Electrophysiological evidence of impaired neuromuscular transmission in exercise‐induced collapse in a labrador retriever

Summary Exercise‐induced collapse (EIC) is a common inherited disorder in labrador retrievers, yet objective functional evidence linking the underlying molecular defect to impaired neuromuscular transmission is scarce. We report electrophysiological findings in a 14‐month‐old labrador retriever homozygous for the dynamin‐1 mutation. Routine nerve conduction studies revealed normal maximum motor nerve conduction velocity and residual latency, but a marked prolongation of compound muscle action potential (CMAP) duration. High‐frequency repetitive nerve stimulation demonstrated a significant CMAP amplitude decrement of 25%–30% during trains of 10 stimuli delivered at 33 Hz. These findings provide functional evidence of impaired neuromuscular transmission in EIC and are consistent with defective synaptic vesicle recycling, likely reflecting a reduced readily releasable vesicle pool and slowed vesicle turnover. Readily available electrophysiological testing may therefore offer supportive diagnostic information in dogs suspected of EIC.