Pharmacological and behavioural manipulation of attention in simple exposure learning

The experiments in this thesis examined mechanisms underlying attentional changes in simple exposure learning. The first set of experiments showed that exposures depressed orienting and subsequent conditioned freezing in rats. A remotely pre-exposed conditioned stimulus (CS) conditioned better and overshadowed a novel CS more than a recently pre-exposed CS. Additional pre-exposures reversed these effects: a remotely pre-exposed CS elicited more orienting, conditioned worse and overshadowed less than a recently pre-exposed CS. Exposure to a compound composed of a novel and a remotely pre-exposed CS resulted in the novel CS subsequently conditioning better than a novel CS exposed in compound with a recently pre-exposed CS. The second set of experiments used rats to investigate the role of dopamine activity in learning to inhibit conditioned fear responses (freezing) as aresult of simple stimulus exposure in extinction. In Experiment 1, rats systemically injected with the D2 dopamine antagonist, haloperidol, froze more across multiple extinction sessions and on a drug-free retention test than control rats. In Experiment 2, rats extinguished under an intracerebroventricular (ICV) infusion of haloperidol suppressed fear responses across extinction but froze more on a subsequent drug-free retention test than control rats. In Experiment 3, rats extinguished under an infusion of haloperidol in the nucleus accumbens were impaired in suppressing fear responses across extinction and froze more on subsequent drug-free retention test than control rats. These results show that learning to inhibit fear responses in extinction requires dopamine activity in the nucleus accumbens. The results were interpreted to mean that stimulus alone exposures produce a loss in associability which recovers across time, that this restoration deepens the loss in associability, and that this deepening is regulated by a common error term. Morover, this reduction in associabilty may be mediated by dopaminergic transmission in the nucleus accumbens