Increase in synapsin I phosphorylation implicates a presynaptic component in septal kindling.

Synaptic plasticity in the CNS is thought to be an important component of learning and memory. Kindling is an animal model of synaptic plasticity in which repetitive local electrical stimulation eventually leads to a generalized motor seizure. Once established, the sensitivity of kindled animals to this epileptic condition is long-lasting. An increase in synaptic efficacy appears to underlie the plastic changes observed in kindling but the molecular mechanisms involved remain unknown. Here we demonstrate that the phosphorylation state of synapsin I, a synaptic vesicle-associated protein which has been implicated in the regulation of neurotransmitter release, is significantly increased in hippocampus and parietal cortex of rats two weeks after the establishment of septal kindling. Furthermore, K(+)-evoked release of L-glutamate is significantly increased in synaptosomes prepared from cerebral cortex of kindled animals. Thus, changes within the presynaptic nerve terminal may contribute, at least in part, to the long-lasting modification in neuronal function induced by kindling.