Research Paper Volume 15, Issue 18 pp 9453—9463
Environmental enrichment enhanced neurogenesis and behavioral recovery after stroke in aged rats
- 1 Department of Laboratory Medicine, The Fourth People’s Hospital of Shenyang of China Medical University, Shenyang, Liaoning, China
- 2 Department of Neurology, The Fourth People’s Hospital of Shenyang of China Medical University, Shenyang, Liaoning, China
- 3 Department of Laboratory Medicine, The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, China
- 4 Department of Acupuncture (Neurology), The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, China
Received: May 6, 2023 Accepted: August 20, 2023 Published: September 8, 2023
https://doi.org/10.18632/aging.205010How to Cite
Copyright: © 2023 Yan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background and Purpose: Age is identified as a significant prognostic factor for poorer outcome after stroke. However, environmental enrichment (EE) has been reported to promote functional recovery after ischemic stroke. The purpose of this study was to investigate whether environmental enrichment was beneficial to ischemic stroke in aged rats.
Methods: Aged rats were randomly assigned as control rats, rats subjected to cerebral ischemia, and rats with cerebral ischemia treated with EE for 30 days. Focal cortical ischemia was induced by intracranial injection of endothelin-1 (ET-1). EE housing began one day after focal ischemia and was maintained for the whole experimental period. We used immunofluorescence staining to analyze the neurogenesis in the subventricular zone (SVZ) and TdT-mediated dUTP-biotin nick-end labeling (TUNEL) assay to evaluate apoptosis. The expression of neuronal nuclei, glial fibrillary acidic protein (GFAP) and Iba-1 around the infarcted area were also measured by double immunohistochemistry.
Results: EE enhanced the proliferation of newborn neurons in the SVZ, as well as increased the long-term survival of newborn neurons. EE also exerted effects on inflammation after stroke. Furthermore, EE suppressed apoptosis and improved the motor functions after stroke in the aged rats.
Conclusions: EE improved post-stroke recovery on the basis of enhancing neurogenesis in aged rats.