Fig. 3.

G_sα transgenic endophenotype is reversed by haloperidol and mimicked by amphetamine: Panel A displays the interaction between haloperidol and genotype for N40 amplitude. Note that transgenic mice have significantly reduced N40 amplitude at baseline, with no significant difference between genotypes after 0.1 mg/kg haloperidol, and the 1.0 mg/kg dose of haloperidol resulting in reversal of baseline deficits, with G_sα transgenic mice displaying significantly larger N40 amplitude than wild type littermates (MS=2533, df=65). These data suggest that full D₂ type DA receptor antagonism unmasks the selective effect of the G_sα transgene on auditory processing. Panel B shows the percent change relative to vehicle for both doses of haloperidol. Panel C displays the interaction between amphetamine and genotype for N40 amplitude. G_sα transgenic mice have significantly reduced amplitude at baseline, as found in both experiments 1 and 2. However, the difference between genotypes is eliminated at all doses of amphetamine due to a dose dependent reduction in N40 amplitude among wild type but not transgenic mice (MS=1568, df=71). * Indicates P<0.05 for wild type (black) vs. transgenic (gray). Panel D shows the percent change relative to vehicle for each dose of amphetamine.