Basolateral amygdala encodes upcoming errors but not response conflict.

Adaptive behavior depends on the detection of potential errors so that ongoing behavior might be corrected. Here, we ask whether basolateral amygdala (ABL) might serve this function by examining activity in rats performing a task in which errors were induced by pitting two behavioral responses against each other. This response competition or conflict was created by forcing rats to respond away from the direction in which they were freely choosing on the majority of trials. Rats were slower and less accurate on these incongruent trial types. We found that activity in ABL fired more strongly prior to errant responses, but did not signal the potential for errors on correctly performed incongruent trials. These data support a role for ABL in processing errors prior to their occurrence and suggest that ABL is not involved in monitoring conflict so that ongoing behavior might be corrected.

Ventral striatum encodes past and predicted value independent of motor contingencies.

The ventral striatum (VS) is thought to signal the predicted value of expected outcomes. However, it is still unclear whether VS can encode value independently from variables often yoked to value such as response direction and latency. Expectations of high value reward are often associated with a particular action and faster latencies. To address this issue we trained rats to perform a task in which the size of the predicted reward was signaled before the instrumental response was instructed. Instrumental directional cues were presented briefly at a variable onset to reduce accuracy and increase reaction time. Rats were more accurate and slower when a large versus small reward was at stake. We found that activity in VS was high during odors that predicted large reward even though reaction times were slower under these conditions. In addition to these effects, we found that activity before the reward predicting cue reflected past and predicted reward. These results demonstrate that VS can encode value independent of motor contingencies and that the role of VS in goal-directed behavior is not just to increase vigor of specific actions when more is at stake.

Attention for learning signals in anterior cingulate cortex.

Learning theory suggests that animals attend to pertinent environmental cues when reward contingencies unexpectedly change so that learning can occur. We have previously shown that activity in basolateral nucleus of amygdala (ABL) responds to unexpected changes in reward value, consistent with unsigned prediction error signals theorized by Pearce and Hall. However, changes in activity were present only at the time of unexpected reward delivery, not during the time when the animal needed to attend to conditioned stimuli that would come to predict the reward. This suggested that a different brain area must be signaling the need for attention necessary for learning. One likely candidate to fulfill this role is the anterior cingulate cortex (ACC). To test this hypothesis, we recorded from single neurons in ACC as rats performed the same behavioral task that we have used to dissociate signed from unsigned prediction errors in dopamine and ABL neurons. In this task, rats chose between two fluid wells that produced varying magnitudes of and delays to reward. Consistent with previous work, we found that ACC detected errors of commission and reward prediction errors. We also found that activity during cue sampling encoded reward size, but not expected delay to reward. Finally, activity in ACC was elevated during trials in which attention was increased following unexpected upshifts and downshifts in value. We conclude that ACC not only signals errors in reward prediction, as previously reported, but also signals the need for enhanced neural resources during learning on trials subsequent to those errors.

ß-III spectrin is critical for development of purkinje cell dendritic tree and spine morphogenesis.

Mutations in the gene encoding ß-III spectrin give rise to spinocerebellar ataxia type 5, a neurodegenerative disease characterized by progressive thinning of the molecular layer, loss of Purkinje cells and increasing motor deficits. A mouse lacking full-length ß-III spectrin (ß-III⁻/⁻) displays a similar phenotype. In vitro and in vivo analyses of Purkinje cells lacking ß-III spectrin, reveal a critical role for ß-III spectrin in Purkinje cell morphological development. Disruption of the normally well ordered dendritic arborization occurs in Purkinje cells from ß-III⁻/⁻ mice, specifically showing a loss of monoplanar organization, smaller average dendritic diameter and reduced densities of Purkinje cell spines and synapses. Early morphological defects appear to affect distribution of dendritic, but not axonal, proteins. This study confirms that thinning of the molecular layer associated with disease pathogenesis is a consequence of Purkinje cell dendritic degeneration, as Purkinje cells from 8-month-old ß-III⁻/⁻ mice have drastically reduced dendritic volumes, surface areas and total dendritic lengths compared with 5- to 6-week-old ß-III⁻/⁻ mice. These findings highlight a critical role of ß-III spectrin in dendritic biology and are consistent with an early developmental defect in ß-III⁻/⁻ mice, with abnormal Purkinje cell dendritic morphology potentially underlying disease pathogenesis.