2017 Lab Photo

One of the rare moments everyone is in the lab at the same time!
No, we didn’t plan to all wear flannel, and no, I don’t have an abnormally long left arm.

L-to-R: Jon Wong, Sunny Zhang, Haley Martin, John Gray, Eden Barragan, Lindsay Cameron

New review article on non-ionotropic NMDA receptor signaling

Gray JA, Zito K, and Hell JW (2016). Non-ionotropic signaling by the NMDA receptor: controversy and opportunity. F1000Research, 5(F1000 Faculty Rev): 1010.

Figure 1-3

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.

My first paper at UC Davis

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.

Stein IS, Gray JA, and Zito K (2015). Non-ionotropic NMDA receptor signaling drives activity-induced dendritic spine shrinkage. Journal of Neuroscience, 35(35): 12303-12308

Stein_&_Zito_7CK_Fig1_v23

John Gray awarded NARSAD Young Investigator Grant

BBRF logoOur 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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