Rationale: The noradrenergic system might be a critical mediator of psychostimulants and opiates hedonic value.
Objectives: The objective of this study is to evaluate the involvement of alpha1-adrenoceptors (alpha1-ARs) in nicotine incentive learning.
Materials and methods: Rats, subjected to an unbiased conditioned place preference (CPP) procedure, received eight 30-min alternating nicotine (0.06 mg/kg) and saline pairings with distinct floor textures. The alpha1-AR antagonist, prazosin (0.125, 0.25, 0.5, or 1 mg/kg), was administered 30 min before nicotine pairings (acquisition) or one of the two 20-min test sessions conducted 24 h and 3 weeks after conditioning (expression).
Results: Pre-pairing injections of prazosin (0.5-1 mg/kg) prevented the acquisition of nicotine-CPP. On pre-test administration, prazosin (0.5 mg/kg) abolished the short-term expression of nicotine-CPP; whereas, none of the tested doses impaired its long-term expression. During a drug-free 3-week test session, nicotine-CPP was also weakened in rats given prazosin (0.5 mg/kg) before the 24-h test, while nicotine-CPP was reduced neither in animals given prazosin immediately after the first test session nor in those not subjected to the 24-h test.
Conclusions: The activation of alpha1-ARs is one of the mechanisms that code for the incentive motivational value of nicotine. It participates also in the short-term, but not the long-term, control of behavior by nicotine-paired stimuli. The latter effect does not result from disruption by prazosin of either memory for the nicotine-cue association or reconsolidation processes at recall. Thus, differences exist in the neurobiological mechanisms that contribute to the incentive motivational value of nicotine and the short- and long-term "memory" of the incentive salience acquired by nicotine-paired cues.