Thalamocortical Dysfunction and Thalamic Injury after Asphyxial Cardiac Arrest in Developing Rats

Details

• Alternative Title:
  J Neurosci
• Personal Author:
  Shoykhet, Michael ; Simons, Daniel J. ; Alexander, Henry ; Hosler, Christina ; Kochanek, Patrick M. ; Clark, Robert S. B.
• Description:
  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.
• Subjects:
  Action Potentials Age Factors Animals Asphyxia Heart Arrest Male Neural Pathways Neurites Rats Rats, Sprague-Dawley Somatosensory Cortex Thalamus Vibrissae

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• Source:
  J Neurosci. 32(14):4972-4981.
• Pubmed ID:
  22492052
• Pubmed Central ID:
  PMC3350787
• Document Type:
  Journal Article
• 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
• Volume:
  32
• Issue:
  14
• Collection(s):
  CDC Public Access
• Main Document Checksum:
  urn:sha256:fe7f9dcb20ae7dc14250ae898aff5268e663cafd86f06ca148335bba1dd3f104
• Download URL:
  https://stacks.cdc.gov/view/cdc/33362/cdc_33362_DS1.pdf
• File Type:
  [PDF - 5.63 MB ]