Nicotine administration attenuates methamphetamine-induced novel object recognition deficits

Paula L. Vieira-Brock, Lisa M. McFadden, Shannon M. Nielsen, Misty D. Smith, Glen R. Hanson, Annette E. Fleckenstein

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Background: Previous studies have demonstrated that methamphetamine abuse leads to memory deficits and these are associated with relapse. Furthermore, extensive evidence indicates that nicotine prevents and/or improves memory deficits in different models of cognitive dysfunction and these nicotinic effects might be mediated by hippocampal or cortical nicotinic acetylcholine receptors. The present study investigated whether nicotine attenuates methamphetamine-induced novel object recognition deficits in rats and explored potential underlying mechanisms. Methods: Adolescent or adult male Sprague-Dawley rats received either nicotine water (10-75 μg/mL) or tap water for several weeks. Methamphetamine (4 × 7.5 mg/kg/injection) or saline was administered either before or after chronic nicotine exposure. Novel object recognition was evaluated 6 days after methamphetamine or saline. Serotonin transporter function and density and α4β2 nicotinic acetylcholine receptor density were assessed on the following day. Results: Chronic nicotine intake via drinking water beginning during either adolescence or adulthood attenuated the novel object recognition deficits caused by a high-dose methamphetamine administration. Similarly, nicotine attenuated methamphetamine-induced deficits in novel object recognition when administered after methamphetamine treatment. However, nicotine did not attenuate the serotonergic deficits caused by methamphetamine in adults. Conversely, nicotine attenuated methamphetamine-induced deficits in α4β2 nicotinic acetylcholine receptor density in the hippocampal CA1 region. Furthermore, nicotine increased α4β2 nicotinic acetylcholine receptor density in the hippocampal CA3, dentate gyrus and perirhinal cortex in both saline- and methamphetamine-treated rats. Conclusions: Overall, these findings suggest that nicotine-induced increases in α4β2 nicotinic acetylcholine receptors in the hippocampus and perirhinal cortex might be one mechanism by which novel object recognition deficits are attenuated by nicotine in methamphetamine-treated rats.

Original languageEnglish (US)
Pages (from-to)1-12
Number of pages12
JournalInternational Journal of Neuropsychopharmacology
Volume18
Issue number12
DOIs
StatePublished - Jan 1 2015

Fingerprint

Methamphetamine
Nicotine
Nicotinic Receptors
Memory Disorders
Hippocampal CA1 Region
Serotonin Plasma Membrane Transport Proteins
Water
Dentate Gyrus
Drinking Water
Cholinergic Agents
Sprague Dawley Rats
Hippocampus
Recurrence

Keywords

  • Methamphetamine
  • Nicotine
  • Nicotinic receptors
  • Novel object recognition memory
  • Serotonin transporter

ASJC Scopus subject areas

  • Pharmacology
  • Psychiatry and Mental health
  • Pharmacology (medical)

Cite this

Nicotine administration attenuates methamphetamine-induced novel object recognition deficits. / Vieira-Brock, Paula L.; McFadden, Lisa M.; Nielsen, Shannon M.; Smith, Misty D.; Hanson, Glen R.; Fleckenstein, Annette E.

In: International Journal of Neuropsychopharmacology, Vol. 18, No. 12, 01.01.2015, p. 1-12.

Research output: Contribution to journalArticle

Vieira-Brock, Paula L. ; McFadden, Lisa M. ; Nielsen, Shannon M. ; Smith, Misty D. ; Hanson, Glen R. ; Fleckenstein, Annette E. / Nicotine administration attenuates methamphetamine-induced novel object recognition deficits. In: International Journal of Neuropsychopharmacology. 2015 ; Vol. 18, No. 12. pp. 1-12.
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AB - Background: Previous studies have demonstrated that methamphetamine abuse leads to memory deficits and these are associated with relapse. Furthermore, extensive evidence indicates that nicotine prevents and/or improves memory deficits in different models of cognitive dysfunction and these nicotinic effects might be mediated by hippocampal or cortical nicotinic acetylcholine receptors. The present study investigated whether nicotine attenuates methamphetamine-induced novel object recognition deficits in rats and explored potential underlying mechanisms. Methods: Adolescent or adult male Sprague-Dawley rats received either nicotine water (10-75 μg/mL) or tap water for several weeks. Methamphetamine (4 × 7.5 mg/kg/injection) or saline was administered either before or after chronic nicotine exposure. Novel object recognition was evaluated 6 days after methamphetamine or saline. Serotonin transporter function and density and α4β2 nicotinic acetylcholine receptor density were assessed on the following day. Results: Chronic nicotine intake via drinking water beginning during either adolescence or adulthood attenuated the novel object recognition deficits caused by a high-dose methamphetamine administration. Similarly, nicotine attenuated methamphetamine-induced deficits in novel object recognition when administered after methamphetamine treatment. However, nicotine did not attenuate the serotonergic deficits caused by methamphetamine in adults. Conversely, nicotine attenuated methamphetamine-induced deficits in α4β2 nicotinic acetylcholine receptor density in the hippocampal CA1 region. Furthermore, nicotine increased α4β2 nicotinic acetylcholine receptor density in the hippocampal CA3, dentate gyrus and perirhinal cortex in both saline- and methamphetamine-treated rats. Conclusions: Overall, these findings suggest that nicotine-induced increases in α4β2 nicotinic acetylcholine receptors in the hippocampus and perirhinal cortex might be one mechanism by which novel object recognition deficits are attenuated by nicotine in methamphetamine-treated rats.

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