Dendritic Spine Dynamics

Bhatt, Dimple H.; Zhang, Shengxiang; Gan, Wen‐Biao

doi:10.1146/annurev.physiol.010908.163140

Cited by 344 publications

(331 citation statements)

References 198 publications

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“…Furthermore, axon guidance cues also play a role in synaptogenesis as they promote or inhibit the formation of presynaptic terminals. 60 After the formation of axon-dendritic complexes, some contacts will become stabilized. At present, the molecular mechanisms underlying the stabilization of synapses remain poorly understood.…”

Section: The Developing Mammalian Brainmentioning

confidence: 99%

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

Donega

Velthoven

Nijboer

et al. 2013

J Cereb Blood Flow Metab

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Neurogenesis continues throughout adulthood. The neurogenic capacity of the brain increases after injury by, e.g., hypoxiaischemia. However, it is well known that in many cases brain damage does not resolve spontaneously, indicating that the endogenous regenerative capacity of the brain is insufficient. Neonatal encephalopathy leads to high mortality rates and long-term neurologic deficits in babies worldwide. Therefore, there is an urgent need to develop more efficient therapeutic strategies. The latest findings indicate that stem cells represent a novel therapeutic possibility to improve outcome in models of neonatal encephalopathy. Transplanted stem cells secrete factors that stimulate and maintain neurogenesis, thereby increasing cell proliferation, neuronal differentiation, and functional integration. Understanding the molecular and cellular mechanisms underlying neurogenesis after an insult is crucial for developing tools to enhance the neurogenic capacity of the brain. The aim of this review is to discuss the endogenous capacity of the neonatal brain to regenerate after a cerebral ischemic insult. We present an overview of the molecular and cellular mechanisms underlying endogenous regenerative processes during development as well as after a cerebral ischemic insult. Furthermore, we will consider the potential to use stem cell transplantation as a means to boost endogenous neurogenesis and restore brain function.

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Section: The Developing Mammalian Brainmentioning

confidence: 99%

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

Donega

Velthoven

Nijboer

et al. 2013

J Cereb Blood Flow Metab

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“…Over the past several decades, studies have mostly focused on the molecular mechanisms underlying the later stages of neuronal morphogenesis, including those mediating polarization [6][7][8][9], dendrite morphogenesis [10][11][12][13][14][15][16], synaptogenesis [17][18][19][20], and spinogenesis [21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Actin Aggregations Mark the Sites of Neurite Initiation

et al. 2016

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A salient feature of neurons is their intrinsic ability to grow and extend neurites, even in the absence of external cues. Compared to the later stages of neuronal development, such as neuronal polarization and dendrite morphogenesis, the early steps of neuritogenesis remain relatively unexplored. Here we showed that redistribution of cortical actin into large aggregates preceded neuritogenesis and determined the site of neurite initiation. Enhancing actin polymerization by jasplakinolide treatment effectively blocked actin redistribution and neurite initiation, while treatment with the actin depolymerizing agents latrunculin A or cytochalasin D accelerated neurite formation. Together, these results demonstrate a critical role of actin dynamics and reorganization in neurite initiation. Further experiments showed that microtubule dynamics and protein synthesis are not required for neurite initiation, but are required for later neurite stabilization. The redistribution of actin during early neuronal development was also observed in the cerebral cortex and hippocampus in vivo.

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“…Despite these behavioral abnormalities, the gross structure of the brain is largely intact in FXS patients and in the mouse model of the disorder. The most consistent anatomical finding is an abnormal profile of dendritic spines, postsynaptic protrusions that receive the vast majority of excitatory input in the brains of diverse species (14)(15)(16)(17).…”

mentioning

confidence: 98%

Dendritic spine instability and insensitivity to modulation by sensory experience in a mouse model of fragile X syndrome

Pan

Aldridge²,

Greenough³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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183

207

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Fragile X syndrome (FXS) is the most common inherited form of mental retardation and is caused by transcriptional inactivation of the X-linked fragile X mental retardation 1 (FMR1) gene. FXS is associated with increased density and abnormal morphology of dendritic spines, the postsynaptic sites of the majority of excitatory synapses. To better understand how lack of the FMR1 gene function affects spine development and plasticity, we examined spine formation and elimination of layer 5 pyramidal neurons in the whisker barrel cortex of Fmr1 KO mice with a transcranial two-photon imaging technique. We found that the rates of spine formation and elimination over days to weeks were significantly higher in both young and adult KO mice compared with littermate controls. The heightened spine turnover in KO mice was due to the existence of a larger pool of "short-lived" new spines in KO mice than in controls. Furthermore, we found that the formation of new spines and the elimination of existing ones were less sensitive to modulation by sensory experience in KO mice. These results indicate that the loss of Fmr1 gene function leads to ongoing overproduction of transient spines in the primary somatosensory cortex. The insensitivity of spine formation and elimination to sensory alterations in Fmr1 KO mice suggest that the developing synaptic circuits may not be properly tuned by sensory stimuli in FXS.autism | imaging | mental retardation | synaptic plasticity | two-photon microscopy F ragile X syndrome (FXS) is the most common form of inherited mental retardation, affecting about 1 in 4,000 males and 1 in 8,000 females (1). Patients who suffer from FXS exhibit various degrees of cognitive, socio-affective, and sensory-motor abnormalities (2). The syndrome is caused by the expansion of a polymorphic CGG trinucleotide repeat in the 5′ untranslated region of the fragile X mental retardation 1 (FMR1) gene located on the X chromosome (3). The fragile X mental retardation protein (FMRP), which is encoded by the FMR1 gene, binds to many mRNAs and is believed to regulate protein translation in various subcellular locations, including dendrites and dendritic spines (4, 5).The Fmr1 KO mice demonstrate many abnormalities found in FXS patients, such as impairments of learning and memory (6-8), social behaviors (9-11), and sensory processing (12, 13), thus providing an excellent model system to study pathogenic mechanisms underlying FXS. Despite these behavioral abnormalities, the gross structure of the brain is largely intact in FXS patients and in the mouse model of the disorder. The most consistent anatomical finding is an abnormal profile of dendritic spines, postsynaptic protrusions that receive the vast majority of excitatory input in the brains of diverse species (14-17).In FXS, the adult dendritic spine phenotype includes increases in spine density and spine length and the number of immaturelooking spines in the various brain regions examined (15,16,18). Similarly, in the visual and somatosensory cortices of adult Fmr1 KO mice, p...

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Dendritic Spine Dynamics

Cited by 344 publications

References 198 publications

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

Actin Aggregations Mark the Sites of Neurite Initiation

Dendritic spine instability and insensitivity to modulation by sensory experience in a mouse model of fragile X syndrome

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