Spaniol and colleagues (2009) analyzed 81 fMRI studies of episodic memory, a subset of which included contrasts of encoding success (subsequent hits greater than misses) and/or retrieval success (hits greater than CR). A quantitative meta-analytic procedure indicated that retrieval success consistently activated striatum across studies, including both dorsal striatum in the left caudate and ventral striatum in regions of caudate, putamen, and nucleus accumbens (also see Kim, 2011). Figure 2 shows this effect

selleck chemicals in an updated recoding and reanalysis of these data conducted for this review. Moreover, a contrast between retrieval success and encoding success showed that the ventral caudate was more reliably associated with retrieval success than encoding success across studies. Importantly, retrieval success in striatum is not dependent on an actual prior experience with an item. Rather, striatum shows greater activation for false

alarms (new items incorrectly judged as old) than CR or misses (Abe et al., 2008). Thus, like most regions showing retrieval success effects (Wagner et al., 2005), striatal activation tracks the perception of an item as being old during a recognition memory task, rather than it having been previously encountered on the study list. Thus, striatal retrieval success effects cannot be trivially explained based Enzalutamide ic50 on a prior association with positive reinforcement formed at encoding. Generally consistent with the neuroimaging data, deficits in patients with Parkinson’s disease (PD)—a disease arising from degeneration of cells in the substantia nigra that are a primary source of dopaminergic input into the striatum (Figure 1B)—indicate that the basal ganglia are broadly necessary for normal levels of recognition memory performance. In particular, though not suffering from the CTP synthase profound amnesias accompanying MTL damage, PD patients do demonstrate deficits in recognition memory relative to controls in studies with sufficient power (Whittington et al., 2000). Accounting for these recognition deficits in PD has proven difficult and multifaceted.

Across studies, deficits have been evident sometimes in recollection (Barnes et al., 2003; Edelstyn et al., 2007, 2010; Drag et al., 2009) and sometimes in familiarity (Davidson et al., 2006; Weiermann et al., 2010). Moreover, there seems ample evidence that at least a portion of memory deficits observed in PD arise from a failure to engage in effective encoding strategies (Knoke et al., 1998; Vingerhoets et al., 2005). However, a recent study has provided convincing evidence for a recollection deficit in PD when encoding strategy was controlled. Cohn et al. (2010) had PD patients and age-matched controls study word pairs under shallow and deep encoding conditions, and estimated familiarity and recollection using the process-dissociation procedure (Yonelinas et al., 1995).

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