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1.  Neural Correlates of Inflexible Behavior in the Orbitofrontal–Amygdalar Circuit after Cocaine Exposure 
Addiction is characterized by compulsive or inflexible behavior, observed both in the context of drug-seeking and in contexts unrelated to drugs. One possible contributor to these inflexible behaviors may be drug-induced dysfunction within circuits that support behavioral flexibility, including the basolateral amygdala (ABL) and the orbitofrontal cortex (OFC). Here we describe data demonstrating that chronic cocaine exposure causes long-lasting changes in encoding properties in the ABL and the OFC during learning and reversal in an odor-guided task. In particular, these data suggest that inflexible encoding in ABL neurons may be the proximal cause of cocaine-induced behavioral inflexibility, and that a loss of outcome-expectant encoding in OFC neurons could be a more distal contributor to this impairment. A similar mechanism of drug-induced orbitofrontal–amygdalar dysfunction may cause inflexible behavior when animals and addicts are exposed to drug-associated cues and contexts.
doi:10.1196/annals.1401.014
PMCID: PMC2587372  PMID: 17846156
addiction; cocaine; orbitofrontal cortex; basolateral amygdala; reversal; associative learning
2.  Reconciling the Roles of Orbitofrontal Cortex in Reversal Learning and the Encoding of Outcome Expectancies 
Damage to orbitofrontal cortex (OFC) has long been associated with decision-making deficits. Such deficits are epitomized by impairments in reversal learning. Historically, reversal learning deficits have been linked to a response inhibition function or to the rapid reversal of associative encoding in OFC neurons. However here we will suggest that OFC supports reversal learning not because its encoding is particularly flexible—indeed it actually is not—but rather because output from OFC is critical for flexible associative encoding downstream in basolateral amygdala (ABL). Consistent with this argument, we will show that reversal performance is actually inversely related to the flexibility of associative encoding in OFC (i.e., the better the reversal performance, the less flexible the encoding). Further, we will demonstrate that associative correlates in ABL are more flexible during reversal learning than in OFC, become less flexible after damage to OFC, and are required for the expression of the reversal deficit caused by OFC lesions. We will propose that OFC facilitates associative flexibility in downstream regions, such as ABL, for the same reason that it is critical for outcome-guided behavior in a variety of setting—namely that processing in OFC signals the value of expected outcomes. In addition to their role in guiding behavior, these outcome expectancies permit the rapid recognition of unexpected outcomes, thereby driving new learning.
doi:10.1196/annals.1401.001
PMCID: PMC2430624  PMID: 17698988
orbitofrontal cortex; basolateral amygdala; reversal; associative learning; expectancies
3.  Should I Stay or Should I Go? 
Animals prefer a small, immediate reward over a larger delayed reward (time discounting). Lesions of the orbitofrontal cortex (OFC) can either increase or decrease the breakpoint at which animals abandon the large delayed reward for the more immediate reward as the delay becomes longer. Here we argue that the varied effects of OFC lesions on delayed discounting reflect two different patterns of activity in OFC; one that bridges the gap between a response and an outcome and another that discounts delayed reward. These signals appear to reflect the spatial location of the reward and/or the action taken to obtain it, and are encoded independently from representations of absolute value. We suggest a dual role for output from OFC in both discounting delayed reward, while at the same time supporting new learning for them.
doi:10.1196/annals.1390.001
PMCID: PMC2430621  PMID: 17344533
reward; orbitofrontal cortex; delay; time discounting; value

Results 1-3 (3)