Astrocytic Neurotransmitter Metabolism After Neonatal Brain Injury From Intermittent Hypoxia

Why It Matters

Identifying persistent astrocytic metabolic dysfunction links a common neonatal insult to long-term neurologic deficits and points to new cellular targets for therapies to mitigate cognitive and epilepsy risks in extremely preterm survivors.

Summary

Dr. Don Lamert presented research using a mouse model of intermittent hypoxia to mimic apnea of prematurity and investigate its effects on astrocytic neurotransmitter metabolism after neonatal brain injury. He reports that intermittent hypoxia disrupts expression and function of astrocytic enzymes in the glutamine–glutamate cycle and impairs astrocytic glutamate uptake, with alterations persisting at least one month post-injury. These findings suggest that early-life intermittent hypoxia can produce sustained changes in astrocyte-mediated neurotransmitter handling. Lamert’s team proposes that such astrocytic dysfunction may underlie long-term neurocognitive and seizure risks seen in extremely preterm infants and could guide targeted therapeutic development.

Original Description

Dr. Dawn Lammert, an epilepsy genetics fellow at The Johns Hopkins Hospital, discusses her research titled Astrocytic Neurotransmitter Metabolism after Neonatal Brain Injury from Intermittent Hypoxia, presented during the 15th annual Hershey Conference on Developmental Brain Injury. Preterm birth affects half a million infants in the United States each year. As neonatal intensive care has improved, mortality has decreased. Although these infants survive, they remain at risk for neurocognitive deficits, neurobehavioral problems and epilepsy. In this study, Dr. Lammert and Dr. Joseph Scafidi’s lab explore how intermittent hypoxia affects brain neurotransmitter metabolism. Learn more at https://www.hopkinsmedicine.org/hershey. #researchsaveschildren #johnshopkinsmedicine #neonatalbraininjury #intermittenthypoxia