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The semiology of epileptic seizures changes during the lifetime. Hence, it can be assumed that age-related changes in brain plasticity influence the patterns of seizure onset, spread and propagation velocity. We employed the 4-aminopyridine model of epilepsy to study seizure-like events in vitro. Combined entorhinal cortex-hippocampus brain slices from juvenile (10-13 days), adult (2-3 months), and senile (24-27 months) rats were examined using electrophysiological recordings and imaging of intrinsic optical signals. In the juvenile group, seizure onset was multifocal in all slice regions including the hippocampus. Onset in adult animals was confined to the entorhinal cortex and to neocortical regions. In slices from senile animals, there was a preponderance of seizure onsets in the neocortex. Spread patterns were highly variable in the juvenile group and became gradually more monomorph with increasing age. Propagation velocities were highest in the adult group, with maximum values of 1.51 +/- 0.68 mm/s. In the juvenile group, they amounted to 0.97 +/- 0.39 mm/s, and to 1.18 +/- 0.42 mm/s in senile slices. The results of this study indicate that age-related changes in brain plasticity profoundly affect spread patterns, which may contribute to the clinically observed changes in seizure semiology during early childhood, adulthood and senescence.

Old age is the most common time for patients to develop epileptic seizures, and due to their frequent unusual clinical presentation the diagnosis of epilepsy is often delayed in the elderly. It is as yet unknown if pronounced alterations in the plastic properties of aging nervous tissue contribute to these phenomena. We employed a non-lesional in vitro epilepsy model to study seizure susceptibility, spread pattern, and propagation velocities in combined hippocampal-entorhinal cortex slices of aged rats and controls using electrophysiological methods and imaging of intrinsic optical signals. In aged animals we saw a less extensive spread of seizure-like events into areas adjacent to the region of onset of activity and a decreased spread velocity in various anatomical regions. In addition, both the activity-dependent shrinkage of the extracellular space (ECS)-volume and the extracellular K(+) concentration were significantly reduced compared to controls. The results of this study are consistent with the clinical observation that epileptic seizures in the elderly have a reduced tendency to spread. In addition, our data suggest that in the absence of structural lesions seizure susceptibility in the aging brain is not increased.