Astrocyte morphogenesis is dependent on BDNF signaling via astrocytic TrkB.T1

Holt, Leanne M.; Hernandez, Raymundo; Pacheco, Natasha L.; Ceja, Beatriz Torres; Hossain, Muhannah; Olsen, Michelle L.

doi:10.7554/elife.44667

Cited by 125 publications

(104 citation statements)

References 71 publications

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“…Given the close relationship between astrocyte processes and synapses, it is not surprising that neurons or neuronal activity or both participate in astrocyte morphogenesis and PAP plasticity 41,[72][73][74][75][76][77][78][79][80][81][82] . Previous studies demonstrated that astrocytes exhibit reduced territory and neuropil infiltration in dark-reared animals, providing evidence for the involvement of neuronal activity in astrocyte morphogenesis 73,74 .…”

Section: Morphological Maturationmentioning

confidence: 99%

Astrocytogenesis: where, when, and how

2020

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Astrocytes are the most abundant cell type in the central nervous system and have diverse functions in blood–brain barrier maintenance, neural circuitry formation and function, and metabolic regulation. To better understand the diverse roles of astrocytes, we will summarize what is known about astrocyte development and the challenges limiting our understanding of this process. We will also discuss new approaches and technologies advancing the field.

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Section: Morphological Maturationmentioning

confidence: 99%

Astrocytogenesis: where, when, and how

2020

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“…5n). Astrocyte functional genes were also significantly decreased in SOX2-defciency mice, for example, glutamate transport genes Slc1a2 and Slc1a3 (38), synaptogenesis regulatory genes Sparcl1 and Megf10 (21,39), astrocytic morphogenesis-promoting gene Ntrk2 (35), and K + -buffering gene Kcnj10 (28) ( Fig. 5n).…”

Section: Sox2 Targets a Cohort Of Genes That Are Crucial For Astrocytmentioning

confidence: 89%

“…In addition, SOX2 also bound to other characteristic astrocyte genes, for example, Gfap, Apq4, Wnt7a, Ntrk2, and Sparcl1 ( Fig. 5g-l), among which Ntrk2 has been shown to promote astrocyte morphological maturation both in vivo and in in vitro (35).…”

Section: Sox2 Targets a Cohort Of Genes That Are Crucial For Astrocytmentioning

confidence: 98%

The stem cell transcription factor SOX2 is essential for astrocyte maturation and controls animal hyperactive behavior

Zhang¹,

Lan²,

Wang³

et al. 2020

Preprint

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Children with SOX2-deficiency develop anophthalmia/microphthalmia and display neurological impairment. Here we report an essential role for astroglial SOX2 in brain anomalies and neurological defects. Sox2-deficiency inhibited postnatal astrocyte maturation without affecting astroglial proliferation and population expansion. Mechanistically, we found that SOX2 directly bound to a cohort of astrocytic signature genes such as those involving in glutamate transport and that Sox2-deficiency remarkably reduced glutamate transporter expression and compromised astrocyte function of glutamate uptake. Behaviorally, astroglial Sox2-deficient mice developed hyperactivity in locomotion while their motor skills, social capability, and learning abilities were unaffected. We found that astroglial Sox2-deficiency results in elevated glutamatergic synapse formation and elevated excitability of striatal medium spiny neurons, which has been shown to trigger hyperactive locomotion. Our study provides new insights into the biological mechanisms underlying brain defects in children with SOX2 mutations and unveils a novel connection between astrocyte SOX2 and brain development and behavior.

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“…Therefore, it may be anticipated that the observed neurodevelopmental effects of STEE in this study were mediated by the activation of TrkB and Rho signaling evident by the upregulation of their downstream effectors Pik3r1 and Limk1 , respectively ( Gupta et al, 2013 ; Tejeda and Diaz-Guerra, 2017 ; Ravindran et al, 2019 ). Particularly, recently explored role of astrocytic TrkB-T1 signaling in astrocyte morphogenesis ( Holt et al, 2019 ) warrants further research on the effect of STEE and its active compounds on TrkB activation.…”

Section: Discussionmentioning

confidence: 99%

Sugarcane (Saccharum officinarum L.) Top Extract Ameliorates Cognitive Decline in Senescence Model SAMP8 Mice: Modulation of Neural Development and Energy Metabolism

Iwata

Ferdousi

et al. 2020

Front. Cell Dev. Biol.

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Age-related biological alterations in brain function increase the risk of mild cognitive impairment and dementia, a global problem exacerbated by aging populations in developed nations. Limited pharmacological therapies have resulted in attention turning to the promising role of medicinal plants and dietary supplements in the treatment and prevention of dementia. Sugarcane ( Saccharum officinarum L.) top, largely considered as a by-product because of its low sugar content, in fact contains the most abundant amounts of antioxidant polyphenols relative to the rest of the plant. Given the numerous epidemiological studies on the effects of polyphenols on cognitive function, in this study, we analyzed polyphenolic constituents of sugarcane top and examined the effect of sugarcane top ethanolic extract (STEE) on a range of central nervous system functions in vitro and in vivo . Orally administrated STEE rescued spatial learning and memory deficit in the senescence-accelerated mouse prone 8 (SAMP8) mice, a non-transgenic strain that spontaneously develops a multisystemic aging phenotype including pathological features of Alzheimer’s disease. This could be correlated with an increased number of hippocampal newborn neurons and restoration of cortical monoamine levels in STEE-fed SAMP8 mice. Global genomic analysis by microarray in cerebral cortices showed multiple potential mechanisms for the cognitive improvement. Gene set enrichment analysis (GSEA) revealed biological processes such as neurogenesis, neuron differentiation, and neuron development were significantly enriched in STEE-fed mice brain compared to non-treated SAMP8 mice. Furthermore, STEE treatment significantly regulated genes involved in neurotrophin signaling, glucose metabolism, and neural development in mice brain. Our in vitro results suggest that STEE treatment enhances the metabolic activity of neuronal cells promoting glucose metabolism with significant upregulation of genes, namely PGK1 , PGAM1 , PKM , and PC . STEE also stimulated proliferation of human neural stem cells (hNSCs), regulated bHLH factor expression and induced neuronal differentiation and astrocytic process lengthening. Altogether, our findings suggest the potential of STEE as a dietary intervention, with promising implications as a novel nutraceutical for cognitive health.

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Astrocyte morphogenesis is dependent on BDNF signaling via astrocytic TrkB.T1

Cited by 125 publications

References 71 publications

Astrocytogenesis: where, when, and how

Astrocytogenesis: where, when, and how

The stem cell transcription factor SOX2 is essential for astrocyte maturation and controls animal hyperactive behavior

Sugarcane (Saccharum officinarum L.) Top Extract Ameliorates Cognitive Decline in Senescence Model SAMP8 Mice: Modulation of Neural Development and Energy Metabolism

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