Post cardiac arrest physical exercise mitigates cell death in the septal and thalamic nuclei and ameliorates contextual fear conditioning deficits in rats.

Autor: Ferrier FJ; Peritz Scheinberg Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.; Neuroscience Program, University of Miami Leonard M. Miller School of Medicine, Miami FL., Saul I; Peritz Scheinberg Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.; Department of Neurology, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA., Khoury N; Peritz Scheinberg Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.; Neuroscience Program, University of Miami Leonard M. Miller School of Medicine, Miami FL., Ruiz AJ; Peritz Scheinberg Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA., Lao EJP; Peritz Scheinberg Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.; Neuroscience Program, University of Miami Leonard M. Miller School of Medicine, Miami FL.; Hussman Institute for Human Genetics, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA., Escobar I; Peritz Scheinberg Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.; Neuroscience Program, University of Miami Leonard M. Miller School of Medicine, Miami FL., Dave KR; Peritz Scheinberg Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.; Neuroscience Program, University of Miami Leonard M. Miller School of Medicine, Miami FL.; Department of Neurology, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA., Young JI; Hussman Institute for Human Genetics, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA., Perez-Pinzon MA; Peritz Scheinberg Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.; Neuroscience Program, University of Miami Leonard M. Miller School of Medicine, Miami FL.; Department of Neurology, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.
Jazyk: angličtina
Zdroj: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism [J Cereb Blood Flow Metab] 2023 Mar; Vol. 43 (3), pp. 446-459. Date of Electronic Publication: 2022 Nov 11.
DOI: 10.1177/0271678X221137539
Abstrakt: A major concern for cardiac arrest (CA) survivors is the manifestation of long-term cognitive impairments. Physical exercise (PE) is a well-established approach to improve cognitive functions under certain pathological conditions. We previously showed that PE post-CA mitigates cognitive deficits, but the underlying mechanisms remain unknown. To define neuroprotective mechanisms, we analyzed whether PE post-CA protects neurons involved in memory. We first performed a contextual fear conditioning (CFC) test to confirm that PE post-CA preserves memory in rats. We then conducted a cell-count analysis and determined the number of live cells in the hippocampus, and septal and thalamic nuclei, all areas involved in cognitive functions. Lastly, we performed RNA-seq to determine PE post-CA effect on gene expression. Following CA, exercised rats had preserved CFC memory than sham PE animals. Despite this outcome, PE post-CA did not protect hippocampal cells from dying. However, PE ameliorated cell death in septal and thalamic nuclei compared to sham PE animals, suggesting that these nuclei are crucial in mitigating cognitive decline post-CA. Interestingly, PE affected regulation of genes related to neuroinflammation, plasticity, and cell death. These findings reveal potential mechanisms whereby PE post-CA preserves cognitive functions by protecting septal and thalamic cells via gene regulation.
Databáze: MEDLINE