NeuroCult™ Chemical Dissociation Kit (Mouse)

Kit for chemical dissociation of mouse neurospheres

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NeuroCult™ Chemical Dissociation Kit (Mouse)

Kit for chemical dissociation of mouse neurospheres

From: 195 USD
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Kit for chemical dissociation of mouse neurospheres
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Product Advantages


  • Obtain cleaner cultures with non-mechanical and non-enzymatic cell dissociation

  • Achieve significantly higher cell viability and total cell number after expansion compared to trituration

  • Ensure minimal cell damage and maintained functional properties of cells

What's Included

  • NeuroCult™ Chemical Dissociation Solution A, 55 mL
  • NeuroCult™ Chemical Dissociation Solution B, 15 mL
  • NeuroCult™ Chemical Dissociation Solution C, 15 mL

Overview

Dissociate neurospheres derived from embryonic or adult mouse central nervous system tissue with NeuroCult™ Chemical Dissociation Kit. This gentle, non-mechanical and non-enzymatic dissociation kit results in minimal damage to the cells, and ensures higher cell variability and total cell number after expansion in comparison with trituration. Functional properties of cells dissociated with the NeuroCult™ Chemical Dissociation Kit are also maintained upon subsequent subculture.
Subtype
Non-Enzymatic
Cell Type
Neural Stem and Progenitor Cells
Species
Mouse
Application
Cell Culture
Brand
NeuroCult
Area of Interest
Neuroscience, Stem Cell Biology

Data Figures

Chemical Dissociation of Mouse Neurospheres

Figure 1. Chemical Dissociation of Mouse Neurospheres

Photomicrographs showing the chemical dissociation of mouse neurospheres at (A) 2 minutes (C) 5 minutes and (E) 7 minutes after the addition of NeuroCult™ Chemical Dissociation Solution B. Figures (B), (D) and (F) are enlargements of the boxed areas in figures (A), (C) and (E), respectively. A single cell suspension is evident in (E) and (F).

Comparison of Percent Viability and Cell Expansion Between the Neurocult™ Chemical Dissociation Kit and Trituration

Figure 2. Comparison of Percent Viability and Cell Expansion Between the Neurocult™ Chemical Dissociation Kit and Trituration

Mouse neurospheres were dissociated at each passage (up to P10) with the NeuroCult™ Chemical Dissociation Kit or trituration. Cells dissociated with the NeuroCult™ Chemical Dissociation Kit had a significantly higher percent viability and total cell number (after expansion) in comparison with trituration.

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

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05707
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All
Language
English
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Technical Manual
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05707
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English
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Safety Data Sheet 1
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05707
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English
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Safety Data Sheet 2
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05707
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English
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Safety Data Sheet 3
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05707
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All
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English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (35)

Cathepsin B Improves ß-Amyloidosis and Learning and Memory in Models of Alzheimer's Disease. Embury CM et al. Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology 2017 JUN

Abstract

Amyloid-ß (Aß) precursor protein (APP) metabolism engages neuronal endolysosomal pathways for Aß processing and secretion. In Alzheimer's disease (AD), dysregulation of APP leads to excess Aß and neuronal dysfunction; suggesting that neuronal APP/Aß trafficking can be targeted for therapeutic gain. Cathepsin B (CatB) is a lysosomal cysteine protease that can lower Aß levels. However, whether CatB-modulation of Aß improves learning and memory function deficits in AD is not known. To this end, progenitor neurons were infected with recombinant adenovirus expressing CatB and recovered cell lysates subjected to proteomic analyses. The results demonstrated Lamp1 deregulation and linkages between CatB and the neuronal phagosome network. Hippocampal injections of adeno-associated virus expressing CatB reduced Aß levels, increased Lamp1 and improved learning and memory. The findings were associated with the emergence of c-fos + cells. The results support the idea that CatB can speed Aß metabolism through lysosomal pathways and as such reduce AD-associated memory deficits.
DNA polymerase β decrement triggers death of olfactory bulb cells and impairs olfaction in a mouse model of Alzheimer's disease. Misiak M et al. Aging cell 2017 FEB

Abstract

Alzheimer's disease (AD) involves the progressive degeneration of neurons critical for learning and memory. In addition, patients with AD typically exhibit impaired olfaction associated with neuronal degeneration in the olfactory bulb (OB). Because DNA base excision repair (BER) is reduced in brain cells during normal aging and AD, we determined whether inefficient BER due to reduced DNA polymerase-β (Polβ) levels renders OB neurons vulnerable to degeneration in the 3xTgAD mouse model of AD. We interrogated OB histopathology and olfactory function in wild-type and 3xTgAD mice with normal or reduced Polβ levels. Compared to wild-type control mice, Polβ heterozygous (Polβ+/- ), and 3xTgAD mice, 3xTgAD/Polβ+/- mice exhibited impaired performance in a buried food test of olfaction. Polβ deficiency did not affect the proliferation of OB neural progenitor cells in the subventricular zone. However, numbers of newly generated neurons were reduced by approximately 25% in Polβ+/- and 3xTgAD mice, and by over 60% in the 3xTgAD/Polβ+/- mice compared to wild-type control mice. Analyses of DNA damage and apoptosis revealed significantly greater degeneration of OB neurons in 3xTgAD/Polβ+/- mice compared to 3xTgAD mice. Levels of amyloid β-peptide (Aβ) accumulation in the OB were similar in 3xTgAD and 3xTgAD/Polβ+/- mice, and cultured Polβ-deficient neurons exhibited increased vulnerability to Aβ-induced death. Olfactory deficit is an early sign in human AD, but the mechanism is not yet understood. Our findings in a new AD mouse model demonstrate that diminution of BER can endanger OB neurons, and suggest a mechanism underlying early olfactory impairment in AD.
EVA1A/TMEM166 Regulates Embryonic Neurogenesis by Autophagy. Li M et al. Stem cell reports 2016 MAR

Abstract

Self-renewal and differentiation of neural stem cells is essential for embryonic neurogenesis, which is associated with cell autophagy. However, the mechanism by which autophagy regulates neurogenesis remains undefined. Here, we show that Eva1a/Tmem166, an autophagy-related gene, regulates neural stem cell self-renewal and differentiation. Eva1a depletion impaired the generation of newborn neurons, both in vivo and in vitro. Conversely, overexpression of EVA1A enhanced newborn neuron generation and maturation. Moreover, Eva1a depletion activated the PIK3CA-AKT axis, leading to the activation of the mammalian target of rapamycin and the subsequent inhibition of autophagy. Furthermore, addition of methylpyruvate to the culture during neural stem cell differentiation rescued the defective embryonic neurogenesis induced by Eva1a depletion, suggesting that energy availability is a significant factor in embryonic neurogenesis. Collectively, these data demonstrated that EVA1A regulates embryonic neurogenesis by modulating autophagy. Our results have potential implications for understanding the pathogenesis of neurodevelopmental disorders caused by autophagy dysregulation.
New look, same high quality and support! You may notice that your instrument or reagent packaging looks slightly different from images displayed on the website, or from previous orders. We are updating our look but rest assured, the products themselves and how you should use them have not changed. Learn more