Isabel Parada

TL;DR: In rats, it was found that the thalamus, a structure that is remote from, but connected to, the injured cortex, was required to maintain cortical seizures, and a closed-loop optogenetic strategy revealed that reducing their activity in real-time was sufficient to immediately interrupt electrographic and behavioral seizures.

TL;DR: Results indicate that epileptogenesis in C1q KO mice is related to a genetically determined failure to prune excessive excitatory synapses during development.

TL;DR: It is shown that tetrodotoxin applied to injured cortex during a critical period early after lesion placement can prevent epileptogenesis in the partial cortical (“undercut”) model of posttraumatic epilepsy, and that treatment markedly attenuates histologic indices of axonal and terminal sprouting and presumably associated aberrant excitatory connectivity.

TL;DR: Results in these models do not support the disinhibitory hypothesis of chronic epileptogenesis, but suggest that GABAergic inhibition may be enhanced in epileptogenic areas associated with chronic cortical injury.

TL;DR: It is shown that comparative transcriptome analyses predict remodeling of extracellular matrix (ECM) as a common response to different types of injuries and insights are provided on how albumin extravasation that occurs upon BBB dysfunction in various brain injuries can predispose neural circuitry to the development of chronic inhibition deficits.