SLC1A2 and ischemic stroke: In a rat model of ischemic stroke, the use of N-acetylcysteine, which can enter cells bypassing EAATs and xc−, led to a significant suppression of xc− expression and an increase in glutamate transporter-1 (GLT-1) expression, which captures glutamate, leading to a decrease in the extracellular pool of glutamate in the brain [59].