Abstract
Synapsin is a vesicle-associated protein that is thought to be involved in synaptogenesis and neurotransmitter release. In this study, we investigated the repeated amygdala kindling-induced changes in levels of synapsin I, a marker of enhanced synaptic activity, using immunohistochemistry. Eight hours after the last seizure, synapsin I immunoreactivity (IR) was increased bilaterally in the polymorphic zone of the dentate gyrus, the hilus and the stratum lucidum in area CA3 of the hippocampus. However, 4 weeks after the last kindled seizures, synapsin I IR was not significantly changed in any of the brain regions studied. Therefore, the increased levels of synapsin I protein observed in these brain regions early after the last seizure may reflect the plastic changes that occur in the specific neural networks of the hippocampus directly after kindling-induced seizure activity.
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