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Fig. 4 | Inflammation and Regeneration

Fig. 4

From: Immune-mediated myogenesis and acetylcholine receptor clustering promote a slow disease progression in ALS mouse models

Fig. 4

Nicotinic acetylcholine receptor activity in fast- and slow-progressing mice. A and B The bar graphs represent mean ± SEM of ACh-evoked currents amplitude (A) and ACh decay time (B). C Representative current traces elicited during prolonged ACh application (500 μM for 60 s) in one oocyte (representative of 12 and 16 for G93A C57 and G93A 129sv, respectively) injected with G93A C57 (blue) or G93A 129Sv muscle membranes. D and E Dose-response curves obtained by plotting the amplitude of currents evoked by ACh concentrations ranging from 1 μM to 1 mM, expressed as a percentage of the maximal current evoked at 1 mM ACh, represented as mean ± SEM and best fitted with Hill curves. Averaged EC50 values and nH in oocytes injected with G93A C57 were 47.0 ± 0.23 μM and 1.9 ± 0.2; in oocytes injected with G93A 129Sv, the values were 54.0 ± 3.0 μM and 1.3 ± 0.1. F ACh-evoked current desensitisation (first six dots) followed by evaluation of current recovery after 5, 10, and 15 minutes of washout from the last pulse of the desensitisation protocol. Currents were normalised at the amplitude of the first ACh application ( = 26.1 ± 6.6 nA, n = 19; = 13.0 ± 1.2 nA, n = 29. (G) Representative ACh-evoked current traces at different time points, as indicated in the panel

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