Human Cortical Neurons

Cat.No.: CSC-C1514

Species: Human

Source: Brain

Cell Type: Neuron

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Cat.No.
CSC-C1514
Description
Human Cortical Neurons are initiated by digestion of minced brain cortical tissue with collagenase. Human Cortical Neurons are guaranteed to further culture under the conditions provided in the data sheet; however, they are not recommended for expanding or long-term cultures since the cells do not proliferate in culture.
Species
Human
Source
Brain
Recommended Medium
It is recommended to use neuronal medium for culturing Human cortical neurons.
Cell Type
Neuron
Disease
Normal
Storage and Shipping
ship in dry ice; store in liquid nitrogen
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

Human Cortical Neurons (HCN) are terminally differentiated neurons that are not immortalized. They are normally obtained from ethically acquired fetal brain tissues from 14-22 gestational weeks. Unlike immortalized cell lines like SH-SY5Y, these cells maintain the phenotypic, molecular, and electrophysiological characteristics of human cortical neurons in vivo. They express key neuronal markers like TUJ1, MAP2, NeuN, and subtype-specific markers for glutamatergic and GABAergic neurons. They build functioning synaptic networks and have mature electrical activity, giving them an extremely physiologically realistic model. HCN are commonly utilized in neurodevelopment, neurodegenerative disease modeling, and CNS drug screening, and have improved clinical translatability than rodent models, despite constraints like as short culture lifetime, donor variability, and expensive cost.

SARS-CoV-2 S1 Protein Induces Endolysosome Dysfunction and Neuritic Dystrophy

Neurological disorders are increasingly associated with COVID-19, yet their pathogenesis remains unclear due to low or undetectable SARS-CoV-2 levels in brain tissue. The spike S1 protein, which can cross the blood-brain barrier and has been detected in neurons, presents a potential alternative mechanism. Datta et al. aimed to test the hypothesis that SARS-CoV-2 S1 protein directly induces neuronal injury.

Using primary human cortical neurons, researchers investigated whether SARS-CoV-2 S1 protein accumulation causes cellular damage underlying COVID-19 neurological complications. Following characterization in CLU199 neuronal cells, we examined S1 effects on endolysosome function in primary human cortical neurons. S1-RBD-GFP (250 ng/ml, 48 h) localized to Lysotracker-, Rab7-, and LAMP1-positive endolysosomes (Fig. 1A). S1 protein (50-100 ng/ml) rapidly and robustly de-acidified endolysosomes, measured by ratiometric pH sensing in LAMP1-positive vesicles (Fig. 1B). Additionally, S1 (100 ng/ml, 30 min) decreased the percentage of endolysosomes containing enzymatically active cathepsin D (Fig. 1C), consistent with findings in CLU199 cells.

SARS-CoV2 S1 protein entered endolysosomes and induced lysosome dysfunction in human neurons.

Fig. 1. SARS-CoV2 S1 protein entered endolysosomes and induced lysosome dysfunction in human neurons (Datta G, Miller N M, et al., 2021).

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