Research line
Chloride cotransporter imbalance, hippocampal network dysfunction, and translational pharmacology.
We investigate how the same chloride cotransporter machinery that fails in epilepsy also contributes to the circuit dysfunction underlying schizophrenia. Using pharmacological and genetic rodent models, we study how altered NKCC1/KCC2 balance disrupts GABAergic inhibition in the hippocampus, contributing to the network-level abnormalities associated with the disorder.
This work has also driven translational efforts to repurpose bumetanide as a candidate antipsychotic, extending our chloride-cotransporter framework from basic mechanism toward potential treatment.
Related work
This line has produced several conference presentations characterizing chloride co-transporter roles in animal models of schizophrenia (Chilean Society for Neuroscience annual meetings, 2013–2018). A dedicated peer-reviewed manuscript from this line is in preparation — check back, or see the full publication list for related mechanistic work.
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