Fig. 8.
The AMP-kinase agonist AICAR accelerates NMJ loss in P15 mice in an ex-vivo model of axonal injury. (A) Representative confocal micrographs of NMJs from deep lumbrical muscles isolated from P15 C57BL/6 J wildtype mice, after 24 h incubation ex-vivo at 28 °C in either standard MPS CO3 ringer solution or MPS CO3 ringer solution +2 mM AICAR. NMJs labelled with antibodies against neurofilament (NF; green) and synaptic vesicle protein 2 (SV2; green) and alpha-bungarotoxin (BTX; red). Note increase in the number of vacant endplates following AICAR treatment. Scale bar = 30 μm (B) Bar chart (Mean ± SEM) confirms significant decrease in the percentage of fully occupied NMJs in AICAR-incubated muscles compared to control. (n = 4 muscles/4 mice per group; *p < 0.05 by Mann-Whitney U test). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)