ArticleeNeuro
Impaired Interneuron Development in a Novel Model of Neonatal Brain Injury.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- From oxidative stress to epigenetic regulation: Molecular mechanisms of preterm brain injury and neuroprotective strategies (Review).Molecular medicine reports · 2026Review
- Adrenomedullin restores the human cortical interneurons migration defects induced by hypoxia.eLife · 2026Article
- Hypoxia-inducible factor signaling regulates embryonic interneuron development, GRIN2B expression and adult cortical function.Developmental cell · 2026Article
- Divergent representation and processing of task cues in sensory and prefrontal cortices of preterm-born mice.Nature communications · 2026Article
- Development of brain metastable dynamics during the equivalent of the third gestational trimester.Developmental cognitive neuroscience · 2025Review
- Prenatal Valproic Acid Exposure Impairs Offspring Cognition Through Disturbing Interneuron Development.CNS neuroscience & therapeutics · 2025Article
- Neurosteroid withdrawal disrupts GABAergic system development in human cortical organoids: implications for preterm birth.Frontiers in cellular neuroscience · 2025Article
- Inflammation mediated brain damage and cytokine expression in a maternally derived murine model for preterm hypoxic-ischemic encephalopathy.Frontiers in systems biology · 2025Article
- Timed fetal inflammation and postnatal hypoxia cause cortical white matter injury, interneuron imbalances, and behavioral deficits in a double-hit rat model of encephalopathy of prematurity.Brain, behavior, & immunity - health · 2024Article
- Immune and metabolic challenges induce changes in pain sensation and related pathways in the hypothalamus.Physiological genomics · 2024Article
- Highly expressed miR-210 in the peripheral blood is closely associated with asphyxiated neonates.Translational pediatrics · 2023Article
- Preterm birth accelerates the maturation of spontaneous and resting activity in the visual cortex.bioRxiv : the preprint server for biology · 2023Article
- Stem cell-based interventions for the prevention and treatment of intraventricular haemorrhage and encephalopathy of prematurity in preterm infants.The Cochrane database of systematic reviews · 2023Review
- Therapeutic Hypothermia Attenuates Cortical Interneuron Loss after Cerebral Ischemia in Near-Term Fetal Sheep.International journal of molecular sciences · 2023Article
- Preterm birth accelerates the maturation of spontaneous and resting activity in the visual cortex.Frontiers in integrative neuroscience · 2023Article
- Excitatory and inhibitory neuron imbalance in the intrauterine growth restricted fetal guinea pig brain: Relevance to the developmental origins of schizophrenia and autism.Developmental neurobiology · 2023Article
- The impact of maternal immune activation on embryonic brain development.Frontiers in neuroscience · 2023Review
- Montelukast reduces grey matter abnormalities and functional deficits in a mouse model of inflammation-induced encephalopathy of prematurity.Journal of neuroinflammation · 2022Article
- Oxidative Stress-Induced Damage to the Developing Hippocampus Is Mediated by GSK3β.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- An Inexpensive Open-Source Chamber for Controlled Hypoxia/Hyperoxia Exposure.Frontiers in physiology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Prematurity is associated with significantly increased risk of neurobehavioral pathologies, including autism and schizophrenia. A common feature of these psychiatric disorders is prefrontal cortex (PFC) inhibitory circuit disruption due to GABAergic interneuron alteration. Cortical interneurons are generated and migrate throughout late gestation and early infancy, making them highly susceptible to perinatal insults such as preterm birth. Term and preterm PFC pathology specimens were assessed using immunohistochemical markers for interneurons. Based on the changes seen, a new preterm encephalopathy mouse model was developed to produce similar PFC interneuron loss. Maternal immune activation (MIA; modeling chorioamnionitis, associated with 85% of extremely preterm births) was combined with chronic sublethal hypoxia (CSH; modeling preterm respiratory failure), with offspring of both sexes assessed anatomically, molecularly and neurobehaviorally. In the PFC examined from the human preterm samples compared to matched term samples at corrected age, a decrease in somatostatin (SST) and calbindin (CLB) interneurons was seen in upper cortical layers. This pattern of interneuron loss in upper cortical layers was mimicked in the mouse PFC following the combination of MIA and CSH, but not after either insult alone. This persistent interneuron loss is associated with postnatal microglial activation that occurs during CSH only after MIA. The combined insults lead to long-term neurobehavioral deficits which parallel human psychopathologies that may be seen after extremely preterm birth. This new preclinical model supports a paradigm in which specific cellular alterations seen in preterm encephalopathy can be linked with a risk of neuropsychiatric sequela. Specific interneuron subtypes may provide therapeutic targets to prevent or ameliorate these neurodevelopmental risks.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.