Skip to main content
. 2017 Dec 27;144(3):241–254. doi: 10.1111/jnc.14263

Figure 1.

Figure 1

Neuronal morphology of hippocampal neurons is normal in the absence of Cgs. (a) Western blot showing the absence of Cgs in brain and adrenal gland lysates from WT and CgA/B−/− P1 mice. (b) qRT‐PCR analysis showing the fold change expression of different members of the Secretogranin family. (c) Example images of control and CgA/B−/− hippocampal neurons (DIV19) stained for the synapse marker Syp1 (green), the dendrite marker microtubule‐associated protein 2 (MAP2) (blue) and the axonal marker SMI312 (red). SMI‐positive (red) nuclei are the astrocytes nuclei, known to contain SMI immunoreactivity (Weigum et al. 2003). (d) Zoomed areas in the boxes shown in (b). (e) Quantification of the dendritic length (MAP2). (f) Quantification of the axonal length (SMI312). (g) Sholl analysis showing the mean number of dendritic branches against the distance from soma. (h) Quantification of the number of synapses (synaptophysin1 puncta on the dendrites) per neuron. (i) Quantification of the number of synapses per μm dendrite per neuron. (j) Quantification of synaptophysin1 intensity per synapse per neuron. (Data shown as mean ± SEM. (b) Control n = 3 mice and CgA/B−/− n = 4 mice MW‐U test. (e–j). Control n = 31 neurons and CgA/B−/− n = 29 neurons from three independent cultures. (e–i) MW‐U test. (j) Student's t‐test.