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Abstract
<p class="first" id="P1">Pediatric cardiac arrest (CA) often leads to poor neurologic
outcomes, including deficits
in learning and memory. The only approved treatment for CA is therapeutic hypothermia,
although its utility in the pediatric population remains unclear. This study analyzed
the effect of mild therapeutic hypothermia after CA in juvenile mice on hippocampal
neuronal injury and the cellular model of learning and memory, termed long-term potentiation
(LTP). Juvenile mice were subjected to cardiac arrest and cardiopulmonary resuscitation
(CA/CPR) followed by normothermia (37 °C) and hypothermia (30 °C, 32 °C). Histological
injury of hippocampal CA1 neurons was performed 3 days after resuscitation using hematoxylin
and eosin (H&E) staining. Field excitatory post-synaptic potentials (fEPSPs) were
recorded from acute hippocampal slices 7 days after CA/CPR to determine LTP. Synaptic
function was impaired 7 days after CA/CPR. Mice exposed to hypothermia showed equivalent
neuroprotection, but exhibited sexually dimorphic protection against ischemia-induced
impairment of LTP. Hypothermia (32 °C) protects synaptic plasticity more effectively
in females, with males requiring a deeper level of hypothermia (30 °C) for equivalent
protection. In conclusion, male and female juvenile mice exhibit equivalent neuronal
injury following CA/CPR and hypothermia protects both males and females. We made the
surprising finding that juvenile mice have a sexually dimorphic response to mild therapeutic
hypothermia protection of synaptic function, where males may need a deeper level of
hypothermia for equivalent synaptic protection.
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