Excitotoxic glutamate levels cause the secretion of resident endoplasmic reticulum proteins.

ABSTRACT: Dysregulation of synaptic glutamate levels can lead to excitotoxicity such as that observed in stroke, traumatic brain injury, and epilepsy. The role of increased intracellular calcium (Ca²⁺) in the development of excitotoxicity is well established. However, less is known regarding the impact of glutamate on endoplasmic reticulum (ER)-Ca²⁺-mediated processes such as proteostasis. To investigate this, we expressed a secreted ER Ca²⁺ modulated protein (SERCaMP) in primary cortical neurons to monitor exodosis, a phenomenon whereby ER calcium depletion causes the secretion of ER-resident proteins that perform essential functions to the ER and the cell. Activation of glutamatergic receptors (GluRs) led to an increase in SERCaMP secretion indicating that normally

SUBMITTER: Dossat AM 

PROVIDER: S-EPMC11401966 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature