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Recent research
employing animal models has shown that adolescent nicotine exposure can
cause long-lasting changes in brain physiology, brain reward systems,
susceptibility to later addiction, and simple behavior (cf.
Abreu-Villaca et al., 2003; Abreu-Villaca, Seidler, & Slotkin, 2003;
Kelley & Middaugh, 1999; Kelley & Rowan, 2004; Trauth, Seidler, &
Slotkin, 2000).
The adolescent
exposure paradigm that we used in our recent studies has been used by
our laboratories and others to study the effects of adolescent nicotine
exposure on adult neurobiology, motivation and reward, and simple forms
of behavior (Abreu-Villaca, Seidler, Qiao and others,
2003;Abreu-Villaca, Seidler, and Slotkin, 2003;Kelley and Middaugh,
1999;Kelley and Rowan, 2004;Trauth, McCook, Seidler and others,
2000;Trauth, Seidler, Ali and others, 2001;Trauth, Seidler, McCook and
others, 1999a;1999b;Trauth, Seidler, and Slotkin, 2000a;2000b). In this
procedure, weanling rats are exposed daily to nicotine for several days
to weeks (Kelley and Middaugh, 1999;Kelley and Rowan, 2004;Trauth,
Seidler, and Slotkin, 2000a). In our present studies, we use the same
5-week adolescent exposure period that has been used in prior studies in
rodents (Kelley and Rowan, 2004;Kelley and Middaugh, 1999). This
exposure period is typically followed by 5 weeks of no exposure to the
drug, which is followed by assessment of long-lasting changes due to
adolescent exposure. The 5-week no-drug period allows the drug to
completely clear the rat’s system so that any changes in the exposure
group relative to controls indicate a long-lasting developmental effect
of the drug rather than direct effects of the drug itself. Early
exposure to nicotine by such methods causes alterations in serotonergic,
dopaminergic, noradrenergic, and cholinergic systems (Abreu-Villaca,
Seidler, Qiao and others, 2003;Abreu-Villaca, Seidler, and Slotkin,
2003;Kelley and Middaugh, 1999;Trauth, Seidler, McCook and others,
1999a), though almost no work has examined the effects of adolescent
nicotine exposure on animal models of complex learning other than our
own. Results of work from our lab, shown in Figure 6, indicate
that adolescent nicotine exposure compromises complex learning and
memory functions in adulthood in rats (Fountain, Rowan, Kelley, Willey,
& Nolley, 2008). These conclusions from neurobiological and behavioral
research are particularly disturbing given the fact that over one-third
of high school students in the United State smoke (National Institutes
of Health, 2001). More recent work has looked more closely at the
effects of adolescent nicotine (Pickens, Rowan, Bevins, & Fountain
(2013) and has also examined similar effects of Ritalin and Prozac
(Rowan, McCarty, Kundey, Osburn, Kelley, Matoushek, & Fountain (2015).
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