Excited that Eden has decided to join the Gray Lab! Eden graduated from UC Irvine where she worked in the lab of Diane O’Dowd studying how mutations in the gene for the voltage-gated sodium channel NaV1.1 lead to epilepsy.
Let’s do some fun science together!
In collaboration with Karen Zito and Johannes Hell, I recently reviewed the emerging literature on possible non-ionotropic signaling by the NMDA receptor, which is classically a ligand-gated ion channel. This conformational-based signaling remains controversial but, if validated, could open the doors for a new era of understanding ion channels and synapse function.
Happy to have Eden Barragan from the Neuroscience Graduate Group rotating in the lab!
Was excited to be able to contribute to an elegant study from the Zito Lab showing that NMDA receptor-mediated spine shrinkage requires glutamate binding but not ion flux through the channel, supporting recent studies showing that the NMDA receptor can signal in an non-ionotropic manner in response to agonist binding.
Our proposal entitled “Genetic ‘Saturation’ of the NMDA Receptor Glycine Co-Agonist Site” was selected for a NARSAD Young Investigator Grant from the Brain and Behavior Research Foundation. We are interested in understanding the fundamental basis for the unique requirement of NMDA receptors to bind both glutamate and a co-agonist (either glycine or D-serine). Even though our understanding is quite limited, in schizophrenia and other neuropsychiatric disorders, significant efforts have been made to clinically enhance NMDA receptor activity though this co-agonist site, either directly by high-dose administration of glycine, D-serine or D-cycloserine (a partial agonist) or indirectly though inhibition of glycine transporters or D-amino acid oxidase. We’re hoping that a deeper understanding of the mechanisms of NMDA receptor function and synapse biology will allow us to develop improved treatments for schizophrenia.
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