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Updated: Apr 13, 2026
Utilizing the Modified T-Maze to Assess Functional Memory Outcomes After Cardiac Arrest
Published on: January 5, 2018
Effect of cardiac arrest on cognitive impairment and hippocampal plasticity in middle-aged rats
Charles H Cohan1, Jake T Neumann2, Kunjan R Dave1
1Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America; Evelyn F. McKnight Brain Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America; Department of Neurology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America; Neuroscience Program, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America.
Insights
Cardiac arrest (CA) in middle-aged rats causes significant spatial memory deficits and synaptic dysfunction. This study establishes a model for investigating cognitive impairments after mild global cerebral ischemia in aging brains.
Area of Science:
- Neuroscience
- Cardiovascular Research
- Gerontology
Background:
- Cardiopulmonary arrest (CA) is a major cause of death and disability, particularly in older adults.
- Global cerebral ischemia following CA leads to neuronal damage and cognitive impairments, especially affecting spatial memory.
- Middle-aged individuals represent an understudied population regarding the long-term cognitive consequences of CA.
Purpose of the Study:
- To establish a reliable animal model of asphyxial cardiac arrest (ACA) in middle-aged rats (9 months old).
- To investigate the impact of mild global cerebral ischemia following ACA on cognitive function, specifically spatial memory.
- To assess synaptic function and neuronal survival in the hippocampus after ACA in this age group.
Main Methods:
- Utilized a model of asphyxial cardiac arrest (ACA) in nine-month-old male Fischer 344 rats.
- Assessed spatial memory using the Barnes circular platform maze and contextual fear conditioning.
- Evaluated synaptic function via field recordings of long-term potentiation (LTP) and paired-pulse facilitation (PPF).
Main Results:
- ACA in nine-month-old rats resulted in impaired spatial memory formation.
- Significant synaptic dysfunction, including paired-pulse facilitation deficits, was observed.
- A reduction in non-compromised hippocampal neurons (Cornu Ammonis 1 and subiculum) was noted post-ACA.
Conclusions:
- Nine-month-old rats undergoing cardiac arrest exhibit reduced survival rates.
- Mild global cerebral ischemia following ACA leads to pronounced deficits in spatial memory formation.
- Synaptic dysfunction in the hippocampus is a key consequence of cardiac arrest in middle-aged rats.
Abstract:
Cardiopulmonary arrest is a leading cause of death and disability in the United States that usually occurs in the aged population. Cardiac arrest (CA) induces global ischemia, disrupting global cerebral circulation that results in ischemic brain injury and leads to cognitive impairments in survivors. Ischemia-induced neuronal damage in the hippocampus following CA can result in the impairment of cognitive function including spatial memory. In the present study, we used a model of asphyxial CA (ACA) in nine month old male Fischer 344 rats to investigate cognitive and synaptic deficits following mild global cerebral ischemia. These experiments were performed with the goals of 1) establishing a model of CA in nine month old middle-aged rats; and 2) to test the hypothesis that learning and memory deficits develop following mild global cerebral ischemia in middle-aged rats. To test this hypothesis, spatial memory assays (Barnes circular platform maze and contextual fear conditioning) and field recordings (long-term potentiation and paired-pulse facilitation) were performed. We show that following ACA in nine month old middle-aged rats, there is significant impairment in spatial memory formation, paired-pulse facilitation n dysfunction, and a reduction in the number of non-compromised hippocampal Cornu Ammonis 1 and subiculum neurons. In conclusion, nine month old animals undergoing cardiac arrest have impaired survival, deficits in spatial memory formation, and synaptic dysfunction.
