We used NGN2-reprogrammed iPSC neurons with glutamatergic hyperactivity and tested phenytoin, perampanel, and carbamazepine.

Read the full paper here 👇
📄 Communications Biology
🔗 http://dx.doi.org/10.1038/s42003-025-08194-6

#Neurotech #SBI #DrugDiscovery #Epilepsy #Organoids #BrainOnAChip #stemcells #bioinformatics #invitromodeling

This shows how DishBrain-like systems could:

go beyond rodent models

reduce reliance on spontaneous activity alone

offer functional assays for epilepsy and beyond

An early proof that SBI systems can support pharmacological discovery.

🔗 http://dx.doi.org/10.1038/s42003-025-08194-6

Traditional readouts miss the bigger picture.

By measuring:

bursting states

criticality (DCC, BR, SC error)

dynamic functional connectivity

…we captured richer, drug-specific neural responses that align with known mechanisms.

🔗 http://dx.doi.org/10.1038/s42003-025-08194-6

Only inhibitory compounds (not all ASMs) improved gameplay.

📉 Spontaneous hyperactivity dropped
📈 Performance during gameplay improved
🧩 Suggesting a link between glutamatergic modulation and goal-directed information processing.

🔗 http://dx.doi.org/10.1038/s42003-025-08194-6

Neural cultures played a simplified Pong game.

Without intervention, hyperactive cultures performed poorly.
💊 After carbamazepine:
✅ Longer rallies
✅ Higher hit/miss ratios
✅ Fewer aces

Structured stimulation reveals functional improvement.

🔗http://dx.doi.org/10.1038/s42003-025-08194-6

Preclinical models rarely test how drugs affect goal-directed neural behavior.

Using DishBrain, we show how epilepsy-linked hyperactivity in human iPSC neurons affects gameplay — and how compounds like carbamazepine restore function.

🔗http://dx.doi.org/10.1038/s42003-025-08194-6