Psychopharmacology

, Volume 184, Issue 3, pp 328–338

β2-Subunit-containing nicotinic acetylcholine receptors are involved in nicotine-induced increases in conditioned reinforcement but not progressive ratio responding for food in C57BL/6 mice

  • Darlene H. Brunzell
  • Jessica R. Chang
  • Brandon Schneider
  • Peter Olausson
  • Jane R. Taylor
  • Marina R. Picciotto
Original Investigation

DOI: 10.1007/s00213-005-0099-z

Cite this article as:
Brunzell, D.H., Chang, J.R., Schneider, B. et al. Psychopharmacology (2006) 184: 328. doi:10.1007/s00213-005-0099-z

Abstract

Rationale

Nicotine administration potentiates conditioned reinforcement in rats, an effect that persists for weeks after chronic exposure. Little is known regarding the nicotinic receptor subtypes that may mediate this effect.

Objective

The purpose of this study was to determine whether β2-subunit-containing nicotinic acetylcholine receptors (β2*nAChRs) are necessary for lasting effects of nicotine on conditioned and primary reinforcement in mice.

Methods

β2 knockout (β2KO) and wild-type (WT) mice received 14 days of nicotine exposure (NIC, 200 μg/ml in 2% saccharin) or saccharin alone (SAC) in their drinking water. Five days later, mice received paired presentations of a conditioned stimulus (CS) with water unconditioned stimulus (US) or explicitly unpaired presentations of the CS and US during Pavlovian discriminative approach training. Training was followed by two conditioned reinforcement tests. Mice were subsequently tested for food-reinforced responding in the absence of explicit cues followed by a progressive ratio test.

Results

During conditioned reinforcement testing, only mice in the paired condition showed increased responding in the CS-reinforced aperture over inactive apertures. WT-NIC mice showed enhanced conditioned reinforcement compared to WT-SAC animals. β2KO-SAC mice showed elevated conditioned reinforcement compared to WT-SAC subjects, but β2KO-NIC and β2KO-SAC mice did not differ in responding with conditioned reinforcement. Prior nicotine exposure did not alter food-reinforced responding but resulted in elevated break points for food in both genotypes.

Conclusion

These data show that nicotine exposure enhances conditioned reinforcement in mice and indicate that β2*nAChRs are necessary for nicotine-dependent enhancement of incentive aspects of motivation but not motivation for primary reinforcement measured by progressive ratio responding.

Keywords

Learning Reward Motivation Mouse Associative learning Pavlovian Drug 

Copyright information

© Springer-Verlag 2005

Authors and Affiliations

  • Darlene H. Brunzell
    • 1
  • Jessica R. Chang
    • 1
  • Brandon Schneider
    • 1
  • Peter Olausson
    • 1
  • Jane R. Taylor
    • 1
  • Marina R. Picciotto
    • 1
  1. 1.Department of Psychiatry, Division of Molecular PsychiatryYale University School of MedicineNew HavenUSA