“…Finally, the absence of injury in other motor areas of the brain (e.g., cortex, striatum, and substantia nigra), as well as areas that may confound behavioral tests (e.g., optic nerve and tract, hippocampus), is an advantage over other models that result in white-matter injury, such as chronic forebrain hypoperfusion, chronic hypertension, intracarotid sodium laurate injection, or capsular photothrombotic lesion. 9,27,[32][33][34][35][36] Of course, ET-1 model has limitations. The mechanism of ischemia does not mimic lacunar pathophysiology, multiple vessels constrict at the same time, the duration of ischemia cannot be precisely controlled, and ET-1 targets not only endothelial and smooth muscle cells but also neurons and glia as a possible confounder.…”