Differential neuroplastic changes in neocortical movement representations and dendritic morphology in epilepsy‐prone and epilepsy‐resistant rat strains following high‐frequency stimulation
- 16 April 2004
- journal article
- research article
- Published by Wiley in European Journal of Neuroscience
- Vol. 19 (8) , 2319-2328
- https://doi.org/10.1111/j.0953-816x.2004.03332.x
Abstract
The epileptogenic-prone (FAST) and epileptogenic-resistant (SLOW) rat strains have become a valuable tool for investigating the neurochemical and neurophysiological basis of epilepsy. This study examined the two strains with respect to their neocortical movement representations and cortical layer III pyramidal cell dendritic morphology in both control and potentiated conditions. FAST and SLOW rats received high-frequency stimulation of the corpus callosum in order to induce long-term polysynaptic potentiation of the transcallosal pathway to the sensorimotor neocortex. Baseline-evoked potentials of this pathway were recorded in the left hemisphere before stimulation, and following 5, 10, 15 and 20 days of high-frequency stimulation. All rats then underwent high-resolution intracortical microstimulation (ICMS) in order to assess functional movement representations of the left caudal forelimb area of the sensorimotor cortex. Immediately following ICMS, the brains were stained with the Golgi-Cox method, and the length, branching and spine density of frontal and occipital neocortical layer III pyramidal neurons were measured. We observed that high-frequency stimulation induced similar increases in polysynaptic potentiation in both rat strains; however, only the FAST strain showed an increase (doubling) in the size of their motor maps. We also observed decreases in dendritic length and branching in the FAST rats, and the opposite profile in the SLOW rats. The potentiated FAST rats also showed an increase in spine density. Our results suggest that differences in susceptibility to epileptogenesis may result in a differential response to stimulation-induced plasticity.Keywords
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