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Abstract
Eight experiments examined the neural mechanisms involved in predictive fear learning, as measured by conditioned suppression in the rat. The first series of experiments examined the contribution of dopamine receptors in amygdala and nucleus accumbens (Acb) subregions to the blocking of Pavlovian fear conditioning. In these experiments, rats in the experimental groups were trained to fear CSA in Stage I by pairings with a shock US, whereas rats in the control groups were not. In Stage II, all rats received compound fear conditioning of CSAB. Rats were later tested for their fear responses to CSB. All rats received microinjections of saline or the dopamine antagonist cis-(z)-flupenthixol prior to Stage II training, targeting either the basolateral amygdala (BLA), central nucleus of the amygdala (CeA), Acb shell subdivision (AcbSh), or Acb core subdivision (AcbC). The associative blocking of fear learning was observed, whereby Stage I fear conditioning of CSA blocked fear learning to CSB during Stage II. Microinjection of cis-(z)-flupenthixol into the BLA, CeA or AcbSh had no effect on fear learning or on blocking. In contrast, microinjection of cis-(z)-flupenthixol into the AcbC attenuated blocking and so enabled fear learning to CSB. These results identify the AcbC as a critical locus for dopamine receptor contributions to blocking of fear learning. The second series of experiments examined the contribution of AMPA glutamate receptors in Acb subregions to the blocking and unblocking of Pavlovian fear conditioning. Increasing US intensity between Stages I and II unblocked learning to CSB. Rats received microinjections of saline or the AMPA antagonist NBQX prior to Stage II training, targeting either AcbSh or AcbC. Intra-AcbSh infusion of NBQX attenuated unblocking and did not affect blocking or fear acquisition. In contrast, intra-AcbC infusion of NBQX attenuated both blocking and unblocking of fear learning, but did not affect fear acquisition. These results were interpreted to mean that Acb dopamine and glutamate are involved in stimulus selection and regulating attention in predictive fear learning, and that the actions of AcbC and AcbSh differ in this role. These findings provide novel insights into the neural mechanisms underlying fear learning and support a critical role for Acb dopamine and glutamate in CS processing.