Hypoxic-brain injury is a major cause of neonatal morbidity and mortality. However, melatonin (N-acetyl-5- methoxytryptamine) has been identified as an indirect anti-oxidant and direct free radical scavenger that could possibly reduce the injurious effects of hypoxic-ischemic brain injury in neonatal infants. Hypoxia-ischemia leads to multiple consequences such as an increase in extracellular glutamate. Yet the many mechanisms involved in melatonin-induced neuroprotection are still under investigation. This blog talks about the feature of melatonin to induce neuroprotection by increasing levels of cystine glutamate exchanger (xCT), an amino acid transporter as shown in previous work in our laboratory.