Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 38, Issue 12, Pages 2223-2235Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X18766421
Keywords
Global ischemia; hippocampus; brain-derived neurotrophic factor; synaptic plasticity; memory and cognition
Categories
Funding
- [R01NS092645]
- [R01NS046072]
- [1K08NS097586]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM125095] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS092645, R01NS046072, K08NS097586] Funding Source: NIH RePORTER
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Global ischemia in childhood often leads to poor neurologic outcomes, including learning and memory deficits. Using our novel model of childhood cardiac arrest/cardiopulmonary resuscitation (CA/CPR), we investigate the mechanism of ischemia-induced cognitive deficits and recovery. Memory is impaired seven days after juvenile CA/CPR and completely recovers by 30 days. Consistent with this remarkable recovery not observed in adults, hippocampal long-term potentiation (LTP) is impaired 7-14 days after CA/CPR, recovering by 30 days. This recovery is not due to the replacement of dead neurons (neurogenesis), but rather correlates with brain-derived neurotrophic factor (BDNF) expression, implicating BDNF as the molecular mechanism underlying impairment and recovery. Importantly, delayed activation of TrkB receptor signaling reverses CA/CPR-induced LTP deficits and memory impairments. These data provide two new insights (1) endogenous recovery of memory and LTP through development may contribute to improved neurological outcome in children compared to adults and (2) BDNF-enhancing drugs speed recovery from pediatric cardiac arrest during the critical school ages.
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