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John
J. Curtin
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Professor of Psychology
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Ph.D.
(Clinical Psychology)
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Research
Interests:
Broadly,
my research program examines the psychological processes and associated
neurobiological substrates that contribute to alcohol and other drug
(AOD) use, abuse, and the poor self-regulation and inappropriate
behavior that are frequently associated with AOD use. More
generally, I maintain an active interest in externalizing behaviors
(e.g., aggression) and related disorders (e.g., antisocial personality
disorder, psychopathy). My research program focuses both on the
etiologically relevant affective processes that support well-learned
and strongly motivated drug use behavior and the cognitive processes
that are essential to regulate or control this drug use motivation when
it is not adaptive. My research program also examines individual
differences in these processes (e.g., variations in stress response,
individual differences in the integrity of cognitive control processes)
to understand how genetic and/or early experience factors affect the
risk for the development of alcohol and drug use disorders.
To accomplish these aims, my research program includes studies that use
drug administration, drug withdrawal, and drug cue exposure
methods. These general methods are applied in samples of social
users of alcohol and other drugs, individuals who are at increased risk
for developing AOD use disorders, and/or currently AOD dependent
users. Basic research and theory from affective and cognitive
science provide the foundation for this research. An emphasis is
placed on the use of well-validated paradigms and sophisticated
psychophysiological indices of key constructs. For example,
research on affective response during drug administration and
withdrawal draws on well-established conceptualizations of affect
(Lang, 1995; Davidson, 1998) and multilevel models of affective
processing incorporating cognitive and neural mechanisms (e.g. Ledoux,
1995; Walker, Toufexis, & Davis, 2003). Assessment of
affective response involves psychophysiological measures of affective
valence (e.g., fear potentiated startle, facial electromyography) and
arousal (skin conductance and heart rate), as well as indices of
neuroendocrine response (e.g. salivary cortisol). Moreover, my research
employs adaptations of basic animal fear conditioning paradigms that
connect this research to animal models in affective science (Davis et
al., 1993) and addiction (e.g., Koob & LeMoal, 2008).
Research on cognitive control processes uses well-validated
cognitive-experimental paradigms (e.g., Stroop, Flanker, n-back) and
cognitive psychophysiological indices (e.g., event related brain
potentials-ERPs). This research is theoretically anchored by
current cognitive neuroscience models on attention networks (Botvinick
et al., 2001; Miller & Cohen, 2001; Posner & DiGirolamo,
2000). My current and near term future research is organized
around two broad aims.
1. Examination of the motivational basis of
addiction. The aim of this research is to understand the
motivational basis of alcohol and other addiction - - that is, what is
the nature and origin of the urge to use drugs? Theorists
indicate that addiction results from neuroadaptive change in
motivational systems in response to repeated AOD exposure. Many
theories highlight adaptation in stress systems as one critical
mechanism in the etiology of addiction across many classes of drugs
(Solomon & Corbit, 1974; Koob & LeMoal, 2008; Baker et al.,
2004). In short, repeated homeostatic adjustments in stress
systems during periods of acute drug intoxication eventually lead to
persistent compensatory adaptations in affective response (e.g.,
increased anxiety) and its neural substrates that result in further
drug-seeking behavior. My research in the service of this aim has
used systematic laboratory drug administration and drug withdrawal
studies in humans to identify and clarify these stress-related
adaptations that motivate addictive drug use.
2. Examination of the cognitive control of AOD use
and associated externalizing behaviors. Acute alcohol
intoxication results in behavioral dysregulation, which has potentially
serious consequences among social and dependent users alike (e.g.,
increased aggressivity, sexual risk taking, drunk driving, and other
potentially harmful behaviors). Current research suggests that
these behaviors may result from impairments in higher-level cognitive
control processes when intoxicated. Other research and
theory suggests that these same cognitive control processes are
critical to adaptively regulate alcohol and other drug use
itself. Therefore, trait-like dysfunction in these cognitive
control processes may represent an important risk mechanism for the
development of AOD use disorders. The primary aim of this
research is to clarify the effects of drug administration, drug
withdrawal and individual differences on various components of
attention function (alerting, sensory orienting, executive cognitive
control) to delineate the contribution of these attention processes to
AOD abuse, harmful intoxicated behavior, and externalizing behavior
more generally.
More detailed description of these research goals
is also available.
Research Interests (extended)
