Figure 1.
A schematic showing the placement of injector tips for animals included in the analysis following treatment of the NAcc shell (open circles) or core (filled circles) during priming-induced reinstatement (Experiments 1A&B, left panel) or cue-induced reinstatement (Experiments 2A&B, right panel).
Numbers represent millimeters anterior to bregma. Drawings were adapted from The Rat Brain in Stereotaxic Coordinates, 4th ed, G. Paxinos and C. Watson, Figures 10, 11, and 13, copyright 1998 [61].
Figure 2.
Effects of NAcc core and shell inactivation on priming-induced reinstatement.
Top panels demonstrate that rats were showing robust lever-pressing on the VR-5, FI-20 schedule by the completion of training (top panels). The middle panels demonstrate a significant effect of NAcc inactivation on priming-induced reinstatement on the previously active lever, regardless of whether the muscimol/baclofen cocktail was injected into the core or the medial shell. There were no changes in pressing on the inactive lever across extinction and reinstatement test conditions. Bottom panels represent the pattern of lever pressing across the reinstatement period and suggest that drug treatment blocked reinstatement early in the session, which then extinguished across time during all test days. Stars (*) on the bar graphs indicate a significant increase in lever pressing on the saline reinstatement day; number signs (#) indicate a significant decrease in lever pressing activity as compared to that observed on the saline reinstatement day (as determined by Tukey's HSD).
Figure 3.
Effects of NAcc core and shell inactivation on cue-induced reinstatement.
Top panels demonstrate that rats were showing robust lever-pressing on the VR-5, FI-20 schedule by the completion of training (top panels). The middle panels demonstrate a significant effect of NAcc inactivation on cue-induced reinstatement on the previously active lever, regardless of whether the muscimol/baclofen cocktail was injected into the core or the medial shell. There were no changes in pressing on the inactive lever across extinction and reinstatement test conditions. Bottom panels represent the pattern of lever pressing across the reinstatement period and suggest that drug treatment blocked reinstatement early in the session, which then extinguished across time during all test days. Statistical symbols are consistent with those used in Fig. 2.
Figure 4.
Although NAcc core and shell inactivation caused a main effect of drug on cue-induced reinstatement (Fig. 3), there was also a significant three-way interaction.
As shown here, the rats who received muscimol/baclofen injections in the NAcc shell on the first reinstatement day did not reinstate food-seeking behavior on the second test when they received saline injections. The star represents a significant difference in responding between animals that received saline injections on the first or second test day. In contrast, rats with NAcc core inhibition showed attenuated reinstatement regardless of which day the drug was given.
Figure 5.
Rats tested for reinstatement following injections of the pharmacological stressor yohimbine did not reinstate food-seeking behavior.
As can be seen, there was no increase in lever pressing following yohimbine, even on the day that rats were tested with saline vehicle injections into either the NAcc shell or core.