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eNeuro. 2017 Jun 30;4(3). pii: ENEURO.0319-16.2017. doi: 10.1523/ENEURO.0319-16.2017. eCollection 2017 May-Jun.

Long-Term Deficits in Cortical Circuit Function after Asphyxial Cardiac Arrest and Resuscitation in Developing Rats.

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Department of Cell Biology and Anatomy, Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112.
Department of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261.
Department of Pediatrics, Washington University in St. Louis School of Medicine, St. Louis, MO 63110.
Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261.
Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, PA 15260.


Cardiac arrest is a common cause of global hypoxic-ischemic brain injury. Poor neurologic outcome among cardiac arrest survivors results not only from direct cellular injury but also from subsequent long-term dysfunction of neuronal circuits. Here, we investigated the long-term impact of cardiac arrest during development on the function of cortical layer IV (L4) barrel circuits in the rat primary somatosensory cortex. We used multielectrode single-neuron recordings to examine responses of presumed excitatory L4 barrel neurons to controlled whisker stimuli in adult (8 ± 2-mo-old) rats that had undergone 9 min of asphyxial cardiac arrest and resuscitation during the third postnatal week. Results indicate that responses to deflections of the topographically appropriate principal whisker (PW) are smaller in magnitude in cardiac arrest survivors than in control rats. Responses to adjacent whisker (AW) deflections are similar in magnitude between the two groups. Because of a disproportionate decrease in PW-evoked responses, receptive fields of L4 barrel neurons are less spatially focused in cardiac arrest survivors than in control rats. In addition, spiking activity among L4 barrel neurons is more correlated in cardiac arrest survivors than in controls. Computational modeling demonstrates that experimentally observed disruptions in barrel circuit function after cardiac arrest can emerge from a balanced increase in background excitatory and inhibitory conductances in L4 neurons. Experimental and modeling data together suggest that after a hypoxic-ischemic insult, cortical sensory circuits are less responsive and less spatially tuned. Modulation of these deficits may represent a therapeutic approach to improving neurologic outcome after cardiac arrest.


Cortex; hypoxia; ischemia; somatosensory; synchrony; thalamus

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