Brain development
Why do preterm brains lose specific interneurons?
Open access · cc by · source: Europe PMC
Human preterm prefrontal cortex had fewer upper-layer SST and calbindin interneurons; a mouse combo of late maternal LPS plus postnatal hypoxia, but not either insult alone, reproduced that loss with later behavioral deficits.
How this study connects
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Study at a glance
- Design
- Animal / in-vitro — Human preterm vs term BA9 immunohistochemistry plus a 2×2 mouse model of late LPS MIA and postnatal chronic sublethal hypoxia
- N
- N=27 · 13 term and 14 preterm human BA9 donors; GAD65-GFP mice, both sexes, four MIA×CSH groups from ≥2 litters each
- Population
- NIH NeuroBioBank term/preterm infant PFC plus C57BL/6 GAD65-GFP mouse offspring of both sexes
- Outcome
- PFC interneuron subtype density (SST, CLB, others), postnatal microglia, and later neurobehavior
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Why do preterm brains lose specific interneurons?
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13 term and 14 preterm infant BA9 sections.
BA9 sections from 13 term and 14 preterm infants were obtained.
LPS 150 µg/kg at E15.5 and E16.5; 10.9% O2 from P3–P10.
Mild, late MIA was induced using 150 µg/kg of lipopolysaccharide (LPS; L6529, from Escherichia coli O55:B5, Millipore Sigma), administered to the pregnant dam intraperitoneally on both E15.5 and E16.5.
Key findings
Upper-layer SST and CLB interneurons were reduced in preterm human PFC. The same pattern appeared in mouse PFC only after MIA+CSH, linked to postnatal microglial activation during hypoxia only after MIA, plus long-term neurobehavioral deficits.
Methodology
Immunostained BA9 from 13 term and 14 preterm infants, then built a mouse model: 150 µg/kg LPS to dams at E15.5 and E16.5 plus 10.9% oxygen from P3–P10, with four MIA×CSH groups assessed anatomically and behaviorally.
Limitations
Postmortem infant samples and a mouse double-hit model cannot prove that targeting SST cells would prevent autism or schizophrenia after preterm birth.
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