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Recovery of Motor Deficit,Cerebellar Serotonin and Lipid Peroxidation Levels in the Cortex of Injured Rats
Authors:Antonio Bueno-Nava  Rigoberto Gonzalez-Pina  Alfonso Alfaro-Rodriguez  Vladimir Nekrassov-Protasova  Alfredo Durand-Rivera  Sergio Montes  Fructuoso Ayala-Guerrero
Institution:1.Depto de Neurofisiologia-Lab. de Cromatografia y Microdialisis,INR, SSA, Calz. Mexico-Xochimilco 289 Col. Arenal de Guadalupe Deleg. Tlalpan,Mexico City,Mexico;2.Depto de Neurofisiologia-Lab. de Neuroplasticidad, Torre de Investigación,Instituto Nacional de Rehabilitación, SSA, Calz. México-Xochimilco 289, Col. Arenal de Guadalupe, Deleg. Tlalpan,Mexico City,Mexico;3.Depto de Neurofisiologia-Lab. de Neuroquimica,INR, SSA,Mexico City,Mexico;4.Depto de Neurofisiologia-Lab. de Neuroprotección,INR, SSA,Mexico City,Mexico;5.Depto de Neuroquimica,INNN MVS, SSA,Mexico City,Mexico;6.Facultad de Psicologia,Universidad Nacional Autonoma de Mexico,Mexico City,Mexico
Abstract:The sensorimotor cortex and the cerebellum are interconnected by the corticopontocerebellar (CPC) pathway and by neuronal groups such as the serotonergic system. Our aims were to determine the levels of cerebellar serotonin (5-HT) and lipid peroxidation (LP) after cortical iron injection and to analyze the motor function produced by the injury. Rats were divided into the following three groups: control, injured and recovering. Motor function was evaluated using the beam-walking test as an assessment of overall locomotor function and the footprint test as an assessment of gait. We also determined the levels of 5-HT and LP two and twenty days post-lesion. We found an increase in cerebellar 5-HT and a concomitant increase in LP in the pons and cerebellum of injured rats, which correlated with their motor deficits. Recovering rats showed normal 5-HT and LP levels. The increase of 5-HT in injured rats could be a result of serotonergic axonal injury after cortical iron injection. The LP and motor deficits could be due to impairments in neuronal connectivity affecting the corticospinal and CPC tracts and dysmetric stride could be indicative of an ataxic gait that involves the cerebellum.
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