Cortical Inhibitory Interneurons
Interneurons are involved in major neurological disease types. But traditional in vitro models rarely include them. Read on to find out how your research can benefit from our latest Early Access product.
Brains need brakes – just ask anyone researching epilepsy.
Interneurons make up about 20-30% of neurons in the neocortex, the location of functions like sensory perception, emotion and cognition. They play an essential role in all higher cortical functions including learning, memory and cognition, helping to integrate and regulate synaptic activity. The brain has excitatory and inhibitory interneurons, with the latter acting as “brakes” in the human CNS, functioning to decrease the likelihood of an action potential occurring.
Disorders of cortical inhibitory interneurons have been implicated in several neurological conditions , including:
- Alzheimer’s Disease
- Parkinson’s Disease
- Seizures & epilepsy
- Neurodevelopmental disorders including autism spectrum disorders, intellectual disability, schizophrenia
Despite this, interneurons are often left out of in vitro brain models or just used in mono-culture, leaving potentially crucial insights behind. Adding interneurons in co-culture with other cells of the brain could produce more physiologically relevant in vitro brain models when studying neurodegenerative diseases.
The value of human iPSCs in modelling the brain
Traditional animal models of neurotoxicity bring translational barriers; for example, there have been contradictory findings when assessing the expression of parvalbumin interneurons (a subtype of inhibitory interneuron) in mouse models of Alzheimer’s disease .
To produce more physiologically-relevant human disease models, cortical inhibitory interneuron progenitors can be derived from human induced pluripotent stem cell (iPSC) interneurons, to add in co-culture with other cell types, such as cortical neurons and astrocytes.
“… iPSCs fill a critical gap in our experimental approaches by providing live, functioning human CNS cells with the genetic backgrounds of patients” 
We recognize the opportunity that iPSCs offer in building isogenic models – where multiple cell types are derived from the same original donor plus patient-derived models. Human iPSC derived cells could be used to build better human models for neurodegenerative disease research.
Early Access axoCellsTM
Interneurons, at their core, work together with other cells. This is why we’ve developed our axoCellsTM cortical inhibitory interneuron progenitor cells in our R&D lab, and actively encourage their use in co- and tri- culture models for better, more physiologically relevant human models.
Our cells are supplied as cortical inhibitory interneuron progenitor cells and take 20 days to become mature interneurons, characterized by key markers such as parvalbumin, somatostatin and PAX-6. At day 30, the mature interneurons display functional calcium imaging responses to glutamic acid and glycine.
Early Access Offer package
Our inhibitory interneurons are available through our Early Access Program where we are offering the following options:
1. When you purchase a co-culture or tri-culture kit, you will receive 1 x a0662 and 1 x ax0667 interneurons free of charge.
2. If you wish to buy interneurons on their own, you can request a 50% discount on the purchase of a twin pack of 1 x ax0662 and 1 x ax0667.
Click the link below to order your interneurons and start building better, more physiologically relevant human disease models for your neurological research.
 Marín O. Interneuron dysfunction in psychiatric disorders. Nat Rev Neurosci. 2012 Jan 18;13(2):107-20. https://doi.org/: 10.1038/nrn3155. PMID: 22251963
 Ruden, J.B., Dugan, L.L. & Konradi, C. Parvalbumin interneuron vulnerability and brain disorders. Neuropsychopharmacol. 46, 279–287 (2021). https://doi.org/10.1038/s41386-020-0778-9
 Hansen Wang, Laurie C. Doering, “Induced Pluripotent Stem Cells to Model and Treat Neurogenetic Disorders”, Neural Plasticity, vol. 2012, Article ID 346053, 15 pages, 2012. https://doi.org/10.1155/2012/346053