ArticleJournal of neuropathology and experimental neurology2010
Loss of cation-chloride cotransporter expression in preterm infants with white matter lesions: implications for the pathogenesis of epilepsy.
Article in Journal of neuropathology and experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Clarifications regarding bumetanide for neonatal seizures.Epilepsia · 2022Trial
- Elucidating the Pivotal Neuroprotective Mechanisms and Therapeutic Variants of Erythropoietin in Neonatal Brain Injury.Current topics in medicinal chemistry · 2025Review
- Umbilical cord-derived mesenchymal stromal cell therapy to prevent the development of neurodevelopmental disorders related to low birth weight.Scientific reports · 2023Article
- Targeting ischemia-induced KCC2 hypofunction rescues refractory neonatal seizures and mitigates epileptogenesis in a mouse model.Science signaling · 2021Article
- The role of KCC2 in hyperexcitability of the neonatal brain.Neuroscience letters · 2020Article
- Intracellular ClPflugers Archiv : European journal of physiology · 2020Review
- Loss of non-canonical KCC2 functions promotes developmental apoptosis of cortical projection neurons.EMBO reports · 2020Article
- Hemodynamic and Metabolic Assessment of Neonates With Punctate White Matter Lesions Using Phase-Contrast MRI and T2-Relaxation-Under-Spin-Tagging (TRUST) MRI.Frontiers in physiology · 2018Article
- Stem cells and cell-based therapies for cerebral palsy: a call for rigor.Pediatric research · 2018Review
- Spinal Hyper-Excitability and Altered Muscle Structure Contribute to Muscle Hypertonia in Newborns After Antenatal Hypoxia-Ischemia in a Rabbit Cerebral Palsy Model.Frontiers in neurology · 2018Article
- Mild Intrauterine Hypoperfusion Leads to Lumbar and Cortical Hyperexcitability, Spasticity, and Muscle Dysfunctions in Rats: Implications for Prematurity.Frontiers in neurology · 2018Article
- Impaired neuronal KCC2 function by biallelic SLC12A5 mutations in migrating focal seizures and severe developmental delay.Scientific reports · 2016Article
- Imaging and serum biomarkers reflecting the functional efficacy of extended erythropoietin treatment in rats following infantile traumatic brain injury.Journal of neurosurgery. Pediatrics · 2016Article
- Erythropoietin Modulates Cerebral and Serum Degradation Products from Excess Calpain Activation following Prenatal Hypoxia-Ischemia.Developmental neuroscience · 2016Article
- Acute TrkB inhibition rescues phenobarbital-resistant seizures in a mouse model of neonatal ischemia.The European journal of neuroscience · 2015Article
- Postnatal Erythropoietin Mitigates Impaired Cerebral Cortical Development Following Subplate Loss from Prenatal Hypoxia-Ischemia.Cerebral cortex (New York, N.Y. : 1991) · 2015Article
- Age- and sex-dependent susceptibility to phenobarbital-resistant neonatal seizures: role of chloride co-transporters.Frontiers in cellular neuroscience · 2015Article
- Prenatal Hypoxia-Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone.Frontiers in cellular neuroscience · 2015Article
- Preclinical Models of Encephalopathy of Prematurity.Developmental neuroscience · 2015Review
- Cation-chloride cotransporters in neuronal development, plasticity and disease.Nature reviews. Neuroscience · 2014Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Epilepsy associated with preterm birth is often refractory to anticonvulsants. Children who are born preterm are also prone to cognitive delay and behavioral problems. Brains from these children often show diffuse abnormalities in cerebral circuitry that is likely caused by disrupted development during critical stages of cortical formation. To test the hypothesis that prenatal injury impairs the developmental switch of gamma-amino butyric acid (GABA)ergic synapses from excitatory to inhibitory, thereby disrupting cortical circuit formation and predisposing to epilepsy, we used immunohistochemistry to compare the expression of cation-chloride transporters that developmentally regulate postsynaptic GABAergic discharges in postmortem cerebral samples from infants born preterm with known white matter injury (n = 11) with that of controls with minimal white matter gliosis (n = 7). Controls showed the expected developmental expression of cation-chloride transporters NKCC1 and KCC2 and ofcalretinin, a marker of a GABAergic neuronal subpopulation. Samples from infants with white matter damage showed a significant loss of expression of both NKCC1 and KCC2 in subplate and white matter. By contrast, there were no significant differences in total cell number or glutamate transporter VGLUT1 expression. Together, these novel findings suggest a molecular mechanism involved in the disruption of a critical stage of cerebral circuit development after brain injury from preterm birth that may predispose to epilepsy.
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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.