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. Author manuscript; available in PMC: 2012 Jul 2.
Published in final edited form as: Science. 2010 Nov 11;330(6008):1238–1240. doi: 10.1126/science.1195320

Figure 2.

Figure 2

Nicotinic receptors mediate adult plasticity in lynx1 KO mice. (A) Mice without MD (open circles, grey KO / blue WT) shift equally after MD during the CP (light blue, KO: mean CBI = 0.48, 6 mice; light grey, WT: CBI = 0.50, 8 mice; P > 0.5, t-test). Adult plasticity (blue, KOMD: CBI = 0.55, 12 mice vs grey, WTMD: CBI = 0.68, 9 mice; *** P < 0.0001, t-test) is abolished by concurrent nAChR antagonists (red, KOMD + mecamylamine: CBI = 0.68, 9 mice vs KOMD, *** P < 0.0001; vs grey, WTMD + mecamylamine: CBI = 0.69, 4 mice, P > 0.7; vs no MD KO + mecamylamine: CBI = 0.68, 7 mice, P > 0.9, t-test; orange, KOMD + DHβE / MLA: CBI = 0.68, 7 mice vs KOMD, *** P < 0.0001, t-test). Darker circles represent cortical mini-pump infusion. (B) Enhanced nicotine response in lynx1 KO mice. Averaged VEP traces (mean ± sem) before (light grey) and 10 minutes after (black) subcutaneous nicotine injection (+ nic) in WT (left) and lynx1 KO mice (right). (C) Integrated VEP (area of first negative peak) for WT (empty bars, 6 mice) and lynx1 KO mice (filled bars, 11 mice). * P < 0.05, t-test; n.s., not significant.