4.5 Article

Enriched environment improves synaptic plasticity and cognitive deficiency in chronic cerebral hypoperfused rats

Journal

BRAIN RESEARCH BULLETIN
Volume 119, Issue -, Pages 34-40

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2015.10.001

Keywords

Brain ischemia; Enriched environment; Electrophysiology; LTP; Field potential recording

Categories

Funding

  1. Research Council of Kerman University of Medical Sciences, Kerman, Iran

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Recent studies have indicated that environmental enrichment (EE) increases the sensorial and social stimulations and leads to strengthened plastic changes in the brain. In models of chronic cerebral hypoperfusion, the ability of an EE to restore the cognition depends on hippocampal synaptic plasticity. The mechanisms for this effect have not, however, been adequately studied. Thus, the aim of the present study was to evaluate the neuroprotective effects and underlying mechanism of environmental enrichment by assessment of spatial memory tasks as well as parameters of synaptic plasticity in rats subjected to occlusion of the bilateral common carotid arteries (2-VO) model. Male Sprague-Dawley rats were used in this study. The model group was established by occlusion of the bilateral common carotid arteries. The animals were tested for learning, memory performance and synaptic plasticity using Morris water maze (MWM), 8-arm Radial Maze (RM), and field potential recording, respectively. The rats subjected to 2-VO in EE exhibited a significantly lower number of working errors and reference errors in RM. Moreover, the enriched environment recovered the memory performance of hypoperfused rats and decreased the swimming time to reach the platform in MWM. In addition, conditions of the environment did not have any effect on baseline synaptic transmission and presynaptic plasticity, but housing the animals in EE rescued the impairment of LTP induction induced by 2-VO. These results suggest that EE ameliorates the LIP and spatial memory impairment induced by 2-VO. Our data indicated that the LTP recovery by EE in the rat models of 2-VO is probably mediated by post-synaptic mechanisms. (C) 2015 Elsevier Inc. All rights reserved.

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