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CA3 axonal sprouting in kainate-induced chronic epilepsy.

Adnan H Siddiqui¹, Shirley A Joseph

¹Department of Neurosurgery, Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA. siddiqua@upstate.edu

|December 20, 2005

Summary

Structural reorganization in the hippocampus, specifically CA3 axon sprouting, occurs after neurological injury. This sprouting may explain the delayed onset of spontaneous recurrent seizures in temporal lobe epilepsy.

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Area of Science:

Neuroscience
Epileptology
Structural Neuroplasticity

Background:

Epilepsy, particularly mesial temporal sclerosis-associated epilepsy, shows a latency between neurological insult and seizure development.
Mossy fiber sprouting in dentate granule cells is a known structural reorganization, but CA3 pyramidal cell outflow alterations are less understood.

Purpose of the Study:

To investigate the aberrant reorganization of CA3 pyramidal cell outflow following kainate-induced seizures.
To provide the first evidence of CA3 structural reorganization and its projections.

Main Methods:

Utilized precise anterograde and retrograde tract tracing methodologies.
Evaluated the reorganization of CA3 pyramidal cell outflow in an epilepsy model.

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Main Results:

Demonstrated widespread CA3 structural reorganization, including sprouting of CA3 axons throughout the hippocampus and entorhinal cortex.
Identified novel CA3 Schaffer collateral projections to the entorhinal cortex and increased projections to CA1 and subiculum.

Conclusions:

Widespread CA3 sprouting may explain how injured hippocampi propagate aberrant excitation to cortical fields.
These sprouting mechanisms could underlie the latency observed in the development of spontaneous recurrent seizures in temporal lobe epilepsy.