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Journal of Neuroscience, Vol 14, 6872-6885, Copyright © 1994 by Society for Neuroscience
Perforant path damage results in progressive neuronal death and somal atrophy in layer II of entorhinal cortex and functional impairment with increasing postdamage age
DA Peterson, CA Lucidi-Phillipi, KL Eagle and FH Gage
Department of Neurosciences, University of California at San Diego, La Jolla 92093-0627.
In vivo model systems that can evaluate neuronal death, survival, and
regeneration are critical to revealing basic mechanisms of neuronal
response and developing strategies for CNS repair. We propose a distinct
experimental model of CNS degeneration following lesions to the perforant
path connecting the hippocampus and the entorhinal cortex. Within 2 weeks
of a unilateral aspirative perforant path lesion, 30% of the ipsilateral
entorhinal cortex layer II (ECL II) projection neurons had died with no
change in the contralateral ECL II population. Although there was no loss
of ECL II neurons with normal aging, animals that survived for 15 months
postlesion experienced an almost 50% loss of ipsilateral neurons compared
to unlesioned controls. This progressive neuronal death was bilateral, with
the contralateral ECL II experiencing a 30% decline in neuronal number
relative to unlesioned controls. The use of unbiased stereology ensured
that estimates of total number were not distorted by changes in the
reference volume. The documented progressive neuronal death resulted in
delayed behavioral impairment in spatial learning and performance (latency
nearly 200% of controls). We propose, therefore, that the perforant path
model is suitable for experimental investigation of neuronal survival and
regeneration following CNS trauma.
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