Several studies have examined the effect of alcohol consumption on P3 amplitude (for a review, see Porjesz and Begleiter 1996). In one study (Porjesz and Begleiter 1996), P3 responses were measured in SOA’s and in men who had no first- or second-degree4 alcoholic relatives. Drinking histories did not differ between groups. Before testing, the subjects consumed sufficient alcohol to raise their blood alcohol concentration (BAC) to approximately 0.06 to 0.07 percent, which is close to the legal limit for intoxication in most States (0.08 percent). Sons of alcoholics exhibited a larger percentage decrease in P3 amplitude than did sons of nonalcoholics during the ascending phase of the BAC (i.e., when blood alcohol levels are climbing). This pattern may indicate greater sensitivity in the high-risk group during the ascending phase of the BAC, a hypothesis proposed by Newlin and Thomson (1990). Alcohol consumption prolonged the latency of the P3 component in both groups. However, during the descending phase of the BAC (i.e., when blood alcohol levels are dropping), the P3 latencies of the high-risk subjects recovered to prealcohol levels more rapidly than did those of the low-risk subjects (see also Schuckit et al. 1988).
