Examination of GABAergic and dopaminergic compounds in the acquisition of nicotine-conditioned hyperactivity in rats

Matthew I. Palmatier, Rick A. Bevins

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

In rats, a distinct environment repeatedly paired with nicotine (0.421 mg/kg base, s.c.) comes to evoke an increase in activity in the absence of any drug. This hyperactivity indicates a Pavlovian-conditioned association between the environment and nicotine. We investigated whether a dopamine D1 receptor antagonist (SCH- 23390), a D2/D3antagonist (eticlopride) or a GABABagonist (baclofen) would prevent the acquisition of nicotine-conditioned hyperactivity. In saline-pretreated rats, acute nicotine suppressed activity during the conditioning phase (i.e. environment-nicotine pairings); chronic nicotine stimulated activity. Pretreatment with SCH-23390 (0.01 mg/kg, i.p.) attenuated the activating effects of nicotine without affecting controls. Eticlopride (0.03-0.07 mg/kg, i.p.) and baclofen (0.625 and 1.25 mg/kg, i.p.) did not affect nicotine-induced activity in a selective manner. Regardless of the pretreatment drug, rats acquired the environment-nicotine association as indexed in a drug-free test. The inability of SCH-23390 to block the acquisition of nicotine-conditioned locomotor activity is notable because in past research SCH-23390 blocked expression of the learned association.

Original languageEnglish (US)
Pages (from-to)87-94
Number of pages8
JournalNeuropsychobiology
Volume45
Issue number2
DOIs
StatePublished - 2002

Keywords

  • Activity
  • Classical conditioning
  • Cravings
  • Dopamine
  • Locomotor
  • Nicotinic acetylcholine
  • Tobacco
  • γ-Aminobutyric acid (GABA)
  • γ-Vinyl-GABA

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Psychiatry and Mental health
  • Biological Psychiatry

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