NeuroCult™ Basal Medium (Mouse & Rat)

Basal medium for culture of mouse and rat neural stem and progenitor cells

More Views

NeuroCult™ Basal Medium (Mouse & Rat)

Basal medium for culture of mouse and rat neural stem and progenitor cells

450 mL
Catalog #05700
82 USD

Required Products

Overview

NeuroCult™ Basal Medium (Mouse & Rat) is a standardized serum-free basal medium designed to be supplemented with NeuroCult™ Proliferation Supplement (Mouse & Rat; Catalog #05701) and appropriate cytokines for the in vitro culture and expansion of mouse and rat neural stem and progenitor cells. NeuroCult™ Basal Medium (Mouse & Rat) can also be supplemented with NeuroCult™ Differentiation Supplement (Mouse & Rat; Catalog #05703) for the differentiation of mouse and rat neural stem and progenitor cells into neurons, astrocytes, and oligodendrocytes. NeuroCult™ Basal Medium (Mouse & Rat) is a component of NeuroCult™ Proliferation Kit (Mouse & Rat; Catalog #05702) and NeuroCult™ Differentiation Kit (Mouse & Rat; Catalog #05704).

NOTE: When preparing Complete NeuroCult™ Proliferation Medium, addition of Human Recombinant EGF (Catalog #78006.1) is required. When culturing cells obtained from adult mouse or rat, Human Recombinant bFGF (Catalog #78003.1) and Heparin Solution (Catalog #07980) are also required.
Subtype:
Basal Media; Specialized Media
Cell Type:
Brain Tumor Stem Cells; Neural Stem and Progenitor Cells
Species:
Mouse; Rat
Application:
Cell Culture; Colony Assay; Differentiation; Expansion; Functional Assay; Spheroid Culture
Brand:
NeuroCult
Area of Interest:
Cancer Research; Disease Modeling; Neuroscience; Stem Cell Biology
Formulation:
Serum-Free

Scientific Resources

Educational Materials

(8)

Product 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.

Data and Publications

Publications

(128)
Neuroscience Letters 2017 MAR

Recombinant insulin-like growth factor binding protein-4 inhibits proliferation and promotes differentiation of neural progenitor cells

Niu H et al.

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.
Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology 2017 JUN

Cathepsin B Improves ß-Amyloidosis and Learning and Memory in Models of Alzheimer's Disease.

Embury CM et al.

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.
Nature genetics 2017 JAN

Qki deficiency maintains stemness of glioma stem cells in suboptimal environment by downregulating endolysosomal degradation.

Shingu T et al.

Abstract

Stem cells, including cancer stem cells (CSCs), require niches to maintain stemness, yet it is unclear how CSCs maintain stemness in the suboptimal environment outside their niches during invasion. Postnatal co-deletion of Pten and Trp53 in mouse neural stem cells (NSCs) leads to the expansion of these cells in their subventricular zone (SVZ) niches but fails to maintain stemness outside the SVZ. We discovered that Qki is a major regulator of NSC stemness. Qk deletion on a Pten-/-; Trp53-/- background helps NSCs maintain their stemness outside the SVZ in Nes-CreERT2; QkL/L; PtenL/L; Trp53L/L mice, which develop glioblastoma with a penetrance of 92% and a median survival time of 105 d. Mechanistically, Qk deletion decreases endolysosome-mediated degradation and enriches receptors essential for maintaining self-renewal on the cytoplasmic membrane to cope with low ligand levels outside niches. Thus, downregulation of endolysosome levels by Qki loss helps glioma stem cells (GSCs) maintain their stemness in suboptimal environments outside their niches.
Molecular and Cellular Biology 2017 JAN

L2hgdh deficiency accumulates L-2-hydroxyglutarate with progressive leukoencephalopathy and neurodegeneration

Ma S et al.

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.
Stem Cell Research & Therapy 2017 DEC

CCL11 promotes migration and proliferation of mouse neural progenitor cells

Wang F et al.

Abstract

BACKGROUND Neonatal hypoxia-ischemia induces massive brain damage during the perinatal period, resulting in long-term consequences to central nervous system structural and functional maturation. Although neural progenitor cells (NPCs) migrate through the parenchyma and home in to injury sites in the rodent brain, the molecular mechanisms are unknown. We examined the role of chemokines in mediating NPC migration after neonatal hypoxic-ischemic brain injury. METHODS Nine-day-old mice were exposed to a 120-minute hypoxia following unilateral carotid occlusion. Chemokine levels were quantified in mouse brain extract. Migration and proliferation assays were performed using embryonic and infant mouse NPCs. RESULTS The neonatal hypoxic-ischemic brain injury resulted in an ipsilateral lesion, which was extended to the cortical and striatal areas. NPCs migrated toward an injured area, where a marked increase of CC chemokines was detected. In vitro studies showed that incubation of NPCs with recombinant mouse CCL11 promoted migration and proliferation. These effects were partly inhibited by a CCR3 antagonist, SB297006. CONCLUSIONS Our data implicate an important effect of CCL11 for mouse NPCs. The effective activation of NPCs may offer a promising strategy for neuroregeneration in neonatal hypoxic-ischemic brain injury.
STEMCELL TECHNOLOGIES INC.’S QUALITY MANAGEMENT SYSTEM IS CERTIFIED TO ISO 13485. PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.