Abstract
Latent inhibition (LI) manifests as poorer conditioning to a CS that has previously been presented without consequence. There is some evidence that LI can be potentiated by reduced mesoaccumbal dopamine (DA) function but the locus within the nucleus accumbens of this effect is as yet not firmly established. Experiment 1 tested whether 6-hydroxydopamine (6-OHDA)-induced lesions of DA terminals within the core and medial shell subregions of the nucleus accumbens (NAc) would enhance LI under conditions that normally disrupt LI in controls (weak pre-exposure). LI was measured in a thirst motivated conditioned emotional response procedure with 10 pre-exposures (to a noise CS) and 2 conditioning trials. The vehicle-injected and core-lesioned animals did not show LI and conditioned to the pre-exposed CS at comparable levels to the non-pre-exposed controls. 6-OHDA lesions to the medial shell, however, produced potentiation of LI, demonstrated across two extinction tests. In a subsequent experiment, haloperidol microinjected into the medial shell prior to conditioning similarly enhanced LI. These results underscore the dissociable roles of core and shell subregions of the NAc in mediating the expression of LI and indicate that reduced DA function within the medial shell leads to enhanced LI.
Highlights
Latent inhibition (LI) refers to the process whereby non-reinforced pre-exposure to a stimulus normally reduces the level of associative learning that the pre-exposed stimulus can support (Lubow and Moore, 1959)
Investigations into the neural substrates of LI have shown that the nucleus accumbens (NAc) and its afferent connections from the entorhinal cortex, hippocampus and basalateral amygdala play a key role in the regulation of LI
Neurotransmitter assay Quantification of the lesions by high-pressure liquid chromatography (HPLC) revealed that 6 animals showed no evidence of NAc DA depletion, these animals were not considered for further analysis
Summary
Latent inhibition (LI) refers to the process whereby non-reinforced pre-exposure to a stimulus normally reduces the level of associative learning that the pre-exposed stimulus can support (Lubow and Moore, 1959). Excitotoxic and electrolytic lesions to the shell disrupt LI but the effect is spared by similar lesions to core NAc (Tai et al, 1995; Weiner et al, 1996; Gal et al, 2005; Pothuizen et al, 2005). Experiment 1 tested the effects of 6-OHDA lesions targeted at the core and medial shell on LI using experimental parameters designed to prevent the emergence of LI in normal rats (weak pre-exposure). This was followed in Experiment 2, by an examination of the effect of haloperidol microinjected prior to conditioning into the core or medial shell using the same behavioral parameters as Experiment 1
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