Abstract W P94: Recovery From Plasticity Impairments in Pediatric But Not Adult Mice Following Cardiac Arrest and Cardiopulmonary Resuscitation
Objectives: The goal of this study was to assess neuronal injury and synaptic plasticity impairments in Purkinje cells in pediatric and adult mice following cardiac arrest and cardiopulmonary resuscitation. We hypothesized that synaptic impairments in pediatrics would be less severe than in adult mice.
Methods: Pediatric ( 21-25 day old) and adult (8-12 week) male mice were subjected to 8 minutes cardiac arrest followed by cardiopulmonary resuscitation or sham surgery. Purkinje cells were labeled using anti-calbindin antibody and cell density was analyzed to examine neuronal injury. To examine synaptic function, whole-cell voltage clamp recording on acute cerebellar slices was performed at 1 and 7 days after CA/CPR or sham surgery. Excitatory postsynaptic currents (EPSCs) resulting from parallel (PF) or climbing fiber (CF) stimulation were recorded. Long-term depression (LTD) was induced by simultaneous parallel and climbing fiber stimulation (1 Hz, 5 min).
Results: Purkinje cell loss was observed in pediatric (24% cell loss) and adult (32% cell loss) mice following CA/CPR. Long-term depression, a reduction of synaptic strength of PF EPSCs was observed in adult and pediatric sham controls following PF+CF stimulation (46.6 ± 10% of baseline n= 5 and 55.4 ± 6.1% n= 3, respectively). LTD was absent in pediatric and adult mice at 24 hours after CA/CPR (96.1 ± 5.2% n =6 and 89.4 ± 4.5% n=2, respectively). At 7 and 30 days after CA/CPR LTD was absent in adult mice (81.6 ± 10.8% n=6 and 86.5 ± 8.9% n=4) but had returned in pediatric mice at 7 days after CA/CPR (70 ± 5.4% n=3).
Conclusions: The results of this study suggest that CA/CPR results in significant Purkinje cell loss in pediatric and adult mice. LTD was absent at 24 hours at both ages and was observed at 7 days after CA/CPR in pediatric but not adult mice. These results suggest enhanced recovery of synaptic plasticity at this developmental stage.
Author Disclosures: N. Quillinan: None. K. Shimizu: None. G. Deng: None. R. Traystman: None. P. Herson: None.
This research has received full or partial funding support from the American Heart Association, SouthWest - Arkansas, Colorado, New Mexico, Oklahoma, Texas, Wyoming.
- © 2015 by American Heart Association, Inc.