Glycine-induced NMDA receptor internalization provides neuroprotection and preserves vasculature following ischemic stroke
Julia Cappelli, Pamela Khacho, Boyang Wang, Alexandra Sokolovski, Wafae Bakkar, Sophie Raymond, Nina Ahlskog, Julian Pitney, Junzheng Wu, Prakash Chudalayandi, Adrian Y. C. Wong, Richard Bergeron
Abstract
, GINI also occurs and provides neuroprotection in the presence of a GlyT1 antagonist (GlyT1-A). Mice pretreated with a GlyT1-A, which increases synaptic glycine levels, exhibited smaller stroke volume, reduced cell death, and minimized behavioral deficits following stroke induction by either photothrombosis or endothelin-1. Moreover, we show evidence that in ischemic conditions, GlyT1-As preserve the vasculature in the peri-infarct area. Therefore, GlyT1 could be a new target for the treatment of ischemic stroke.
Topics & Concepts
NMDA receptorNeuroprotectionGlutamate receptorGlycinePharmacologyAgonistStroke (engine)NimodipineInternalizationAntagonistChemistryReceptorNeuroscienceMedicineBiologyBiochemistryInternal medicineAmino acidEngineeringMechanical engineeringCalciumNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration MechanismsRetinal Development and Disorders