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Neural Substrates Underlying Eyeblink Classical Conditioning in Adults With Alcohol Use Disorders
Author(s) -
Cheng Dominic T.,
Rice Laura C.,
McCaul Mary E.,
Rilee Jessica J.,
Faulkner Monica L.,
Sheu YiShin,
Mathena Joanna R.,
Desmond John E.
Publication year - 2020
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.14288
Subject(s) - eyeblink conditioning , psychology , functional magnetic resonance imaging , classical conditioning , conditioning , hyperactivation , alcohol use disorder , audiology , neuroscience , cognition , developmental psychology , alcohol , medicine , biochemistry , statistics , chemistry , mathematics
Background Excessive alcohol consumption produces changes in the brain that often lead to cognitive impairments. One fundamental form of learning, eyeblink classical conditioning (EBC), has been widely used to study the neurobiology of learning and memory. Participants with alcohol use disorders (AUD) have consistently shown a behavioral deficit in EBC. The present functional magnetic resonance imaging (fMRI) study is the first to examine brain function during conditioning in abstinent AUD participants and healthy participants. Methods AUD participants met DSM‐IV criteria for alcohol dependence, had at least a 10‐year history of heavy drinking, and were abstinent from alcohol for at least 30 days. During fMRI, participants received auditory tones that predicted the occurrence of corneal airpuffs. Anticipatory eyeblink responses to these tones were monitored during the experiment to assess learning‐related changes. Results Behavioral results indicate that AUD participants showed significant conditioning deficits and that their history of lifetime drinks corresponded to these deficits. Despite this learning impairment, AUD participants showed hyperactivation in several key cerebellar structures (including lobule VI) during conditioning. For all participants, history of lifetime drinks corresponded with their lobule VI activity. Conclusions These findings suggest that excessive alcohol consumption is associated with abnormal cerebellar hyperactivation and conditioning impairments.