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Alcohol and study list repetition were used to manipulate encoding quality to gain insight into the mechanisms underlying false memories. The DRM paradigm (Deese 1959b; Roediger & McDermott 1995) was used to elicit false memories. Participants studied lists of words (veridical items) which were semantically related to a critical non-presented item, which, if erroneously endorsed, served as the measure of false memory. Implicit and explicit tests of memory were used, and remember know judgments were also taken. An anterograde impairment of memory after alcohol was obtained for veridical items using explicit tests, although no effect of alcohol was found using implicit measures. Alcohol reduced false memory levels relative to placebo for material viewed once at encoding. In accordance with previous en1pirical research, repetition was found to increase, decrease or have no effect on false memory levels. The introduction of distinctive pictorial stimuli at encoding resulted in an inverted U -shaped relationship between repetition and false memories, though this effect was confined to remember judgments only. The increase in false memories as a function of repetition was greater in the alcohol group than in the placebo group_ whilst the placebo group was better able to use extended repetitions to reduce false memories. These results are accounted for using the Activation and Monitoring Framework (Gallo & Roediger 2002). It is suggested that reduced levels of false memories under alcohol for material viewed once can be attributed to reduced activation within semantic networks resulting from superficial encoding under alcohol (Craik 1977) and impoverished attentional resources when intoxicated (Steele & Josephs 1988). The selective impairment of recollective traces under alcohol (Duka et al. 2001) may limit the potential for extended repetitions to diminish false memories under alcohol. The role of metacognitive factors in affecting false memory endorsement is also discussed.

Neurocognitive and functional outcome deficits have long been acknowledged in schizophrenia and are considered a core feature of the disorder. Neurocognition has been found to account for functional disability to a greater extent than psychopathology however much of the variance in functional outcome still remains unexplained. How functional outcome is measured also requires clarification. By investigating the relationship between neurocognition and functional outcome in First-Episode Psychosis (FEP), much can be learnt about the trajectory of disability and the course of illness in schizophrenia. Metacognition, or thinking about thinking, has been proposed as a mediating variable between neurocognition and functional outcome. Despite different theoretical backgrounds, authors generally converge on there being higher-order, explicit, conscious metacognitive knowledge and lower-order, implicit metacognitive processes. How these relate to each other requires clarification. The prefrontal cortex (PFC) has been implicated in higher order thought and metacognitive processing, and deficits have been observed in PFC Grey Matter (GM) volume in schizophrenia. These metacognitive deficits may contribute to the relationship between cognitive ability and community functioning. A preliminary meta-analysis demonstrated that a moderate effect size is found between neurocognition and metacognition and a moderate effect size exists between metacognition and functional outcome. The present thesis investigated whether metacognition mediates the relationship between neurocognition and functional outcome in FEP (N=80). Path models were created to investigate the different relationships between neurocognition, metacognition and both capacity to perform everyday tasks and objective functioning in the community. A secondary Voxel-based Morphometry (VBM) analysis was also conducted investigating perceptual metacognitive accuracy and its relationship to GM volume in both FEP (N=41) and a matched healthy control sample (N=21). Current findings support the model that metacognition and negative symptoms mediate the relationship between neurocognition and functional capacity in FEP. Path models also demonstrated a significant mediation effect of metacognition between neorocognition and objective function, and functional capacity and objective function. Significant group differences were found between FEP and controls in perceptual metacognitive accuracy however no significant relationship was found between metacognition and GM volume in the PFC. The present thesis suggests that metacognitive deficits are present at first episode and may account for the relationship between cognitive ability and functioning in the community. Findings also suggest that cognitive remediation programmes may wish to focus on metacognition to maximise the transfer of cognitive skills to community functioning. The findings also suggest the presence of two metacognitive processing routes; explicit, declarable, higher-order knowledge and implicit, intuition-based, lower-order experience which can be accounted for by Nelson and Narens (1990) metacognitive model.

Dopamine and 3',5'-cyclic adenosine monophosphate-regulated neuronal phosphoprotein (DARPP-32) is a critical mediator of neuroplasticity in striatal medium spiny neurons (MSNs). The work presented in this thesis used a global gene knockout (KO) construct to investigate the role of DARPP-32 in reward-based learning and performance. Global deletion of the DARPP-32 gene disturbed performance during the intertemporal (delay) discounting procedure. DARPP-32 KO mice were less sensitive than their wildtype (WT) littermates during long delays to reinforcement. In comparison to WT mice, DARPP-32 KO mice also developed a risk-sensitive pattern of choices during a probability discounting task. Unlike the effects of DARPP-32 deletion on reinforcement along dimensions of time and risk, DARPP-32 knockout did not affect the degree of effort that subjects were willing to invest during food-reinforced progressive ratio testing. DARPP-32 KO mice also failed to exhibit Pavlovian-to-instrumental transfer and this impairment could not be rescued by administering methylphenidate prior to test. Finally, DARPP-32 KO mice were indistinguishable from WT mice during an amphetamine psychomotor sensitisation study. Overall, the data in this thesis suggest DARPP-32 is involved in adaptive reward-based learning and performance.