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. Author manuscript; available in PMC: 2010 Mar 2.
Published in final edited form as: J Neurosci. 2009 Sep 2;29(35):10788–10801. doi: 10.1523/JNEUROSCI.2132-09.2009

Figure 2.

Figure 2

Neuromuscular synapse defects in APP/APLP2 motor neuron (N-dCKO) and muscle (M-dCKO) knockout mice. A. Whole mount immunostaining of control, dKO, N-dCKO or M-dCKO P0 diaphragm muscles with antibodies against synaptophysin (Syn) or neurofilament (NF). α-BTX staining was used to mark the AchRs. Both the germline and conditional mutants showed diffused pre- and postsynaptic distribution and nerve terminal sprouting. B. Quantification of the average band width of AchR-positive endplates. C. Quantification of the number of AchR-positive endplates outside the central 200 μM band zone. D. Measurement of the number of endplate per unit area. B-D are expressed as mean ± SEM (6 animals/genotype). E. Higher magnification images of synapse structures with representative endplates poorly covered by Syn marked by arrowheads and extra-synaptic Syn staining by arrows. F. Quantification of the percentage of AchR-positive endplates covered by Syn (average ± SEM of 20 endplates/genotype). Asterisks above each bar are in comparison with the control. Asterisks on top of the brackets are in comparison with the dKO mice. ***p<0.001, **p<0.01, *p<0.05, NS: non-significant (p>0.05) (one way ANOVA). Scale bar in A: 100 μM; in E: 20 μM.