Habit formation: implications for alcoholism research.
Characteristics of individuals with severe alcohol use disorders include heightened cue sensitivity, compulsive seeking, craving, and continued alcohol use in the face of negative consequences. Animal models are useful for understanding behavioral and neurological mechanisms underlying problematic alcohol use. Seeking of operant reinforcers including alcohol is processed by two mechanisms, commonly referred to as "goal-directed" (action-outcome) and "habitual" (stimulus-response). As substance use disorders are characterized by continued use regardless of unfavorable outcomes, it is plausible that drug use causes an unnatural disruption of these mechanisms. We present a critical analysis of literature pertaining to behavioral neuroscience alcoholism research involving habit formation. Traditionally, when operant behavior is unaffected by a loss of subjective value of a reinforcer (devaluation), the behavior is considered habitual. Acquisition of instrumental behavior requires corticostriatal mechanisms that depend heavily on the prefrontal cortex and ventral striatum, whereas practiced behavior is more predominantly controlled by the dorsal striatum. Dopaminergic signaling is necessary for the neurological adaptations involved in stimulus-response action, and drugs of abuse appear to facilitate habitual behavior through high levels of dopamine release. Evidence suggests that the use of alcohol as a reinforcer expedites habit formation, and that a history of alcohol use produces alterations in striatal morphology, aids habit learning for non-psychoactive reinforcers, and promotes alcohol drinking despite aversive adulterants. In this review, we suggest directions for future alcoholism research that seeks to measure action made despite a devalued outcome, including procedural modifications and genotypic, pharmacological, or neurological manipulations. Most alcoholism models currently in use fail to reach substantial blood ethanol concentrations, a shortcoming that may be alleviated through the use of high-drinking rodent lines. Additionally, satiety, one common mechanism of devaluing reinforcers, is not recommended for alcohol research because the psychoactive effects of alcohol depress response rates, mimicking devaluation effects. Overall, further research of habit formation and potentially related perseverative behaviors could be invaluable in discovering genetic variance, traits that correlate with persistent alcohol seeking, implicated neural structures and processes of alcohol use, and eventually novel pharmacological treatment for alcoholism.
Department of Psychology, Indiana University - Purdue University Indianapolis, Indianapolis, IN, USA.
David
D
O'Tousa
Department of Psychology, Indiana University - Purdue University Indianapolis, Indianapolis, IN, USA. Electronic address: ngrahame@iupui.edu.
Nicholas
N
Grahame
D019973:Alcohol-Related Disorders / Q000503:physiopathology; D000437:Alcoholism; D000818:Animals; D016739:Behavior, Addictive; D003216:Conditioning, Operant / Q000502:physiology; D003342:Corpus Striatum; D004298:Dopamine / Q000378:metabolism; D000431:Ethanol / Q000494:pharmacology; D005260:Female; D006184:Habits; D006801:Humans; D008297:Male; D023421:Models, Animal; D012107:Research Design; D012737:Sex Factors
D000431:Ethanol; D004298:Dopamine
Alcohol; Animal model; Goal-directed behavior; Habit learning; Reinforcer devaluation; Self-administration