A critical physiological mechanism contributing to injury to the brain in the acute phase of stroke is a breakdown of the blood-brain barrier (BBB). The clinical research in this field bears certain limitations that do not exist in the preclinical setting. In preclinical research, experimental models of ischemic stroke show differences in lesion evolution and BBB permeability between adult and neonatal rats. However, little is known about these factors in the juvenile stage. Here, we describe a photothrombotic ring model of stroke that involves inducing ischemic cortical lesions using a fiber optic cold light source to induce photothrombosis that forms thrombi that interrupt local cerebral blood flow. This technique produces substantial local vasogenic and cytotoxic edema comparable to that seen in human ischemic stroke (Provenzale JM, Jahan R, Naidich TP, Fox AJ, Radiology, 2003. https://doi.org/10.1148/radiol.2292020402 ). In a modified version, a ring filter provides a central area within the lesioned cortex that has not been optically thrombosed, and this area is considered the penumbra. The “ring” in the model facilitates a reproducible study of the penumbra, where the potentially compromised tissue lies within, rather than perifocal, to an ischemic locus. The pathophysiological mechanisms involved in the evolution of ischemic damage are considered characteristic of the evolution of clinical thromboembolic stroke with penumbra. Our goal is to provide the reader with guidelines on how to execute the ring-lesion photothrombotic procedure, with notes highlighting the advantages and limitations of the method. We also include directions on how to conduct the techniques used to evaluate the permeability of the BBB including histology procedures Evans blue (EB) extravasation and TTC (triphenyl tetrazolium chloride), diffusion MRI (DWI), and dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), a technique used to evaluate BBB permeability applied in a rat model of juvenile stroke.