During intensive care after premature birth, babies may experience hypoxia, a lack of oxygen in their tissues and cells. Hypoxia is associated with poor brain health and lifelong memory loss, but the mechanisms are unclear. Researchers led by Art Riddle and Stephen Buck at Oregon Health and Science University discovered the contributing mechanism by creating a mouse model of mild hypoxia after preterm birth. “Historically, the field has focused on how hypoxia damages the brain’s white matter and destroys neurons,” Riddle said. “This study is the first to explore how mild hypoxia changes brain development during this neonatal period, without direct brain damage.”
As introduced in them, JNeurosci Mild hypoxia shortly after birth impairs learning and memory into adulthood, according to the paper, and researchers have discovered at least part of the mechanism for this effect. It is a change in communication between neurons in the hippocampus. The researchers investigated the molecular mechanisms and found that hypoxia after preterm birth affects protein channels involved in communication between neurons and memory that develop in the hippocampus during adolescence. They also identified a second protein involved in the effects of hypoxia on channel function. When the researchers targeted this second protein in adult mice, the channel’s function was restored. Riddle added: “When we looked at surrounding brain regions, we also found that this protein was altered by mild hypoxia, suggesting that other brain regions may also be susceptible to hypoxia.” In future studies, the researchers plan to assess how hypoxia affects these areas.
According to the authors, this study reveals how hypoxia in preterm infants affects neuronal transmission in memory-related brain regions, impeding learning and memory into adulthood. As for clinical implications, Riddle said, “The subtle impairments of mild hypoxia that we studied here are common in clinical practice in preterm infants.” The researchers also plan to search for early developmental molecular targets, since the molecules they identified are not expressed when infants are in hypoxia.
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Reference magazines:
Riddle, A. others. (2026). Mild neonatal hypoxia targets synaptic maturation, disrupts adult hippocampal learning and memory, and is associated with loss of CK2-mediated synaptic calcium-activated potassium channel KCNN2 activity. neuroscience journal. DOI: 10.1523/JNEUROSCI.1643-25.2026. https://www.jneurosci.org/content/early/2026/03/12/JNEUROSCI.1643-25.2026
