Interactive Effects of Naturalistic Drinking Context and Alcohol Sensitivity on Neural Alcohol Cue‐Reactivity Responses

Abstract

Background: Considerable evidence indicates that a low level of subjective response to alcohol's acute effects (i.e., low sensitivity) is associated with enhanced risk for alcohol use disorder (AUD). Recent work suggests that the highest risk response profile consists of blunted sensitivity to alcohol's sedation-like effects, coupled with enhanced sensitivity to alcohol's stimulation-like effects (i.e., differential sensitivity). A largely separate body of work indicates that enhanced reactivity to alcohol-related cues is associated with increased AUD risk.Aims: The current research examined the extent to which variability in alcohol response phenotypes is associated with enhanced P3 event-related potential (ERP) responses to alcohol-related pictures (ACR-P3), and whether this reactivity varies according to depicted drinking contexts.Methods: Eighty young adults (aged 18 to 33 years) completed a self-report measure of alcohol sensitivity (the Alcohol Sensitivity Questionnaire) and viewed images depicting drinking in naturalistic contexts, alcohol and nonalcohol beverages in isolation (devoid of naturalistic drinking context), and neutral nonbeverage control images while ERPs were recorded.Results: Results indicated that blunted sensitivity to alcohol's sedative-like effects was differentially associated with enhanced ACR-P3 but reduced P3 reactivity to nonalcohol cues. Variation in sensitivity to alcohol's stimulant-like effects was not associated with differential ACR-P3. Contrary to predictions, these effects were not potentiated by drinking contexts.Conclusions: The current results replicate and extend previous work linking low alcohol sensitivity with enhanced incentive salience for alcohol-related cues and suggest that cues depicting drinking contexts are less likely to differentiate high-risk from low-risk drinkers.

Transfer of incentive salience from a first‐order alcohol cue to a novel second‐order alcohol cue among individuals at risk for alcohol use disorder: electrophysiological evidence

“…Following previous demonstrations of larger neurophysiological response to alcohol but not to other appetitive visual CS 1 among LS versus HS individuals [31,32,36], we expected larger LPC amplitude for alcohol but not for other olfactory CS 1 among LS compared to HS individuals (H6). Because alcohol CS 2 -CS 1 pairings involved presentation of alcohol CS 1 without subsequent alcohol ingestion [unconditional stimulus [US)], alcohol CS 2 acquisition involved de-facto alcohol CS 1 extinction (US omission).…”

“…The current study represented an attempt at translation of some of the ISTA's tenets-including its emphasis on individual differences [7,74,75]-into a human laboratory model. Improving upon previous studies [31][32][33][34][35][36], the current study adopted a Pavlovian conditioning paradigm such as those used in pre-clinical tests of ISTA and tested for individual differences in the incentive value of a novel cue across its conditioning and extinction. Given these similarities, the current study provides a strong first test of the ISTA in humans with a known phenotypical risk for development of AUD.…”

“…LS is known to confer risk for AUD [27][28][29], and can be observed in both humans and rodents [30]. Additionally, LS is associated with exaggerated alcohol cue-reactivity in both laboratory [31][32][33][34][35][36] and natural environments [37,38]. Moreover, the genetic variants-particularly dopaminergic (DRD3, DRD4), cannabinoid (CB1) and μ1 opioid receptors (OPRM1)-associated with LS [39][40][41][42] are also associated with cue-induced alcohol craving [43,44] and alcohol cue-reactivity [45][46][47].…”

Neuropsychophysiological Measures of Alcohol Dependence: Can We Use EEG in the Clinical Assessment?

“…P3 to alcohol cues in an oddball task is also found increased in alcohol dependence, indicating the alteration of higher-order processing such as controlled attentional allocation ( 42 ). This preferential processing of alcohol cues also appear in individuals at risk, ERP changes being observed in social drinkers ( 43 ) with heavy use ( 44 ), that show increased P1 latencies and LPP amplitudes toward alcohol images, and in individuals with a low sensitivity to alcohol effects, that have increased P3 amplitudes ( 45 , 46 ). In this way, since early stages of alcohol consumption and in individuals at risk (low alcohol sensitivity), substance-related cues seem to be processed faster and with a high motivational salience, and ERP monitoring could help predict substance-related problems.…”

Neurobiology and the Hierarchical Taxonomy ofPsychopathology: progress toward ontogenetically informed and clinically usefulnosology

“…Evidence for these points comes from ERP research demonstrating variability in the neural responses to substance-related cues among individuals with varying severity of SPs, as well as longitudinal changes in these responses within SP-diagnosed individuals who experience recovery. One robust electrocortical indicator of incentive sensitization is the alcohol cue reactivity P3 response (ACR-P3 46 - 48 ), which is evoked by alcohol-related cues in the context of a larger visual categorization task. The ACR-P3 appears to capture incentive valuation (ie, degree of “wanting”) of alcohol and is greater in heavier-drinking individuals.…”