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Fig. 8 | Translational Neurodegeneration

Fig. 8

From: Impaired dynamic interaction of axonal endoplasmic reticulum and ribosomes contributes to defective stimulus–response in spinal muscular atrophy

Fig. 8

BDNF stimulation does not increase the Smn levels in both control and Smn-deficient motoneurons. a Representative Western blots of total protein lysates obtained from cultured Smn+/+;SMN2tgtg, Smn+/−;SMN2tgtg and Smn−/−;SMN2tgtg motoneurons, which have been exposed to 1-min BDNF and probed against Smn and Calnexin. b Quantification of Western blot shows reduced total levels of Smn in unstimulated Smn−/−;SMN2tgtg neurons compared to unstimulated Smn+/+;SMN2tgtg and Smn+/−  ;SMN2tgtg (*P = 0.0500; n = 3 independent experiments). c Quantification of Western blot shown in a indicates no significant increase in Smn levels after 1-min BDNF stimulation in either genotype (n.s., P = 0.5000; n = 3 independent experiments). d Representative Western blot of total protein lysates obtained from Smn+/+;SMN2tgtg and Smn−/−;SMN2tgtg motoneurons shows no changes in total Smn levels after 10 min BDNF stimulation. e Representative images of growth cones of cultured Smn+/+;SMN2tgtg, Smn+/−;SMN2tgtg and Smn−/−;SMN2tgtg motoneurons immunostained against Smn (green) and Tau (red) following 1-min BDNF pulse. Smn levels do not increase after 1-min BDNF stimulation in any of the investigated genotypes. Calnexin was used as loading control in a and d, and for normalization in b and c. Data are presented in bar diagrams; error bars represent mean ± SEM. Statistical analyses were done by one-tailed Mann Whitney test

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