permeable transient receptor potential vanilloid 3(TRPV3) channel protects against cerebral ischemia/reperfusion(I/R) injury. TRPV3 expression is upregulated in mice subjected to cerebral I/R injury. Silencing of TRPV3 reduces intrinsic neuronal excitability, excitatory synaptic transmissions, and also attenuates cerebral I/R injury in mouse model of transient middle cerebral artery occlusion(tMCAO). Conversely, overexpressing or re-expressing TRPV3 increases neuronal excitability, excitatory synaptic transmissions and aggravates cerebral I/R injury. Furthermore, specific inhibition of TRPV3 by natural forsythoside B decreases neural excitability and attenuates cerebral I/R injury. Taken together, our findings for the first time reveal a causative role of neuronal TRPV3 channel in progressive cell death after stroke, and blocking overactive TRPV3 channel may provide therapeutic potential for ischemic brain injury.

关键词： TRPV3 Ca^(2+)influx Acidosis Cerebral ischemia/reperfusion injury Excitotoxicity neural excitability Forsythoside B tMACO OGD TRP

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Neurexin regulates night-time sleep through modulating neural excitability

Neurexin regulates night-time sleep through modulating neura...

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2015年中国中西医结合学会时间生物医学专业委员会学术...

作者： Huawei Tong Qian Li Junhai Han Institute of Life Sciences the Key Laboratory of Developmental Genes and Human DiseaseSoutheast University

Sleep is a universal,essential and evolutionarily conserved behavior among animal species,which is regulated by various neural circuits and closely related to synaptic function.Neurexins are cell adhesion molecules that function in various neural circuits through mediating synapse formation and synaptic transmission.However,the neuronal circuits and the potential role of Neurexins in sleep regulation are not clear.Here,we show that lack of the Drosophila homolog of α-Neurexin significantly reduce night-time sleep and depletion of Neurexin from different kenyon cell populations either increase or decrease night-time sleep.We further identified the role of different KC populations in night-time sleep regulation.Using calcium image analysis,we reveal that nrx mutant KCs exhibits an elevated neural excitability,which results in a decreased night-time sleep.Finally,we demonstrate that Neurexin associates with Na/K-ATPase and promotes its plasma membrane location,which is essential to govern the neural excitability.Our study indicate that different KCs populations play variant roles in night-time sleep regulation and Neurexin regulates night-time sleep through modulating the excitability of KCs,which offers the insights into the neural circuit mechanism of sleep regulation and the molecular function of Neurexin.

关键词： Sleep neural circuit Mushroom body Kenyon cell Neurexin Na+/K+-ATPase neural excitability

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