Neural Progenitor Cells <i>Rptor</i> Ablation Impairs Development but Benefits to Seizure‐Induced Behavioral Abnormalities

Chen, Linglin; Wu, Meiling; Zhu, Feng; Kai, Jiejing; Dong, Jie; Wu, Ximei; Zeng, Ling‐Hui

doi:10.1111/cns.12607

Cited by 11 publications

(6 citation statements)

References 42 publications

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“…The generation of Raptor deficient animal models has been a robust approach for demonstrating that mTORC1-signalling is critical for the development and function of several major cell types within the CNS. Conditional deletion of Rptor in NPCs during embryonic development leads to microcephaly and aberrant oligodendrocyte differentiation while Rptor inactivation in postnatal mice induces reactive astrogliosis (Bercury et al, 2014; Chen et al, 2016; Cloetta et al, 2013; Zhang et al, 2017). Furthermore, treatment of experimental models with pharmacological mTORC1 inhibitors leads to long-term learning and memory deficits (Blundell et al, 2008; Tischmeyer et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Reduced mTORC1-signaling in retinal progenitor cells leads to visual pathway dysfunction

2019

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Development of the vertebrate central nervous system involves the co-ordinated differentiation of progenitor cells and the establishment of functional neural networks. This neurogenic process is driven by both intracellular and extracellular cues that converge on the mammalian target of rapamycin complex 1 (mTORC1). Here we demonstrate that mTORC1-signalling mediates multi-faceted roles during central nervous system development using the mouse retina as a model system. Downregulation of mTORC1-signalling in retinal progenitor cells by conditional ablation of Rptor leads to proliferation deficits and an over-production of retinal ganglion cells during embryonic development. In contrast, reduced mTORC1-signalling in postnatal animals leads to temporal deviations in programmed cell death and the consequent production of asymmetric retinal ganglion cell mosaics and associated loss of axonal termination topographies in the dorsal lateral geniculate nucleus of adult mice. In combination these developmental defects induce visually mediated behavioural deficits. These collective observations demonstrate that mTORC1-signalling mediates critical roles during visual pathway development and function.

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Section: Introductionmentioning

confidence: 99%

Reduced mTORC1-signaling in retinal progenitor cells leads to visual pathway dysfunction

2019

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“…Alternatively, female Gulo −/− pups supplemented with or without 3.3 g/L of VC, were peritoneally injected with or without l -NAME at 0.8 mg/10 body weight, once daily, for four consecutive weeks. These groups of pups were then subjected to the tests for learning and memory abilities by using a Morris water maze as described previously [ 30 ].…”

Section: Methodsmentioning

confidence: 99%

Vitamin C deficiency induces hypoglycemia and cognitive disorder through S-nitrosylation-mediated activation of glycogen synthase kinase 3β

et al. 2022

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“…The approach-response test and touch-response test were used to determine the excitability and sensory responsiveness of mice as previously described . (1) Approach-response test: a pen is vertically slowly moved toward the face of the animal.…”

Section: Methodsmentioning

confidence: 99%

“…The approach-response test and touch-response test were used to determine the excitability and sensory responsiveness of mice as previously described. 18 (1) Approach-response test: a pen is vertically slowly moved toward the face of the animal. Responses were scored as follows: 1, no reaction; 2, the mouse sniffs at the object; 3, the mouse moves away from the object; 4, the mouse freezes; 5, the mouse jerks away from the object; 6, the mice jump with or without vocalizations.…”

Section: Test For Behavioral Hyperexcitabilitymentioning

confidence: 99%

Time Course of Metabolic Alterations Associated with the Progression of Systemic Lupus Erythematosus in MRL/lpr Mice Based on GC/MS

Zhang

Wang

et al. 2020

J. Proteome Res.

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Exploring the dynamic changes of metabolites and metabolic pathways during the development of the disease can help to further understand the etiology and pathogenesis of systemic lupus erythematosus (SLE). In this study, serum metabolomics based on gas chromatography/mass spectrometry (GC/MS) was employed to investigate the metabolic alterations at different stages of SLE using lupus-prone mice (MRL/lpr) of 9, 11, and 13 weeks of age. Multivariate statistical analysis was performed to view the alterations of metabolic profiles between MRL/lpr mice and age-matched C57BL/6 mice, and t-test and fold change criteria were used to identify differential metabolites at each stage. 11 changed metabolites were found in MRL/lpr mice at 9 weeks of age, which were mainly involved in the tricarboxylic acid (TCA) cycle, glycolysis, and butanoate metabolism; with the increase of week age, the TCA cycle was still disturbed, and the biosynthesis of fatty acids was significantly upregulated since 11 weeks of age; in addition, urea, urate, and indole-3-lactate were increased at 13 weeks of age. We found a time course of metabolic alterations in MRL/lpr mice, which may be related to the progression of SLE. These findings could provide a reference for studying the mechanism of SLE and judging the pathological stage and severity of the disease. The MS data have been deposited in Mendeley (https://www.mendeley.com/).

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Neural Progenitor Cells Rptor Ablation Impairs Development but Benefits to Seizure‐Induced Behavioral Abnormalities

Abstract: Loss of the Rptor gene in mice neural progenitor cells affects normal development in young age and may contribute to alleviate KA seizure-induced behavioral abnormalities, suggesting that raptor protein plays an important role in seizure comorbidities.

Cited by 11 publications

References 42 publications

Reduced mTORC1-signaling in retinal progenitor cells leads to visual pathway dysfunction

Reduced mTORC1-signaling in retinal progenitor cells leads to visual pathway dysfunction

Vitamin C deficiency induces hypoglycemia and cognitive disorder through S-nitrosylation-mediated activation of glycogen synthase kinase 3β

Time Course of Metabolic Alterations Associated with the Progression of Systemic Lupus Erythematosus in MRL/lpr Mice Based on GC/MS

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