RATIONALE: Lithium-pilocarpine-induced status epilepticus (SE) generates neuronal lesions in the limbic forebrain, cerebral cortex and thalamus that lead to circuit reorganization and spontaneous recurrent seizures. The process of reorganization in regions with neuronal damage is not fully clarified. METHODS: In the present study, we evaluated by immunohistochemistry the early reorganization during the latent period with two neuronal markers, synaptophysin and growth-associated protein 43 (GAP-43) in rats subjected to SE at PN21 and as adults. RESULTS: Synaptophysin immunoreactivity increased between 24 h and 3 weeks post-SE in regions with severe and rapidly occurring neuronal loss, namely thalamus, amygdala, piriform and entorhinal cortices. GAP-43 expression decreased at 1 and 3 weeks in the same regions. The immunoreactivity of synaptophysin and GAP-43 increased in the inner molecular layer of dentate gyrus from 24 h after SE, and decreased in the outer molecular layer from 72 h after SE. These changes likely result from the death of hilar neurons and the reduction of the input from the entorhinal cortex. In 21-day-old rats that experience less SE-induced neuronal loss, increased immunoreactivity of synaptophysin was only found in piriform and entorhinal cortex while no changes occurred in GAP-43 expression. CONCLUSION: These findings suggest that there is an age-related relation between the extent and rapidity of the process of neuronal death and the expression of these markers. Synaptophysin appears to be a more sensitive marker of plasticity induced by SE than GAP-43.
RATIONALE: Lithium-pilocarpine-induced status epilepticus (SE) generates neuronal lesions in the limbic forebrain, cerebral cortex and thalamus that lead to circuit reorganization and spontaneous recurrent seizures. The process of reorganization in regions with neuronal damage is not fully clarified. METHODS: In the present study, we evaluated by immunohistochemistry the early reorganization during the latent period with two neuronal markers, synaptophysin and growth-associated protein 43 (GAP-43) in rats subjected to SE at PN21 and as adults. RESULTS:Synaptophysin immunoreactivity increased between 24 h and 3 weeks post-SE in regions with severe and rapidly occurring neuronal loss, namely thalamus, amygdala, piriform and entorhinal cortices. GAP-43 expression decreased at 1 and 3 weeks in the same regions. The immunoreactivity of synaptophysin and GAP-43 increased in the inner molecular layer of dentate gyrus from 24 h after SE, and decreased in the outer molecular layer from 72 h after SE. These changes likely result from the death of hilar neurons and the reduction of the input from the entorhinal cortex. In 21-day-old rats that experience less SE-induced neuronal loss, increased immunoreactivity of synaptophysin was only found in piriform and entorhinal cortex while no changes occurred in GAP-43 expression. CONCLUSION: These findings suggest that there is an age-related relation between the extent and rapidity of the process of neuronal death and the expression of these markers. Synaptophysin appears to be a more sensitive marker of plasticity induced by SE than GAP-43.