ArticleBrain, behavior, and immunity2018
Lung-injury depresses glutamatergic synaptic transmission in the nucleus tractus solitarii via discrete age-dependent mechanisms in neonatal rats.
Article in Brain, behavior, and immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 17 citations in OpenAlex.
- Peritoneal sepsis caused by Escherichia coli triggers brainstem inflammation and alters the function of sympatho-respiratory control circuits.Journal of neuroinflammation · 2024Article
- Synapse Regulation.Advances in neurobiology · 2024Review
- Cannabinoid Receptor mRNA Expression in Central and Peripheral Tissues in a Rodent Model of Peritonitis.Cannabis and cannabinoid research · 2023Article
- Dynamics of ventilatory pattern variability and Cardioventilatory Coupling during systemic inflammation in rats.Frontiers in network physiology · 2023Article
- A Minimally Invasive Method for Intratracheal Instillation of Drugs in Neonatal Rodents to Treat Lung Disease.Journal of visualized experiments : JoVE · 2021Article
- Effects of allergic airway inflammation and chronic intermittent hypoxia on systemic blood pressure.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Peripheral-to-central immune communication at the area postrema glial-barrier following bleomycin-induced sterile lung injury in adult rats.Brain, behavior, and immunity · 2020Article
- Impact of inflammation on developing respiratory control networks: rhythm generation, chemoreception and plasticity.Respiratory physiology & neurobiology · 2020Review
- Acute lung injury in neonatal rats causes postsynaptic depression in nucleus tractus solitarii second-order neurons.Respiratory physiology & neurobiology · 2019Article
- Ventilatory pattern variability as a biometric for severity of acute lung injury in rats.Respiratory physiology & neurobiology · 2019Article
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4 authors at 2 institutions in 1 country.
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Abstract
Transition periods (TPs) are brief stages in CNS development where neural circuits can exhibit heightened vulnerability to pathologic conditions such as injury or infection. This susceptibility is due in part to specialized mechanisms of synaptic plasticity, which may become activated by inflammatory mediators released under pathologic conditions. Thus, we hypothesized that the immune response to lung injury (LI) mediated synaptic changes through plasticity-like mechanisms that depended on whether LI occurred just before or after a TP. We studied the impact of LI on brainstem 2nd-order viscerosensory neurons located in the nucleus tractus solitarii (nTS) during a TP for respiratory control spanning (postnatal day (P) 11-15). We injured the lungs of Sprague-Dawley rats by intratracheal instillation of Bleomycin (or saline) just before (P9-11) or after (P17-19) the TP. A week later, we prepared horizontal slices of the medulla and recorded spontaneous and evoked excitatory postsynaptic currents (sEPSCs/eEPSCs) in vitro from neurons in the nTS that received monosynaptic glutamatergic input from the tractus solitarii (TS). In rats injured before the TP (pre-TP), neurons exhibited blunted sEPSCs and TS-eEPSCs compared to controls. The decreased TS-eEPSCs were mediated by differences in postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic-acid receptors (AMPAR). Specifically, compared to controls, LI rats had more Ca
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