BEHAVIORAL AND ELECTROPHYSIOLOGICAL STUDIES OF ENTORHINAL CORTEX LESIONS IN THE RAT

Bilateral ibotenic acid injections aimed at the entorhinal cortex (EC) lesioned the EC and subiculum in 30% of animals (group EC/S) and caused additional hippocampal damage in 50% (group RH). Both lesions increased acetylcholinesterase (AChE) staining in the intermediate molecular layer of the dentate gyrus. EC/S lesions increased diurnal deep sleep and the incidence of spindles but decreased REM sleep. RH lesions increased nocturnal deep sleep and decreased nocturnal quiet sleep. Both lesions reduced power over the theta frequency range from 6-10 Hz for epochs of REM sleep and quiet waking but not deep sleep. Peak frequency was unaffected. The RH group and a subset of the EC/S group were nocturnally, but not diurnally, hyperactive. Six weeks after the lesion there was no evidence for hyperactivity in a novel open field. The EC/S lesion impaired exploration as indicated by reduced motility and rearing in an open field and by the failure of EC/S-lesioned rats to increase contact time in response to a novel olfactory cue. Place navigation learning in a Morris maze was not affected by EC/S or RH lesions. However, when the spatial location of the hidden platform was shifted EC/S-lesioned rats were impaired. The sprouting response, reduced theta power and exploration deficits resemble those reported following electrolytic lesions, but the lack of effect on place navigation learning contrasts with reports of impaired spatial learning following electrolytic lesions. The data prompt a reexamination of the role which the EC projection to the hippocampus plays in spatial learning.