Authors: Christa W. Habela, Shiyu Liu, Arens Taga, Sean Oddoye, Raha Dastgheyb, Norman Haughey, Dwight E. Bergles, Hongjun Song, Guo-Li Ming, and Nicholas J. Maragakis
Translational Psychiatry, 29 August 2025
Scientists use the Maestro MEA platform to reveal how a common chromosomal deletion disrupts brain development and function.
Deletions in the chromosome 15q11.2 locus occur in ~1.5% of epilepsy patients and are also strongly linked to schizophrenia and intellectual disability, but their effects on neuronal function remain unclear. To investigate, researchers in this study generated an iPSC line carrying this deletion and monitored the maturation of human neuronal networks.
With Axion BioSystems’ noninvasive Maestro Edge multielectrode array (MEA), the team recorded activity from co-cultures of glutamatergic and GABAergic neurons with astrocytes. They found that the 15q11.2 deletion led to shorter, less complex dendrites, delayed maturation, and disrupted excitatory-inhibitory balance, resulting in reduced network activity. Pharmacological assays with CNQX and bicuculline further highlighted altered AMPA/kainate receptor signaling and impaired GABAergic responses.
These results shed light on how 15q11.2 deletion impacts brain circuitry and provide a mechanistic link to epilepsy, schizophrenia, and other neurodevelopmental and neuropsychiatric disorders associated with this genomic variant.
