Special Theme: Neurotransmission and Addiction: Recent Translational Findings

Neuropsychopharmacology (2009) 34, 299–306; doi:10.1038/npp.2008.96; published online 25 June 2008

Long-Lasting Cognitive Deficits Resulting from Adolescent Nicotine Exposure in Rats

Danielle S Counotte1, Sabine Spijker1, Linda H Van de Burgwal1, François Hogenboom2, Anton N M Schoffelmeer2, Taco J De Vries1,2, August B Smit1 and Tommy Pattij2

  1. 1Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Vrije Universiteit, Amsterdam, The Netherlands
  2. 2Department of Anatomy and Neurosciences, Center for Neurogenomics and Cognitive Research, VU University Medical Center, Amsterdam, The Netherlands

Correspondence: Dr T Pattij, Department of Anatomy and Neurosciences, Center for Neurogenomics and Cognitive Research, VU University Medical Center, Van der Boechorststraat 7, Amsterdam 1081 BT, Netherlands. Tel: +3 120 444 8089; E-mail: t.pattij@vumc.nl

Received 18 February 2008; Revised 23 May 2008; Accepted 23 May 2008; Published online 25 June 2008.

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Abstract

Adolescence is a developmental period, during which the brain and particularly medial prefrontal cortical (mPFC) regions thereof have not fully matured. Because epidemiological data have suggested that adolescent nicotine use may result in disturbances in cognitive function in adulthood, we investigated the long-term effects of adolescent nicotine exposure in rats. Male Wistar rats were exposed to either nicotine (three times daily, 0.4 mg/kg s.c.) or saline for 10 days during (postnatal day (PND) 34–43) or following (PND 60–69) adolescence. After 5 weeks during adulthood, separate groups of animals were tested in operant paradigms taxing attention and distinct measures of impulsivity. Visuospatial attention and impulsive action were tested in the five-choice serial reaction time task, whereas impulsive choice was assessed in the delayed reward task. Our data show that adolescent, but not postadolescent, nicotine exposure affects cognitive performance in adulthood and results in diminished attentional performance and increments in impulsive action, while leaving impulsive choice intact. This altered cognitive performance appeared to be associated with enhanced releasability of dopamine in the mPFC. Together, these data suggest that adolescence is a time window during which the brain is vulnerable to long-lasting cognitive disturbances resulting from nicotine exposure.

Keywords:

adolescence, nicotine, attention, impulsivity, prefrontal cortex

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