D-cycloserine selectively decreases nicotine self-administration in rats with low baseline levels of response.

Published

Journal Article

Expanding the variety of treatments available to aid smoking cessation will allow the treatments to be customized to particular types of smokers. The key is to understand which subpopulations of smokers respond best to which treatment. This study used adult female Sprague-Dawley rats to evaluate the efficacy of D-cycloserine, a partial NMDA glutamate receptor agonist, in reducing nicotine self-administration. Rats were trained to self-administer nicotine (0.03 mg/kg/infusion, i.v.) via operant lever response (FR1) with a secondary visual reinforcer. Two studies of D-cycloserine effects on nicotine self-administration were conducted: an acute dose-effect study (0, 10, 20 and 40 mg/kg, s.c.) and a chronic study with 40 mg/kg given before each test session for two weeks. Effects on rats with low or high pretreatment baseline levels of nicotine self-administration were assessed. In the acute study there was a significant interaction of D-cycloserine×baseline level of nicotine self-administration. In the low baseline group, 10 mg/kg D-cycloserine significantly decreased nicotine self-administration. In the high baseline group, 40 mg/kg significantly increased nicotine self-administration. In the repeated injection study, there was also a significant interaction of d-cycloserine×baseline level of nicotine self-administration. Chronic D-cycloserine significantly reduced nicotine self-administration selectively in rats with low baseline nicotine use, but was ineffective with the rats with higher levels of baseline nicotine self-administration. NMDA glutamate treatments may be particularly useful in helping lighter smokers successfully quit smoking, highlighting the need for diverse treatments for different types of smokers.

Full Text

Duke Authors

Cited Authors

  • Levin, ED; Slade, S; Wells, C; Petro, A; Rose, JE

Published Date

  • April 2011

Published In

Volume / Issue

  • 98 / 2

Start / End Page

  • 210 - 214

PubMed ID

  • 21192967

Pubmed Central ID

  • 21192967

Electronic International Standard Serial Number (EISSN)

  • 1873-5177

Digital Object Identifier (DOI)

  • 10.1016/j.pbb.2010.12.023

Language

  • eng

Conference Location

  • United States