Lesions to the basolateral amygdala and the orbitofrontal cortex but not to the medial prefrontal cortex produce an abnormally persistent latent inhibition in rats
- PMID: 15450350
- DOI: 10.1016/j.neuroscience.2004.06.020
Lesions to the basolateral amygdala and the orbitofrontal cortex but not to the medial prefrontal cortex produce an abnormally persistent latent inhibition in rats
Abstract
Repeated nonreinforced preexposure to a stimulus interferes with the establishment of conditioned responding to this stimulus when it is subsequently paired with reinforcement. This stimulus-preexposure effect is known as latent inhibition (LI). Rather remarkably, LI appears to be resistant to the effects of numerous lesions, including the prefrontal cortex (PFC) and the basolateral amygdala (BLA). However, intact behavioral expression of LI following damage to given brain regions does not preclude the possibility that such regions participate in the regulation of LI expression in the intact brain. The present study showed that lesions of the BLA and the orbitofrontal cortex (OFC) but not of the medial PFC (mPFC) led to an abnormally persistent LI which emerged under conditions that disrupted LI in control rats. LI was measured in a thirst motivated conditioned emotional response procedure by comparing suppression of drinking in response to a tone in rats which received 0 (nonpreexposed) or 40 tone presentations (preexposed) followed by either two or five tone-shock pairings. Control rats showed LI with 40 preexposures and two conditioning trials, but raising the number of conditioning trials to five disrupted LI. OFC- and BLA-lesioned rats showed LI under the former condition but in addition persisted in exhibiting LI under the latter condition. Rats with lesion of the mPFC did not show persistent LI. Thus, although LI does not depend on the integrity of BLA and OFC (because it is present in BLA- and OFC- lesioned rats even under conditions disrupting the phenomenon in normal rats), these regions play an important role in the modulation of its expression, more specifically, in the control of the non-expression of LI when the impact of conditioning increases beyond a certain level.
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