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Central Pain Syndrome Cell Model Products

Introduction Types Advantages Applications FAQs Related Product Sections Product List

Introduction

Elucidating the pathophysiology of Central Pain Syndrome (CPS)—a condition originating from lesions within the central nervous system—presents a formidable scientific challenge. Key molecular drivers, such as neuronal hyperexcitability and persistent glial activation, have proven difficult to model effectively. Consequently, preclinical progress has long been constrained by the poor clinical translatability of animal systems and the inherent variability and scarcity of primary human cells.

To address these critical limitations, highly characterized human iPSC-derived cellular platforms have now been engineered to faithfully recapitulate fundamental aspects of CPS pathogenesis. These reproducible, ready-to-use systems provide a crucial, human-specific context for the precise interrogation of disease mechanisms and the high-throughput screening of novel therapeutic compounds, thereby surmounting previous obstacles in the field. Contact our scientists for expert guidance in finding the perfect model for your study and to learn how you can accelerate your research.

Alternatively, you can find specific products by consulting our complete Product List.

Types of CPS Models Offered

Types Description
iPSC-Derived Sensory Neuron Monocultures These highly pure monocultures, enriched for nociceptive sensory neurons, provide a direct and clean system for interrogating neuronal hyperexcitability. They are ideal for high-fidelity electrophysiological studies and high-throughput screening campaigns targeting key pain-related ion channels like Nav1.7, Nav1.8, and TRPV1, allowing you to precisely assess changes in spontaneous firing rates and evoked potentials in response to your compounds.
Neuron-Astrocyte Co-Cultures This system recapitulates the critical bidirectional communication between neurons and astrocytes, which is fundamental to central sensitization. It is specifically designed for investigating how reactive astrocytes contribute to the pain state through mechanisms like glutamate dysregulation, release of pro-inflammatory cytokines (e.g., TNF-α, IL-1β), and altered gliotransmission, providing a far more complete and physiologically relevant picture of the neuro-inflammatory environment than monocultures alone.
Neuron-Microglia Co-Cultures These models place neurons in direct contact with the CNS's resident immune cells, the microglia, essential for studying the innate immune aspects of central pain. They are optimized for modeling the initiation and propagation of neuroinflammation driven by microglial activation. Use this system to screen for compounds that prevent microglial polarization (M1/M2 states), inhibit aberrant synaptic pruning, and suppress the secretion of key pain-mediating factors like BDNF and CCL2.
Custom-Engineered Models Move beyond correlation to causation by definitively validating your specific genetic target. Our expert team collaborates with you to design and execute precise genomic alterations using CRISPR/Cas9, including complete gene knockouts, SNP insertions mimicking patient genetics, or the introduction of fluorescent reporters. We deliver fully validated, clonally-derived isogenic cell lines, providing the ultimate control for definitively linking a genotype to a pain-related phenotype.

Advantages

Choosing Creative Biolabs CPS models gives your project a distinct competitive edge:

Achieve Unmatched Human Relevance

Move away from the translational gap of animal models. Investigate human-specific pathways and targets directly in a human genetic context.

Generate Reproducible, Reliable Data

Eliminate the frustrating variability of primary cells and the inconsistencies between different animal subjects. Our stringent QC guarantees models you can trust, experiment after experiment.

Accelerate Your Timeline

Skip the months-long, complex process of differentiating iPSCs yourself. Our models are pre-differentiated, characterized, and cryopreserved. Go from your freezer to your experiment in days, not months.

Recreate the Critical Neuro-Glia Axis

Central sensitization is driven by complex interactions between neurons and glial cells. Our co-culture and tri-culture systems allow you to study this critical crosstalk in a controlled environment.

Gain Clear Mechanistic Insights

The defined nature of our in vitro systems enables you to dissect specific molecular pathways and cellular contributions to CPS pathology without the confounding variables of an in vivo system.

Applications

Put our models to work in a range of critical applications:

Applications Description
Mechanism of Disease Studies Dissect the molecular signaling pathways that initiate and maintain central sensitization and neuronal hyperexcitability.
High-Throughput Screening (HTS) Screen compound libraries to identify novel analgesics that modulate neuronal firing or glial activation.
Therapeutic Target Validation Confirm the role of specific ion channels, receptors, or signaling proteins in CPS pathology.
Neuroinflammation Research Investigate the specific role of astrocytes and microglia in the neuroinflammatory processes that drive chronic central pain.
Predictive Toxicology Assess the potential for developmental compounds to induce neuronal hyperexcitability or neurotoxicity.
A picture that presents the Schematic illustration. (Kuan, et al., 2016) (OA Literature)Fig.1 Schematic illustration of P2X receptors' involvement in nociceptive transmission and modulation in central pain syndrome.1

FAQs

  • Can we request a custom model with a specific genetic mutation not in your catalog?
    Absolutely. Our custom engineering service is a core part of our offering. We can introduce specific knockouts, point mutations, or reporter genes using CRISPR technology. We encourage you to contact our scientific team to discuss the feasibility and timeline for your specific target.
  • How are the cells shipped, and what should I do if I encounter an issue?
    The cells are shipped cryopreserved on dry ice via a priority courier. We guarantee their viability upon arrival when handled according to our protocols. In the rare event of an issue, our dedicated technical support team is available to help troubleshoot and ensure your success.
  • Can I re-freeze the cells once thawed?
    No. Like most cryopreserved primary and iPSC-derived cells, these are intended for a single thaw. Re-freezing will severely compromise cell health and function.
  • Do you provide technical support?
    Yes! Our team of PhD scientists who developed these models is available to help you with any questions from initial setup to data interpretation.
  • Can I create my own co-culture by purchasing the monoculture vials separately?
    Yes, you can. We provide detailed protocols for combining the individual cell populations. However, for guaranteed results and convenience, we recommend our pre-validated co-culture systems, which have been optimized for cell ratios and stable integration.

The Creative Biolabs platforms for Central Pain Syndrome are engineered to expedite the preclinical development of novel therapeutics, extending far beyond the provision of standard cellular reagents. Each system is rigorously validated and supported by a comprehensive characterization dataset. This foundation of stringent quality control, coupled with expert technical consultation, provides the robust and reproducible framework necessary for researchers to execute their most critical programs with confidence. Contact our team of specialists to answer your questions, discuss how our CPS models can fit into your research, and get help designing your next experiment.

Related Product Sections

For more categories of Pain & Functional Disease related Research Tools, please visit the following links:

Reference

  1. Kuan, Yung-Hui, and Bai-Chuang Shyu. "Nociceptive transmission and modulation via P2X receptors in central pain syndrome." Molecular brain 9.1 (2016): 58. DOI: 10.3389/fneur.2019.00935. Use under Open Access license CC BY 4.0, without modification.