Environmental Enrichment as a Modifier of Gait Following Ischemic Stroke in Hypertensive Rats

Long-term disability from ischemic stroke is considered a major global health burden, and rehabilitation strategies need to be refined to help combat this issue. Prior research has examined some of the physical impairments resulting from induced ischemic stroke via middle cerebral artery occlusion (MCAO) in male spontaneously hypertensive rats (SHRs). The objective of this study was to examine the effects of MCAO on gait in male SHRs exposed to environmental enrichment. We hypothesized that rehabilitation in the form of enriched housing (EH) improves the gait of SHRs recovering from MCAO compared to standard housing (SH) conditions. Following MCAO or sham procedure, SHRs were randomized to either an EH or SH rehabilitation treatment group. Each animal was instructed to traverse a glass plate towards a goal box, and their footprints were recorded and analyzed using the Catwalk XT (Noldus) gait analysis system 2-weeks prior- and then 3-weeks and 8-weeks post-MCAO. When compared to sham animals, MCAO animals displayed a significant decrease in left and right front paw max intensities (arbitrary units). EH also caused a significant decrease in front paw max intensities MCAO animals at 3 weeks post-MCAO compared to Sham+SH & Sham+EH. No significant differences were found between groups for other parameters, such as duty cycle (%) and regularity index (%), stride lengths (cm), or the base of support (cm) for the front or hind paws. These findings suggest that compared to sham, MCAO and EH do not cause significant changes in gait cycle efficiency or interlimb coordination over time. However, MCAO does appear to induce changes in body weight distribution, which may be temporarily exacerbated by EH. For future studies, a more comprehensive analysis with additional parameters will be done to fully characterize the modification of gait by environmental enrichment following ischemic stroke in hypertensive rats. GC Cross-Disciplinary Science Institute (X-SIG), VA BX000347 & IK6 BX004471, NIH RF1 NS083559 & R01 NS104573; NIH T32HL007260 & F32HL158011; SC Clin. & Transl. Res. (SCTR2201) This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.