The effects of excitotoxic lesion of the medial prefrontal cortex on latent inhibition, prepulse inhibition, food hoarding, elevated plus maze, active avoidance and locomotor activity in the rat
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Abstract
Latent inhibition is a measure of retarded conditioning to a previously presented
nonreinforced stimulus that is impaired in schizophrenic patients and in rats treated
with amphetamine. In terms of neural substrates, latent inhibition depends on the
integrity of the nucleus accumbens and the inputs to this structure from the hippocampal
formation and adjacent cortical areas. Since another major source of input to the
nucleus accumbens is the medial prefrontal cortex, and there are numerous demonstrations
that manipulations of this region can modify ventral striatal dopamine, we investigated
the effects of N-methyl-D-aspartate lesion to the medial prefrontal cortex on latent
inhibition, assessed in an off-baseline conditioned emotional response procedure in
rats licking for water. In addition, the effects of the medial prefrontal cortex lesion
were assessed on a battery of tasks potentially sensitive to medial prefrontal cortex
damage, including spontaneous and amphetamine-induced activity, elevated plus maze
exploration, food hoarding, prepulse inhibition, and active avoidance. The lesion
decreased hoarding behaviour and increased spontaneous exploratory activity in the
open field, while exerting only mild effects on amphetamine-induced activity. Prepulse
inhibition, exploration of the elevated plus maze, and the acquisition of two-way
active avoidance were unaffected by the lesion. Likewise, latent inhibition was left
intact following the lesion, suggesting that neither the destruction of the intrinsic
cells of the medial prefrontal cortex nor any potential lesion-induced changes in
subcortical dopamine, affect latent inhibition.