Dendritic morphology is typically highly branched,and the branching and synaptic abundance of dendrites can enhance the receptive range of neurons and the diversity of information received,thus providing the basis for...Dendritic morphology is typically highly branched,and the branching and synaptic abundance of dendrites can enhance the receptive range of neurons and the diversity of information received,thus providing the basis for information processing in the nervous system.Once dendritic development is aberrantly compromised or damaged,it may lead to abnormal connectivity of the neural network,affecting the function and stability of the nervous system and ultimately triggering a series of neurological disorders.Research on the regulation of dendritic developmental processes has flourished,and much progress is now being made in its regulatory mechanisms.Noteworthily,dendrites are characterized by an extremely complex dendritic arborization that cannot be attributed to individual protein functions alone,requiring a systematic analysis of the intrinsic and extrinsic signals and the coordinated roles among them.Actin cytoskeleton organization and membrane vesicle trafficking are required during dendrite development,with actin providing tracks for vesicles and vesicle trafficking in turn providing material for actin assembly.In this review,we focus on these two basic biological processes and discuss the molecular mechanisms and their synergistic effects underlying the morphogenesis of neuronal dendrites.We also offer insights and discuss strategies for the potential preventive and therapeutic treatment of neuropsychiatric disorders.展开更多
Autism Spectrum Disorder(ASD)is marked by early-onset neurodevelopmental anomalies,yet the tem-poral dynamics of genetic contributions to these processes remain insufficiently understood.This study aimed to elu-cidate...Autism Spectrum Disorder(ASD)is marked by early-onset neurodevelopmental anomalies,yet the tem-poral dynamics of genetic contributions to these processes remain insufficiently understood.This study aimed to elu-cidate the role of the Shank3 gene,known to be associated with monogenic causes of autism,in early developmental processes to inform the timing and mechanisms for poten-tial interventions for ASD.Utilizing the Shank3B knockout(KO)mouse model,we examined Shank3 expression and its impact on neuronal maturation through Golgi staining for dendritic morphology and electrophysiological recordings to measure synaptic function in the anterior cingulate cortex(ACC)across different postnatal stages.Our longitudinal analysis revealed that,while Shank3B KO mice displayed normal neuronal morphology at one week postnatal,signifi-cant impairments in dendritic growth and synaptic activity emerged by two to three weeks.These findings highlight the critical developmental window during which Shank3 is essential for neuronal and synaptic maturation in the ACC.展开更多
Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic...Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumetanide 200 μg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These findings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia.展开更多
基金supported by the National Natural Science Foundation of China(32100784)the Natural Science Foundation of Jiangsu Province(BK20221458)the Fundamental Research Funds for the Central Universities(also known as the Southeast University Zhishan Young Scholars Program,2242024RCB0031)。
文摘Dendritic morphology is typically highly branched,and the branching and synaptic abundance of dendrites can enhance the receptive range of neurons and the diversity of information received,thus providing the basis for information processing in the nervous system.Once dendritic development is aberrantly compromised or damaged,it may lead to abnormal connectivity of the neural network,affecting the function and stability of the nervous system and ultimately triggering a series of neurological disorders.Research on the regulation of dendritic developmental processes has flourished,and much progress is now being made in its regulatory mechanisms.Noteworthily,dendrites are characterized by an extremely complex dendritic arborization that cannot be attributed to individual protein functions alone,requiring a systematic analysis of the intrinsic and extrinsic signals and the coordinated roles among them.Actin cytoskeleton organization and membrane vesicle trafficking are required during dendrite development,with actin providing tracks for vesicles and vesicle trafficking in turn providing material for actin assembly.In this review,we focus on these two basic biological processes and discuss the molecular mechanisms and their synergistic effects underlying the morphogenesis of neuronal dendrites.We also offer insights and discuss strategies for the potential preventive and therapeutic treatment of neuropsychiatric disorders.
基金supported by the Natural Science Foundation of China(32394032,82201699,and 82221001)the Natural Science Foundation of Zhejiang Province(LTGD24H250001)+1 种基金the Kay R&D Program of Shaanxi Province(2023-YBSF-093),the Young Talent Fund of University Association for Science and Technology in Shaanxi(20220306)the Joint Founding Project of Innovation Research Institute,Xijing Hospital(LHJJ24JH02).
文摘Autism Spectrum Disorder(ASD)is marked by early-onset neurodevelopmental anomalies,yet the tem-poral dynamics of genetic contributions to these processes remain insufficiently understood.This study aimed to elu-cidate the role of the Shank3 gene,known to be associated with monogenic causes of autism,in early developmental processes to inform the timing and mechanisms for poten-tial interventions for ASD.Utilizing the Shank3B knockout(KO)mouse model,we examined Shank3 expression and its impact on neuronal maturation through Golgi staining for dendritic morphology and electrophysiological recordings to measure synaptic function in the anterior cingulate cortex(ACC)across different postnatal stages.Our longitudinal analysis revealed that,while Shank3B KO mice displayed normal neuronal morphology at one week postnatal,signifi-cant impairments in dendritic growth and synaptic activity emerged by two to three weeks.These findings highlight the critical developmental window during which Shank3 is essential for neuronal and synaptic maturation in the ACC.
文摘Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumetanide 200 μg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These findings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia.
