Adolescent Vulnerabilities to Chronic Alcohol or
Nicotine Exposure: Findings From Rodent Models
Susan Barron, Aaron White, H. Scott Swartzwelder, Richard L. Bell, Zachary A. Rodd, Craig J. Slawecki, Cindy L. Ehlers,
Edward D. Levin, Amir H. Rezvani, and Linda P. Spear
This article presents an overview of the proceedings from a symposium entitled “Is adolescence special?
Possible age-related vulnerabilities to chronic alcohol or nicotine exposure,” organized by Susan Barron
and Linda Spear and held at the 2004 Research Society on Alcoholism Meeting in Vancouver, British
Columbia. This symposium, cosponsored by the Fetal Alcohol Syndrome Study Group and the Neurobe-
havioral Teratology Society, focused on our current knowledge regarding the long-term consequences of
ethanol and/or nicotine exposure during adolescence with the emphasis on data from rodent models. The
support from these two societies represents the understanding by these research groups that adolescence
represents a unique developmental stage for the effects of chronic drug exposure and also marks an age in
which many risky behaviors including alcohol consumption and smoking typically begin. The speakers
included (1) Aaron White, who presented data on the effects of adolescent ethanol exposure on subsequent
motor or cognitive response to an ethanol challenge in adulthood; (2) Richard Bell, who presented data
suggesting that genetic differences could play a role in adolescent vulnerability to ethanol; (3) Craig
Slawecki, who presented data looking at the effects of chronic exposure to alcohol or nicotine on neuro-
physiologic and behavioral end points; and (4) Ed Levin, who presented data on acute and long-term
consequences of adolescent nicotine exposure. Finally, Linda Spear provided some summary points and
recommendations regarding unresolved issues and future directions.
young as 11 to 12 and spanning the teenage years), al-
though some researchers expand their definition of adoles-
cence to include the early 20s as well. Adolescents are more
likely to experiment with a variety of unsafe behaviors,
including drug use (Martin et al., 2002). It has been shown
repeatedly that this is often a time for the first use of both
alcohol and tobacco (Grant et al., 1987; Kandel and
Yamaguchi 1985; Nelson et al., 1995; Webster et al., 1994).
Individuals who do not start using these drugs during ado-
DOLESCENCE IN HUMANS is typically defined as
spanning the second decade of life (i.e., starting as
lescence rarely initiate use in later life (Chen and Kandel,
1995; Kandel and Logan, 1984). The consequence of these
findings is that a considerable amount of research now
focuses on the adolescent, as we try to understand the
unique nature of this age group. Although numerous envi-
ronmental and peer-related explanations for this increase
in risky behaviors exist, we now have a better understanding
of some of the considerable pharmacologic and neuroana-
tomic changes occurring in the organism at this age (see
Spear, 2000 for review). For example, the dorsolateral pre-
frontal cortex, an area that has been implicated in impulse
control, continues to undergo considerable development
during adolescence (e.g., Giedd, 2004; Sowell et al., 2001).
Furthermore, there are marked changes in sensitivity to
pharmacologic challenges during adolescence that probably
contribute to the increased risk for adolescent drug use
(Chambers et al., 2003).
Because the adolescent brain continues to undergo con-
siderable growth and change, there is currently much con-
cern regarding the long-term consequences of drug expo-
sure during this critical period. Clinical studies are
beginning to suggest that there can be marked conse-
quences of chronic exposure during adolescence to a num-
ber of drugs, including ethanol (Grant et al., 1997), and,
more recently, nicotine (Jacobsen et al., 2005), but much
more work is needed in this area. Animal models have been
extremely useful and important in beginning to address
these questions. The papers discussed below present data
From the Psychology Department, University of Kentucky, Lexington, KY
(SB); Indiana University School of Medicine, Institute of Psychiatric Re-
search, Indianapolis, Indiana (RLB, ZAR); the Department of Psychiatry
and Behavioral Sciences, Duke University Medical Center, Durham, North
Carolina (AW, HSS, EDL, AHR); Scripps Research Institute, La Jolla,
California (CJS, CLE); and the Center for Developmental Psychobiology,
Department of Psychology, Binghamton University, Binghamton, New York
Received for publication May 2, 2005; accepted May 16, 2005.
Supported in part by grants AA12600 and AA14032 (to SB), AA10256 and
AA11261 (to RLB), AA12478 and VA Senior Research Career Scientist
Award (to HSS), AA00298 and AA014339 (to CJS), AA06059 (to CLE),
DA015756 and MH64494 (to EDL), and AA12150 and AA12525 (to LPS).
Reprint requests: Dr. Susan Barron, Kastle Hall, Lexington, KY, 40506-
0044; Fax: 606-323-1979; E-mail: email@example.com
Copyright © 2005 by the Research Society on Alcoholism.
ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH
Vol. 29, No. 9
Alcohol Clin Exp Res, Vol 29, No 9, 2005: pp 1720–1725
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ADOLESCENT VULNERABILITY TO ALCOHOL OR NICOTINE EXPOSURE