Selenium deficiency impedes maturation of parvalbumin interneurons, perineuronal nets, and neural network activity

Authors: Alexandru R. Sasuclark, Marissa Watanabe, Kai Roshto, Victor W. Kilonzo, Yiqiang Zhang, and Matthew W. Pitts

Redox Biology, 13 February 2025

Scientists use Axion BioSystems’ next-generation Maestro MEA platform to explore links between selenium deficiency and neuropsychiatric disease.

Selenium is an essential component of redox signaling, especially for parvalbumin-expressing interneurons (PVI) and perineuronal net (PNN) formation. Developmental deficits in PVI and PNN maturation have been associated with neuropsychiatric disorders, and evidence from in vivo studies has indicated a role for imbalanced redox signaling. In this study, scientists evaluated the role of selenium in redox signaling and PVI development using primary cortical neurons. In addition to deficits observed in antioxidant activity, PNN formation, and PVI synaptic connectivity when cultured in selenium-deficient media, the authors also used Axion BioSystems noninvasive Maestro multielectrode (MEA) platform to evaluate functional activity in real time. Using MEA, the team found that selenium-deficient cultures exhibited decreased activity, network bursts, long-term potentiation, and response to electrical stimulation.  

Overall, the authors report that these findings “show the vital role of selenium for the development of GABAergic inhibitory circuits,” and “further suggest that dietary Se supplementation may be beneficial for certain individuals at risk for neurodevelopmental disorders characterized by aberrant excitatory/inhibitory balance, such as epilepsy and schizophrenia.”