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. 2019 Aug 7;39(32):6233–6250. doi: 10.1523/JNEUROSCI.2984-18.2019

Figure 1.

Figure 1.

Loss of CHL1 increases spine density on apical dendrites of cortical pyramidal neurons in early adolescence and adulthood. A–F, Representative images of apical and basal dendrites from Golgi-labeled pyramidal neurons and quantification of spine density in PFC layer 2/3 and V1, layer 4 of adolescent WT and CHL1-null (KO) mice at P21. Mean spine density per neuron (±SEM) was significantly increased on apical but not basal dendrites of pyramidal neurons in CHL1-null mice compared with WT at P21 (*p = 1.70E-07 (PFC), 0.0377 (V1); two-tailed t test). Number of mice: 3 per genotype. Number of neurons scored: WT, n = 11 (apical), n = 10 (basal); CHL1-null, n = 10 (apical), n = 10 (basal). Scale bar, 10 μm. The total number of spines counted in each condition ranged from 280 to 563. G–L, Representative images of apical and basal dendrites from Golgi-labeled pyramidal neurons and quantification of spine density in PFC layer 2/3 and V1 layer 4 of adult WT and CHL1 KO mice at P60. Mean spine density per neuron (±SEM) was significantly increased on apical but not basal dendrites of pyramidal neurons in CHL1-null mice compared with WT at P60 (*p = 0.017 (PFC), 0.0176 (V1); two-tailed t test). Number of mice: 3 per genotype. Number of neurons scored: WT, n = 10 (apical), n = 10 (basal); CHL1-null, n = 10 (apical), n = 10 (basal). Scale bar, 10 μm. The total number of spines counted in each condition ranged from 450 to 863.