How does a stroke manifest in rats? - briefly
In rodent models, ischemic injury leads to focal neurological deficits—including unilateral weakness, impaired coordination, and reduced sensorimotor performance—alongside a localized brain infarct detectable by imaging or histology. These impairments are commonly quantified using tests such as the adhesive removal, cylinder, and ladder rung assays.
How does a stroke manifest in rats? - in detail
Stroke in laboratory rats produces a reproducible set of neurological and physiological alterations that can be observed across acute, sub‑acute, and chronic phases. Immediately after induction of focal cerebral ischemia—commonly via middle‑cerebral‑artery occlusion—rats display loss of righting reflex, reduced spontaneous movement, and unilateral motor weakness. The affected forelimb shows diminished grip strength and impaired coordination, often quantified with the forelimb placing test or the cylinder test, which records asymmetric forepaw use during vertical exploration.
Within the first 24 hours, the animal may develop facial palsy, decreased whisker movement, and neglect of the contralateral side. Sensory deficits become evident in the adhesive removal test, where latency to detect and remove a tape strip from the impaired paw increases markedly. Cognitive disturbances emerge during the sub‑acute period (days 3–7), manifesting as reduced performance in the Morris water maze and novel object recognition tasks, indicating hippocampal involvement.
Physiological markers accompany behavioral signs. Cerebral blood flow measured by laser‑Doppler flowmetry falls to 10–30 % of baseline during occlusion and remains depressed for several hours after reperfusion. Electroencephalography shows a shift toward low‑frequency activity in the ischemic hemisphere. Blood plasma exhibits elevated levels of glutamate, interleukin‑1β, and matrix‑metalloproteinase‑9, reflecting excitotoxicity and inflammation.
Histopathological examination reveals infarcted tissue confined to the striatum and overlying cortex. Hematoxylin‑eosin staining shows necrotic cells with eosinophilic cytoplasm and pyknotic nuclei. Immunohistochemistry detects activated microglia (Iba1‑positive) and astrocytic gliosis (GFAP‑positive) beginning at day 3 and peaking around day 14. Edema appears as increased brain weight and ventricular compression on magnetic‑resonance imaging, while diffusion‑weighted imaging highlights restricted water movement in the core lesion.
Long‑term outcomes (weeks to months) include persistent motor asymmetry, chronic neuroinflammation, and progressive atrophy of the damaged region, measurable by serial MRI volumetry. Rehabilitation interventions—such as treadmill training or enriched environment exposure—can attenuate these deficits, emphasizing the model’s utility for testing therapeutic strategies.