This work was supported by the VA Research Service and grants from NIH (DA13186 and DA016663 to MPP, AA13419 to SFT, and AA005526 to MAS).
Alcohol Attenuates Load-related Activation During a Working Memory Task: Relation to Level of Response to Alcohol
Article first published online: 25 JUL 2006
Alcoholism: Clinical and Experimental Research
Volume 30, Issue 8, pages 1363–1371, August 2006
How to Cite
Paulus, M. P., Tapert, S. F., Pulido, C. and Schuckit, M. A. (2006), Alcohol Attenuates Load-related Activation During a Working Memory Task: Relation to Level of Response to Alcohol. Alcoholism: Clinical and Experimental Research, 30: 1363–1371. doi: 10.1111/j.1530-0277.2006.00164.x
- Issue published online: 25 JUL 2006
- Article first published online: 25 JUL 2006
- Received for publication September 2, 2005; accepted April 21, 2006.
- Working Memory;
- Functional MRI;
- Risk Factors
Background: A low level of response to alcohol is a major risk factor for the development of alcohol dependence, but neural correlates of this marker are unclear.
Method: Ten healthy volunteers were classified by median split on level of response to alcohol and underwent 2 sessions of functional magnetic resonance imaging following ingestion of a moderate dose of alcohol and a placebo. The blood oxygen level–dependent activation to an event-related visual working memory test was examined.
Results: The subjects exhibited longer response latencies and more errors as a function of increasing working memory load and showed a load-dependent increase in activation in dorsolateral prefrontal cortex, posterior parietal cortex, and visual cortex. Alcohol did not affect performance (errors or response latency), but attenuated the working memory load–dependent activation in the dorsolateral prefrontal cortex. During the placebo condition, individuals with a low level of response to alcohol showed greater activation in dorsolateral prefrontal cortex and posterior parietal cortex than those with a high level of response to alcohol. During the alcohol condition, groups showed similar attenuation of load-dependent brain activation in these regions.
Conclusion: Low-level responders relative to high-level responders exhibited an increased working memory load–dependent activation in dorsolateral prefrontal cortex and posterior parietal cortex when not exposed to alcohol. This increase in brain response was attenuated in low-level responders after ingesting a moderate dose of alcohol.