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Thalamocortical Dysfunction and Thalamic Injury after Asphyxial Cardiac Arrest in Developing Rats
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Thalamocortical Dysfunction and Thalamic Injury after Asphyxial Cardiac Arrest in Developing Rats
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    Global hypoxia-ischemia interrupts oxygen delivery and blood flow to the entire brain. Previous studies of global brain hypoxia-ischemia have primarily focused on injury to the cerebral cortex and to the hippocampus. Susceptible neuronal populations also include inhibitory neurons in the thalamic reticular nucleus. We therefore investigated the impact of global brain hypoxia-ischemia on the thalamic circuit function in the somatosensory system of young rats. We used single neuron recordings and controlled whisker deflections to examine responses of thalamocortical neurons to sensory stimulation in rat survivors of 9 min of asphyxial cardiac arrest incurred on postnatal day 17. We found that 48-72 h after cardiac arrest, thalamocortical neurons demonstrate significantly elevated firing rates both during spontaneous activity and in response to whisker deflections. The elevated evoked firing rates persist for at least 6-8 weeks after injury. Despite the overall increase in firing, by 6 weeks, thalamocortical neurons display degraded receptive fields, with decreased responses to adjacent whiskers. Nine minutes of asphyxial cardiac arrest was associated with extensive degeneration of neurites in the somatosensory nucleus as well as activation of microglia in the reticular nucleus. Global brain hypoxia-ischemia during cardiac arrest has a long-term impact on processing and transfer of sensory information by thalamic circuitry. Thalamic circuitry and normalization of its function may represent a distinct therapeutic target after cardiac arrest.

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  • Funding:
    5K12-HD047349-08/HD/NICHD NIH HHS/United States
    K12 HD001487/HD/NICHD NIH HHS/United States
    K12 HD001487-15/HD/NICHD NIH HHS/United States
    K12 HD047349/HD/NICHD NIH HHS/United States
    K12 HD047349-09/HD/NICHD NIH HHS/United States
    K12-HD01487/HD/NICHD NIH HHS/United States
    ND045968/ND/ONDIEH CDC HHS/United States
    NS07003/NS/NINDS NIH HHS/United States
    NS19950/NS/NINDS NIH HHS/United States
    NS30318/NS/NINDS NIH HHS/United States
    R01 HD045968/HD/NICHD NIH HHS/United States
    R01 HD045968-05/HD/NICHD NIH HHS/United States
    R01 NS019950/NS/NINDS NIH HHS/United States
    R01 NS019950-28/NS/NINDS NIH HHS/United States
    R21 NS070003/NS/NINDS NIH HHS/United States
    R21 NS070003-01/NS/NINDS NIH HHS/United States
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