134 / 218
132
Chapter 6
have established a role for the AcbC in helping animals to choose the best action based on
prospective rewards. Disrupted functioning of the AcbC in these studies generally reduces
the facilitation of appropriate responses, for example assessed with general Pavlovian to
instrumental transfer (g-PIT) or cue-induced reinstatement (Floresco et al., 2008b; Corbit
and Balleine, 2011). In a PIT procedure, animals receive instrumental- (learning to press a
lever to obtain a food reward) and Pavlovian conditioning (learning that a cue predicts the
delivery of an outcome), followed by a test on which the Pavlovian stimulus (CS) is delivered
with the levers present. The presence of a CS increases lever pressing, i.e. the association
between a cue and a reward facilitates instrumental performance, but only in animals with an
intact AcbC (Corbit and Balleine, 2011). In addition to this general enhancement of reward-
related cues, Pavlovian cues can also selectively increase performance on the basis of the
specific outcome predicted by the cue. Animals with lesions of the AcbC are still able to show
this specific PIT effect. In the current study, optimal behaviour would entail the facilitation
of flexible control in the high reward context over the low reward context. This facilitation
of flexible control under high reward was impaired after lesions of the AcbC. Also, lesions
of the AcbC are known to reduce the inhibition of inappropriate actions, during outcome
devaluation (Shiflett and Balleine, 2010) (Corbit et al., 2001), (but see de Borchgrave et al.,
2002). After instrumental training on two levers which deliver two distinct outcomes, the
value of one of the outcomes is reduced (e.g. by allowing animals to consume one of the
outcomes freely). During a subsequent test, animals with an intact AcbC reduce responding
to the lever which previously delivered the devalued outcome. After lesions of the AcbC
however, animals no longer show this inhibition. In the current study, the suboptimal strategy
would be to maximize cognitive control in the low reward context over the high reward
context. In line with a role for the AcbC in the inhibition of inappropriate behaviour, we
observed that animals with lesions of the AcbC exhibited more cognitive control in the low
reward context than did animals with sham lesions. Combined, these results suggest that the
AcbC is necessary to facilitate appropriate responses (e.g. when a CS predicts a reward) and
to inhibit irrelevant responses (e.g. when the outcome is undesirable).
Another field of research suggesting a role for the AcbC in facilitating and suppressing
goals shows that animals without an intact AcbC are impaired when facing a situation that
requires a shift in strategy (Floresco et al., 2006a). However, this deficit was clearly distinct
from set-shifting deficits typically observed after lesions of cognitive control areas, such as the
dorsomedial striatum (DMS) or the prelimbic cortex (PL). Animals with lesions in the DS and
PL generally fail to make the initial shift (i.e. they persevere on the old rule (Ragozzino et al.,
2002; Ragozzino, 2007). After lesions of the AcbC on the other hand, animals show no deficit
on the initial switch. Instead, their deficit is characterized by an inability to eliminate irrelevant
responses after they initially switch, i.e. animals occasionally go back to the previously correct
(i.e. now incorrect) response. These studies fit well with a role for the AcbC in orienting
behaviour to optimize cognitive control in order to obtain rewards (Floresco et al., 2006a). A
failure to optimize cognitive control may result in inefficient facilitation of control in a low