Informal Seminar
Abstract:
Absence seizures affect children with episodes of brief unconsciousness. Even with effective medications, these children often suffer from cognitive deficits. Our study sought to identify alterations of neuronal circuits relevant for cognition in a mouse model of absence seizures. Using optogenetics and electrophysiological recordings, we found deficiencies in thalamic inputs to the prefrontal cortex, crucial for higher cognition. Changes were noted in depolarization dynamics, synaptic integration, and excitation-inhibition balance. Surprisingly, this circuit didn't trigger seizures like other thalamic inputs. The research highlights changes in functional connectivity within the seizure model that are likely to contribute to cognitive deficits, rather than seizure generation.