Nucleus Accumbens Core and Delay Discounting

Several studies have implicated the nucleus accumbens core in delay discounting. These studies have predominantly been in rodents and have generally suggested that the nucleus accumbens core promotes choice of the delayed reinforcer (less delay discounting). Additionally, a few studies  have shown that delay discounting correlates with elements of the physiological makeup of the nucleus accumbens core.

Human imaging studies using functional magnetic resonance imaging (fMRI) have heavily implicated the ventral striatum (which contains the nucleus accumbens core) in delay discounting, but the resolution of fMRI studies is insufficient to determine if the nucleus accumbens core is driving this effect (see Ventral Striatum and Delay Discounting).

Role of the nucleus accumbens core in delay discounting


Several studies have investigated the role of the nucleus accumbens core in delay discounting. Although there are a few exceptions, the majority of these have found that lesioning or inactivating the nucleus accumbens core increases choice of the small, immediate reinforcer (increased delay discounting, see Table 1 below). This suggests that the intact nucleus accumbens core promotes delayed choice.

The exact mechanism by which the nucleus accumbens core modulates delay discounting is currently unknown. A number of studies performed by Bradshaw and colleagues have suggested that the nucleus accumbens core is specifically involved in sensitivity to delay   (as opposed to sensitivity to magnitude, see Components of Delay Discounting). This data is corroborated by a study that found that lesion of the accumbens core impaired rats' ability to learn an instrumental response paired with a delayed reward, but had no effect on non-delayed instrumental learning.

However, not all studies suggest that the accumbens core acts on sensitivity to delay. One study has suggested that the nucleus accumbens core may modulate sensitivity to magnitude instead. The authors provided evidence suggesting that the effects of accumbens lesions on magnitude sensitivity were due to its effect on reinforcer value, rather than any effects on magnitude discrimination, and also found no effects of accumbens core lesion on ability to perceive delays. Another study found that accumbens core inactivation altered delay discounting, but had no effect on tasks measuring sensitivity to delay or magnitude in isolation.

It is also important to consider both other brain regions that input into the accumbens core, as well as the role that the accumbens core plays in tasks that are partially distinct from delay discounting (e.g. probability and effort discounting). Several inputs into the nucleus accumbens core, most notably the basolateral amygdala, but also the hippocampus, medial prefrontal cortex, and ventral tegmental area, have been implicated in delay discounting as well. Therefore, it may be that upstream neural substrates are responsible for delay sensitivity, with the nucleus accumbens core being either a relay or an integrator of this and other information. Supporting the "integrator" role for the nucleus accumbens core are several studies that have shown the accumbens core to be involved in effort discounting as well (the literature for probability discounting is somewhat mixed).

Relationship between delay discounting and nucleus accumbens core physiology
In addition to studies examining the direct role that the nucleus accumbens plays in delay discounting, several studies have investigated the relationship between delay discounting and the physiology of the nucleus accumbens core. These studies have varied in their methods, examining gene expression, neuronal firing, and neurotransmitter levels (see Table 2 below).

Some studies have investigated the relationship between individual differences in delay discounting and individual differences in nucleus accumbens core physiology. These studies have primarily focused on dopamine. Although delay discounting does not correlate with dopamine receptor levels in the nucleus accumbens core, rats with low delay discounting exhibit higher evoked dopamine in the nucleus accumbens core than do rats with high delay discounting. This may suggest that dopaminergic inputs from the ventral tegmental area play a role in determining a given individual's level of delay discounting.

Additionally, a number of studies have examined neuronal activity in the ventral striatum during delay discounting, although none have specifically investigated the nucleus accumbens core. Within the animal literature, one study generally found that separate populations of neurons independently tracked delay and magnitude, suggesting that the nucleus accumbens core maintains two separate representations of delay and magnitude. However, another study found that neurons that tracked one also tended to track the other, suggesting an integrator role for the nucleus accumbens core. The differences in findings may relate to both the different species and different tasks used.