Nicotine provokes impulsive‐like action by stimulating α4β2 nicotinic acetylcholine receptors in the infralimbic, but not in the prelimbic cortex

Abstract

Nicotine, a major addictive component of tobacco, has been suggested to provoke impulsivity by activating central α4β2 nicotinic acetylcholine receptors (nAChRs). Although lesion studies have demonstrated the involvement of the medial prefrontal cortex (mPFC) in impulsive action, the precise brain sites responsible for nicotine‐induced impulsive action have not been identified. Our goal was to determine whether α4β2 nAChRs in the prelimbic cortex (PL) and/or infralimbic cortex (IL), which are subregions of the mPFC, mediate nicotine‐provoked impulsive‐like action in the 3‐choice serial reaction time task (3‐CSRTT). The 3‐CSRTT is a rodent model of impulsive action in which the animal is required to inhibit the response until a light stimulus is presented randomly in one of three holes. Following the completion of the training, rats were bilaterally injected with dihydro‐β‐erythroidine (DHβE) (6 and 18 μg/side), a selective α4β2 nAChRs antagonist, into the PL or IL before systemic injection of nicotine (0.2 mg/kg, s.c.). Intra IL DHβE infusions dose‐dependently blocked nicotine‐induced impulsive‐like action, whereas infusions of DHβE into the PL failed to block the effects. Our data provide evidence for the involvement of α4β2 nAChRs in the IL in nicotine‐provoked impulsive‐like action.