Fig. 2.

G_sα mice have normal auditory threshold with reduced ABR and N40 gain. ABR (mean+SEM) measured as the P3–N5 amplitude in wild type and transgenic mice is shown at 58–90 dB in panel A. Note that there is no overall difference in ABR amplitude between transgenic and wild type mice, indicating there is no deficit for auditory threshold or at any individual intensity. Comparison of ABR amplitude between wild type (black) vs. transgenic (gray) mice at each intensity using Fisher LSD post hoc analyses (Ms=0.56, df=84) are 58 dB (P=0.456), 66 dB (P=0.846), 74 dB (P=0.733), 82 dB (P=0.441), 90 dB (P=0.281). However, there are differences in the amount of increased in ABR amplitude with increasing stimulus intensity (gain) within each genotype. Panel B shows baseline reduction in N40 amplitude and intensity function (gain) in G_sα transgenic mice relative to wild type littermates. Note that transgenic mice have significantly lower amplitude of N40 response at both 85 and 95 dB, but not at 75 dB (MS=1732, df=61), 75 dB (P=0.849), 85 dB (P=0.006), and 95 dB (P<0.001). Panel C demonstrates that haloperidol (across doses) reverses the G_sα transgenic deficit for N40 amplitude. Panel D demonstrates that amphetamine (across doses) causes a reduction in the overall amplitude and intensity function for N40 amplitude (gain) for wild type but not transgenic mice (MS=969, df=37) 75 dB (P=0.761), 85 dB (P=0.105), and 95 dB (P=0.033). Note the similarity between panels B and D for overall pattern of N40 intensity function. Taken together, these data suggest that the G_sα transgene and increased DA activity result in a schizophrenia-like pattern of reduced N1 amplitude. Wild type mice are shown in black and G_sα transgenic mice in gray in all panels. * Indicates P<0.05 for wild type vs. transgenic mice.