Neuronal activity in the nucleus accumbens is necessary for performance-related increases in cortical acetylcholine release

Abstract

In vivo microdialysis was used to determine the necessity of neuronal activity in the nucleus accumbens (NAC) for task-induced increases in cortical acetylcholine (ACh) efflux. Rats were trained in a behavioral task in which they were required to perform a defined number of licks of a citric acid solution in order to gain access to a palatable, cheese-flavored food. Upon reaching a consistent level of performance, rats were implanted with microdialysis cannula in the medial prefrontal cortex (mPFC) and either the ipsilateral shell of the NAC or in the dorsal striatum (STR; control site). Dialysis samples from the mPFC were analyzed for ACh concentrations and samples from the NAC were analyzed for dopamine (DA) concentrations. Performance in the task was associated with increases in both ACh efflux in the cortex (150–200%) and DA efflux in the NAC (50–75%). These increases were blocked by administration of tetrodotoxin (TTX; 1.0 μM) via reverse dialysis into the NAC. Administration of TTX into the dorsal STR control site was ineffective in blocking performance-associated increases in cortical ACh. The D2 antagonist sulpiride (10 or 100 μM) administered into the NAC via reverse dialysis was ineffective in blocking increases in cortical ACh efflux. The present data reveal that neuronal activity in the NAC is necessary for behaviorally induced increases in cortical ACh efflux and that this activation does not require increases in D2 receptor activity.