NeuroCult™ Differentiation Kit (Mouse & Rat)

Medium kit for differentiation of mouse and rat neural stem and progenitor cells

NeuroCult™ Differentiation Kit (Mouse & Rat)

Medium kit for differentiation of mouse and rat neural stem and progenitor cells

NeuroCult™ Differentiation Kit (Mouse & Rat)
1 Kit
250 USD
Catalog # 05704

Medium kit for differentiation of mouse and rat neural stem and progenitor cells

What's Included

  • NeuroCult™ Basal Medium (Mouse & Rat), 450 mL (Catalog #05700)
  • NeuroCult™ Differentiation Supplement (Mouse & Rat), 50 mL (Catalog #05703)

Overview

NeuroCult™ Differentiation Kit (Mouse & Rat) is a standardized medium and supplement kit for the differentiation of mouse and rat neural stem and progenitor cells into neurons, astrocytes, and oligodendrocytes.
Contains
Serum
Subtype
Specialized Media
Cell Type
Brain Tumor Stem Cells, Neural Stem and Progenitor Cells
Species
Mouse, Rat
Application
Cell Culture, Differentiation, Functional Assay
Brand
NeuroCult
Area of Interest
Neuroscience, Stem Cell Biology

Data Figures

Differentiation of Mouse Neural Stem Cells Using NeuroCult™

Figure 1. Differentiation of Mouse Neural Stem Cells Using NeuroCult™

(A) Immunofluorescent staining of neural cell body and processes (red) with mouse monoclonal ß-Tubulin III antibody. (B) Immunofluorescent staining of astrocytes (green) with rabbit polyclonal GFAP antibody and neurons (red) with mouse monoclonal MAP2 antibody. (C) Immunofluorescent staining of oligodendrocytes (green) with mouse monoclonal O4 Oligodendrocyte Marker antibody. (D) Immunofluorescent staining of GABA-nergic neurons (green) with rabbit polyclonal GABA antibody.

Protocols and Documentation

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

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
05704
Lot #
All
Language
English
Catalog #
05704
Lot #
All
Language
English
Document Type
Technical Manual
Catalog #
05704
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
05704
Lot #
All
Language
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 (30)

Recombinant insulin-like growth factor binding protein-4 inhibits proliferation and promotes differentiation of neural progenitor cells Niu H et al. Neuroscience Letters 2017 MAR

Abstract

Insulin-like growth factor (IGF) is involved in regulating many processes during neural development, and IGF binding protein-4 (IGFBP4) functions as a modulator of IGF actions or in an IGF-independent manner (e.g., via inhibiting Wnt/β-catenin signaling). In the present study, neural progenitor cells (NPCs) were isolated from the forebrain of newborn mice to investigate effects of IGFBP4 on the proliferation and differentiation of NPCs. The proliferation of NPCs was evaluated using Cell Counting Kit-8 (CCK-8) after treatment with or without IGFBP4 as well as blockers of IGF-IR and β-catenin. Phosphorylation levels of Akt, Erk1, 2 and p38 were analyzed by Western blotting. The differentiation of NPCs was evaluated using immunofluorescence and Western blotting. It was shown that exogenous IGFBP4 significantly inhibited the proliferation of NPCs and it did not induce a more pronounced inhibition of cell proliferation after blockade of IGF-IR but it did after antagonism of β-catenin. Akt phosphorylation was significantly decreased and phosphorylation levels of Erk1, 2 and p38 were not significantly changed in IGFBP4-treated NPCs. Excessive IGFBP4 significantly promoted NPCs to differentiate into astrocytes and neurons. These data suggested that exogenous IGFBP4 inhibits proliferation and promotes differentiation of neural progenitor cells mainly through IGF-IR signaling pathway.
L2hgdh deficiency accumulates L-2-hydroxyglutarate with progressive leukoencephalopathy and neurodegeneration Ma S et al. Molecular and Cellular Biology 2017 JAN

Abstract

L-2-hydroxyglutarate aciduria (L-2-HGA) is an autosomal recessive neurometabolic disorder caused by a mutation in the L-2-hydroxyglutarate dehydrogenase ( L2HGDH ) gene. In this study, we generated L2hgdh knockout (KO) mice and observed a robust increase of 2-hydroxyglutarate (L-2-HG) levels in multiple tissues. The highest levels of L-2-HG were observed in the brain and testis with a corresponding increase in histone methylation in these tissues. L2hgdh KO mice exhibit white matter abnormalities, extensive gliosis, microglia-mediated neuroinflammation, and an expansion of oligodendrocyte progenitor cells (OPCs). Moreover, L2hgdh deficiency leads to impaired adult hippocampal neurogenesis and late-onset neurodegeneration in mouse brains. Our data provide in vivo evidence that L2hgdh mutation leads to L-2-HG accumulation, leukoencephalopathy, and neurodegeneration in mice, thus offering new insights into the pathophysiology of L-2-HGA in humans.
Exercise protects against methamphetamine-induced aberrant neurogenesis. Park M et al. Scientific reports 2016 SEP

Abstract

While no effective therapy is available for the treatment of methamphetamine (METH)-induced neurotoxicity, aerobic exercise is being proposed to improve depressive symptoms and substance abuse outcomes. The present study focuses on the effect of exercise on METH-induced aberrant neurogenesis in the hippocampal dentate gyrus in the context of the blood-brain barrier (BBB) pathology. Mice were administered with METH or saline by i.p. injections for 5 days with an escalating dose regimen. One set of mice was sacrificed 24 h post last injection of METH, and the remaining animals were either subjected to voluntary wheel running (exercised mice) or remained in sedentary housing (sedentary mice). METH administration decreased expression of tight junction (TJ) proteins and increased BBB permeability in the hippocampus. These changes were preserved post METH administration in sedentary mice and were associated with the development of significant aberrations of neural differentiation. Exercise protected against these effects by enhancing the protein expression of TJ proteins, stabilizing the BBB integrity, and enhancing the neural differentiation. In addition, exercise protected against METH-induced systemic increase in inflammatory cytokine levels. These results suggest that exercise can attenuate METH-induced neurotoxicity by protecting against the BBB disruption and related microenvironmental changes in the hippocampus.

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