Computational analysis of cortical neuronal excitotoxicity in a large animal model of neonatal brain injury.

ABSTRACT:

Background

Neonatal hypoxic brain injury is a major cause of intellectual and developmental disability. Hypoxia causes neuronal dysfunction and death in the developing cerebral cortex due to excitotoxic Ca²⁺-influx. In the translational piglet model of hypoxic encephalopathy, we have previously shown that hypoxia overactivates Ca²⁺/Calmodulin (CaM) signaling via Sarcoma (Src) kinase in cortical neurons, resulting in overexpression of proapoptotic genes. However, identifying the exact relationship between alterations in neuronal Ca²⁺-influx, molecular determinants of cell death, and the degree of hypoxia in a dynamic system represents a significant challenge.

Methods

We used experimental and computational methods to identify molecular events c

SUBMITTER: Kratimenos P 

PROVIDER: S-EPMC8966144 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature