Affiliations: Department of Neurosurgery, Kinki University, School of Medicine, Osaka-Sayama (Japan) | Department of Neurosurgery, Osaka University, Medical School, Osaka (Japan) | Department of Pharmacology, Nippon Shinyaku Co., Ltd., Kyoto (Japan)
Note: [] Correspondence: K. Kataoka, Department of Neurosurgery, Kinki University School of Medicine, 377-2, Ohno-Higashi, Osaka-Sayama, Osaka 589, Japan. Fax: (81)(723) 66 0206.
Abstract: We compared the functional and anatomical alterations of somatosensory circuits in the acute (1–3 days after infarct) and chronic (3 months after infarct) stage after subcortical striatal infarct in Wistar rats. Occlusion of the left middle cerebral artery produced subcortical striatal infarct in approximately 69% of the rats. The others developed cortical infarct. The function of the somatosensory circuits was evaluated by [14C]2-deoxyglucose autoradiography during physiological stimulation of the right vibrissae and face. In rats with subcortical infarct, the areas activated by sensory stimulation of the right vibrissae and face, applied 1 and 3 days after occlusion, were reduced compared to sham-operated controls (P < 0.05). In the chronic stage of subcortical infarct, the areas of metabolic activation of the left anterior vibrissal and facial sensory area were increased compared to rats with acute subcortical infarct (P < 0.05). To evaluate the anatomical changes in the somatosensory pathway, at 1 day and 3 months after occlusion, we injected wheat germ agglutinin-horseradish peroxidase solution as an axonal transport substance bilaterally into the anterior vibrissal and facial sensory area. Tract tracing studies in both the acute and chronic stage of subcortical infarct showed a reduction in the peroxidase-positive area in the left thalamus compared to the control hemispheres (P < 0.01). The functional disturbance and recovery of the somatosensory circuits after subcortical infarct are discussed.
Keywords: Local cerebral glucose utilization, Middle cerebral artery occlusion, Rat, Somatosensory circuit, Subcortical infarction
