ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Early Life Inflammation Increases CA1 Pyramidal Neuron Excitability in a Sex and Age Dependent Manner through a Chloride Homeostasis Disruption.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Increased Ih Current Is Associated with Reduced Hippocampal CA1 Excitability in a Mouse Model of Multiple Sclerosis.eNeuro · 2026Article
- How to train your neuron: developing a detailed, up-to-date, multipurpose model of hippocampal CA1 pyramidal cells.Frontiers in computational neuroscience · 2026Article
- Aromatase inhibition modulates intrinsic properties and excitability of hippocampal CA1 pyramidal cells in the APP/PS1 mouse model of Alzheimer's disease.Experimental neurology · 2025Article
- Neonatal immune stimulation results in sex-specific changes in ultrasonic vocalizations but does not affect seizure susceptibility in neonatal mice.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2024Article
- Novel Insights into Changes in Gene Expression within the Hypothalamus in Two Asthma Mouse Models: A Transcriptomic Lung-Brain Axis Study.International journal of molecular sciences · 2024Article
- Maternal antibiotic administration during gestation can affect the memory and brain structure in mouse offspring.Frontiers in cellular neuroscience · 2023Article
- Severe inflammation in new-borns induces long-term cognitive impairment by activation of IL-1β/KCC2 signaling during early development.BMC medicine · 2022Article
- Inhibition of Connexin 36 attenuates HMGB1-mediated depressive-like behaviors induced by chronic unpredictable mild stress.Brain and behavior · 2022Article
- Increased Excitatory Synaptic Transmission Associated with Adult Seizure Vulnerability Induced by Early-Life Inflammation in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Inhibition of the NKCC1/NF-κB Signaling Pathway Decreases Inflammation and Improves Brain Edema and Nerve Cell Apoptosis in an SBI Rat Model.Frontiers in molecular neuroscience · 2021Article
- Magnetic Resonance Imaging Correlates of White Matter Gliosis and Injury in Preterm Fetal Sheep Exposed to Progressive Systemic Inflammation.International journal of molecular sciences · 2020Article
- The Frail Male: Early Life Inflammation Promotes Chloride Loading in Adult Male Mice.Epilepsy currents · 2020Article
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4 authors at 1 institution in 1 country.
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Abstract
Early life, systemic inflammation causes long-lasting changes in behavior. To unmask possible mechanisms associated with this phenomenon, we asked whether the intrinsic membrane properties in hippocampal neurons were altered as a consequence of early life inflammation. C57BL/6 mice were bred in-house and both male and female pups from multiple litters were injected with lipopolysaccharide (LPS; 100 μg/kg, i.p.) or vehicle at postnatal day (P)14, and kept until adolescence (P35-P45) or adulthood (P60-P70), when brain slices were prepared for whole-cell and perforated-patch recordings from CA1 hippocampal pyramidal neurons. In neurons of adult male mice pretreated with LPS, the number of action potentials elicited by depolarizing current pulses was significantly increased compared with control neurons, concomitant with increased input resistance, and a lower action potential threshold. Although these changes were not associated with changes in relevant sodium channel expression or differences in capacitance or dendritic architecture, they were linked to a mechanism involving intracellular chloride overload, revealed through a depolarized GABA reversal potential and increased expression of the chloride transporter, NKCC1. In contrast, no significant changes were observed in neurons of adult female mice pretreated with LPS, nor in adolescent mice of either sex. These data uncover a potential mechanism involving neonatal inflammation-induced plasticity in chloride homeostasis, which may contribute to early life inflammation-induced behavioral alterations.
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