An experimental study on the course of trans-synaptic propagation of neural activity and plasticity in the hippocampus in kainate-induced epilepsy.
To investigate the course of trans-synaptic propagation of neural activity and plasticity in temporal lobe epilepsy, time-dependent changes in the level of synapsin I, a synaptic vesicle protein that is a marker of enhanced synaptic activity and synaptogenesis, were examined following kainate-induced epileptic status in rats. Compared with the control, the level of synapsin I protein increased in the bilateral stratum oriens of CA3 (28.8-40.2%) and CA1 (28.0-34.6%), and the stratum radiatum of CA1 (34.0%) ipsilateral to the injection site at 8 h after intra-amygdala administration of kainate. At 24 h, and 2 and 4 weeks after the kainate treatment, however, synapsin I levels returned to normal levels in most of the regions studied in spite of the extended neural loss in the hippocampus, which suggested the axonal sprouting on the remaining cells. The synapsin I mRNA levels time-dependently decreased bilaterally in CA1-CA3 and the hilus, while no significant changes were observed in the dentate gyrus. These results suggest that the synaptic input to CA3 and CA1 through the stratum oriens was enhanced in this model. A different mode of hippocampal neural activity and plasticity between kainate and kindling models of epilepsy may be stressed.[1]References
- An experimental study on the course of trans-synaptic propagation of neural activity and plasticity in the hippocampus in kainate-induced epilepsy. Sato, K., Abe, K. Brain Res. Bull. (2001) [Pubmed]
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