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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Increases in mRNA levels for synapsin I but not synapsin II in the hippocampus of the rat kindling model of epilepsy.

We studied brain synapsin I and II mRNA levels using the amygdala kindling model of epilepsy. There were significant increases in the synapsin I mRNA level in the granule cell layer of the hippocampal bilateral dentate gyrus. One to 8 h after seizures, the level in the dentate gyrus ipsilateral to stimulation increased by 44.2-73.2%, compared with the control level. Of the time points investigated, the greatest increase in expression was observed 8 h after the kindled seizures. Furthermore, the synapsin I mRNA levels in the dentate gyrus contralateral to stimulation increased by 28.0% and 51.1%, 2 and 8 h, respectively, after the kindled seizures. Expression of this mRNA, however, did not change significantly in other areas examined, including CA1, CA2, CA3 and the polymorphic layer of the hippocampus and the perirhinal and temporal cortices. Synapsin II mRNA levels did not change significantly in any of the regions studied for up to 24 h after the seizures and synapsin II was presumed to have little involvement in kindling. We considered the locally elevated synapsin I mRNA levels in the bilateral dentate gyrus associated with kindling indicate that excitatory changes occur in the synaptic circuit in which the dentate granule cells participate. Synapsin I may be involved in the presynaptic molecular mechanisms underlying the neuronal plasticity in kindling.[1]

References

  1. Increases in mRNA levels for synapsin I but not synapsin II in the hippocampus of the rat kindling model of epilepsy. Morimoto, K., Sato, K., Sato, S., Suemaru, S., Sato, T., Yamada, N., Hayabara, T. Seizure : the journal of the British Epilepsy Association. (1998) [Pubmed]
 
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