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. Author manuscript; available in PMC: 2010 Aug 1.
Published in final edited form as: Nat Neurosci. 2010 Jan 10;13(2):163–172. doi: 10.1038/nn.2477

Figure 2. Tsc2+/− mice have defects in ipsilateral retinogeniculate projections.

Figure 2

(a–b) A series of coronal sections from the anterior (top) to the posterior (bottom) showing retinogeniculate projections into dLGN in P16 Tsc2+/+ (a) and Tsc2+/− (b) mice. Alexa594 (red) and Alexa488 (green) conjugated CTB are injected to left and right eyes, respectively. D, dorsal; L, lateral. Dashed lines represent the borders of dLGN in sections displaying the ipsilateral projections. Scale bar, 100 µm. (c) In some Tsc2+/− mice, ipsilateral projection formed multiple patches rather than a single central patch. Axons from the ipsilateral eye are in green on top and red at the bottom. Scale bar, 100 µm. (d) Multi-threshold analysis of the percentage of ipsilateral projections in dLGN in wild-type versus Tsc2+/− littermates at P16. Tsc2+/− mice have larger ipsilateral territories than wild-type littermates, regardless of threshold. Data are expressed as mean ± s.e.m. (n = 6 mice for each genotype; * P < 0.05 by t-test). (e) Quantification of the percentage of contralateral projections in dLGN. No significant difference exists at any threshold between wild-type and Tsc2+/− littermates. (f) Quantification of dLGN receiving contra-ipsi overlapping projections. No significant difference exists at any threshold between wild-type and Tsc2+/− littermates. (g) The center of the ipsilateral projection in the dLGN was shifted ventrally and laterally in Tsc2+/− mice. Line scan technique was used to calculate the mean pixel intensity along the dorsomedial (DM, 0%) to ventrolateral (VL, 100%) axes in 10 wild-type and 11 Tsc2+/− littermates. Error bars represent s.e.m. and ** P = 0.0014 by Mann Whitney test.