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. Author manuscript; available in PMC: 2019 Aug 2.
Published in final edited form as: J Comp Neurol. 2016 Nov 21;525(5):1216–1233. doi: 10.1002/cne.24131

Figure 8.

Figure 8.

VsEP amplitudes. A: Normalized p1n1 amplitudes for responses recorded at the highest stimulus level (+6 dB re:1 g/msec). WT (solid circles), α9 KO (downward triangles) and α9/10 KO (upward triangles), α7/9 KO (open circles), α7 KO (squares), and α10 KO (diamonds) are shown. Amplitudes for p1n1 were significantly reduced for both α9 KO and α/10 KO groups at +6 dB re:1 g/msec (significance indicated with an asterisk; *P < 0.007). Amplitudes of α9/10 KO animals were also lower than those of α9 KO animals (asterisk). At the highest stimulus level, the amplitude of p2n1 was also significantly reduced com-pared with WT for α9/10 KO animals (not shown in A; see D). B: VsEP latencies for p1, n1, and p2 at the highest stimulus levels (+6 dB re:1 g/msec). WT, α9/10 KO, α9/10 KO, α7/9 KO, α7 KO, and α10 KO are represented. Peripheral latencies (p1, n1) were either the same or significantly shorter than in WT knockout groups. The shortest latencies were found in α7 KO and α10 KO animals (*P < 0.003). C,D: p1n1 (C) and p2n1 (D) amplitudes at the three highest stimulus levels (0, +3, +6 dB re:1 g/msec). Both α9 KO and α9/10 KO mice consistently had significantly reduced amplitudes (*P < 0.0031) compared with WT, and α9/10 KO amplitudes were less than α9 KO amplitudes (*P< 0.021).