Epilepsy
How NKCC1-driven chloride dysregulation produces the hyperexcitability behind chronic seizures — and how bumetanide might help treat it.
Read moreNeurophysiology Lab · Universidad de Santiago de Chile
We study how neural circuits break down, using electrophysiological recordings in rodent models to investigate the mechanisms underlying epilepsy, and autism spectrum disorder. Though these conditions differ widely in presentation, our work traces each back to a shared point of failure: disrupted chloride cotransport and GABAergic inhibition in hippocampal circuits.
Chloride cotransporters — NKCC1 and KCC2 — set the intracellular chloride balance that determines whether GABA acts as an inhibitory signal in the brain. In our pilocarpine model of epilepsy, elevated NKCC1 activity disrupts this balance in the hippocampus, weakening inhibition in ways that make circuits prone to seizures. In our VPA model of autism spectrum condition, we study this same chloride machinery in dentate gyrus granule cells, where altered excitability may help explain the well-documented overlap between autism and epilepsy. This shared mechanism is also the basis for our translational work repurposing bumetanide, an NKCC1 inhibitor, as a candidate therapeutic.
Research lines
We approach epilepsy and autism spectrum condition not as unrelated conditions, but as different behavioral outcomes of a shared vulnerability in inhibitory signaling.
How NKCC1-driven chloride dysregulation produces the hyperexcitability behind chronic seizures — and how bumetanide might help treat it.
Read moreHow disrupted excitation-inhibition balance in the VPA model connects autism spectrum disorder to its frequent overlap with epilepsy.
Read moreApproach
We combine in vitro hippocampal electrophysiology with EEG and behavioral phenotyping in genetic and pharmacological rodent models — work that has also driven translational studies repurposing chloride cotransporter inhibitors as candidate therapeutics.
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