BrainPhys™ Without Phenol Red

Serum-free neurophysiological basal medium for improved neuronal function

BrainPhys™ Without Phenol Red

Serum-free neurophysiological basal medium for improved neuronal function

BrainPhys™ Without Phenol Red
500 mL
123 USD
Catalog # 05791

Serum-free neurophysiological basal medium for improved neuronal function

Product Advantages

• More representative of the brain’s extracellular environment
• Improved neuronal function and a higher proportion of synaptically active neurons
• Perform functional assays without changing media and shocking cells
• Supports long-term culture of ES/iPS cell- and CNS-derived neurons
• Rigorous raw material screening and quality control ensure minimal lot-to-lot variability


Promote, rather than inhibit, neuronal activity and maturity in your cultured primary or human pluripotent stem cell (hPSC)-derived neurons in a phenol red-free environment.

Based on the formulation by Bardy and Gage (Bardy C et al. PNAS, 2015), BrainPhys™ serum-free neuronal basal medium is optimized to yield a higher proportion of synaptically active neurons by mimicking the central nervous system extracellular environment. Use BrainPhys™ Without Phenol Red to culture primary neurons, differentiate and mature hPSC-derived neurons, record microelectrode array-based neuronal activity, live-fluorescent image neurons, and transdifferentiate somatic cells to neurons without hormonal signaling.

To ensure cell survival in long-term serum-free culture, BrainPhys™ Without Phenol Red must be combined with an appropriate serum-replacement supplement, such as NeuroCult™ SM1 Neuronal Supplement (Catalog #05711) and/or N2 Supplement-A (Catalog #07152).
Basal Media, Specialized Media
Cell Type
Neural Cells, PSC-Derived, Neurons, Pluripotent Stem Cells
Human, Mouse, Rat
Cell Culture, Differentiation, Maintenance
Area of Interest
Disease Modeling, Drug Discovery and Toxicity Testing, Neuroscience, Stem Cell Biology

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 (2)

Mutations in ACTL6B Cause Neurodevelopmental Deficits and Epilepsy and Lead to Loss of Dendrites in Human Neurons. S. Bell et al. American journal of human genetics 2019


We identified individuals with variations in ACTL6B, a component of the chromatin remodeling machinery including the BAF complex. Ten individuals harbored bi-allelic mutations and presented with global developmental delay, epileptic encephalopathy, and spasticity, and ten individuals with de novo heterozygous mutations displayed intellectual disability, ambulation deficits, severe language impairment, hypotonia, Rett-like stereotypies, and minor facial dysmorphisms (wide mouth, diastema, bulbous nose). Nine of these ten unrelated individuals had the identical de novo c.1027G{\textgreater}A (p.Gly343Arg) mutation. Human-derived neurons were generated that recaptured ACTL6B expression patterns in development from progenitor cell to post-mitotic neuron, validating the use of this model. Engineered knock-out of ACTL6B in wild-type human neurons resulted in profound deficits in dendrite development, a result recapitulated in two individuals with different bi-allelic mutations, and reversed on clonal genetic repair or exogenous expression of ACTL6B. Whole-transcriptome analyses and whole-genomic profiling of the BAF complex in wild-type and bi-allelic mutant ACTL6B neural progenitor cells and neurons revealed increased genomic binding of the BAF complex in ACTL6B mutants, with corresponding transcriptional changes in several genes including TPPP and FSCN1, suggesting that altered regulation of some cytoskeletal genes contribute to altered dendrite development. Assessment of bi-alleic and heterozygous ACTL6B mutations on an ACTL6B knock-out human background demonstrated that bi-allelic mutations mimic engineered deletion deficits while heterozygous mutations do not, suggesting that the former are loss of function and the latter are gain of function. These results reveal a role for ACTL6B in neurodevelopment and implicate another component of chromatin remodeling machinery in brain disease.
iPSC-derived familial Alzheimer's PSEN2 N141I cholinergic neurons exhibit mutation-dependent molecular pathology corrected by insulin signaling. C. L. Moreno et al. Molecular neurodegeneration 2018


BACKGROUND Type 2 diabetes (T2D) is a recognized risk factor for the development of cognitive impairment (CI) and/or dementia, although the exact nature of the molecular pathology of T2D-associated CI remains obscure. One link between T2D and CI might involve decreased insulin signaling in brain and/or neurons in either animal or postmortem human brains as has been reported as a feature of Alzheimer's disease (AD). Here we asked if neuronal insulin resistance is a cell autonomous phenomenon in a familial form of AD. METHODS We have applied a newly developed protocol for deriving human basal forebrain cholinergic neurons (BFCN) from skin fibroblasts via induced pluripotent stem cell (iPSC) technology. We generated wildtype and familial AD mutant PSEN2 N141I (presenilin 2) BFCNs and assessed if insulin signaling, insulin regulation of the major AD proteins Abeta$ and/or tau, and/or calcium fluxes is altered by the PSEN2 N141I mutation. RESULTS We report herein that wildtype, PSEN2 N141I and CRISPR/Cas9-corrected iPSC-derived BFCNs (and their precursors) show indistinguishable insulin signaling profiles as determined by the phosphorylation of canonical insulin signaling pathway molecules. Chronic insulin treatment of BFCNs of all genotypes led to a reduction in the Abeta$42/40 ratio. Unexpectedly, we found a CRISPR/Cas9-correctable effect of PSEN2 N141I on calcium flux, which could be prevented by chronic exposure of BFCNs to insulin. CONCLUSIONS Our studies indicate that the familial AD mutation PSEN2 N141I does not induce neuronal insulin resistance in a cell autonomous fashion. The ability of insulin to correct calcium fluxes and to lower Abeta$42/40 ratio suggests that insulin acts to oppose an AD-pathophysiology. Hence, our results are consistent with a potential physiological role for insulin as a mediator of resilience by counteracting specific metabolic and molecular features of AD.

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