Aspiration lesions of rat ventral hippocampus disinhibit responding in conditioned suppression or extinction, but spare latent inhibition and the partial reinforcement extinction effect

A. J.M. Clark, J. Feldon, J. N.P. Rawlins

Research output: Contribution to journalArticlepeer-review

Abstract

Latent inhibition refers to a decrement in learning about a stimulus as a result of its prior non-reinforced presentation. There is evidence that lesions of nucleus accumbens and conventional hippocampal lesions both disrupt the development of latent inhibition. The partial reinforcement extinction effect reflects the observation that resistance to extinction is normally greater in animals that have been rewarded on a 50% random proportion of acquisition trials than in those rewarded on every trial. Conventional hippocampal lesions, excitotoxic lesions of hippocampus plus subiculum, or conventional lesions of nucleus accumbens abolish this effect. The present experiments examined the possibility that a projection originating in the ventral [temporal in the nomenclature proposed by Blackstad: (1956) J. comp. Neurol. 105, 417-537] subiculum and terminating in nucleus accumbens underlies the normal development of latent inhibition and the partial reinforcement extinction effect, by evaluating the performance on these two behaviours of rats with aspiration lesions in the ventral hippocampal region. There was equally clear evidence of latent inhibition and of a partial reinforcement extinction effect in controls and in rats with ventral hippocampal damage. However, superimposed on this, the hippocampal lesion induced a loss of behavioural inhibition in both paradigms. Subsequent anatomical analyses indicated that cell bodies in nearby retrohippocampal cortex had maintained intact projections to nucleus accumbens. We suggest that these extra-hippocampal projections may underlie the ability to learn to ignore irrelevant stimuli.

Original languageEnglish
Pages (from-to)821-829
Number of pages9
JournalNeuroscience
Volume48
Issue number4
DOIs
StatePublished - Jun 1992

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