Motor nerve terminals must be prepared for sudden increases in energy demand associated with vesicular release and recycling. This article summarizes studies using functional fluorescence imaging and electrophysiological recording that demonstrate that vertebrate motor terminals rely on their abundant mitochondria not only for adenosine triphosphate production but also for efficient, sustained sequestration of large stimulation-induced Ca2+ loads. Ca2+ influx into the mitochondria is essential for sustaining neuromuscular transmission during repetitive stimulation and is a major stimulant for mitochondrial respiration in motor terminals. Their heavy reliance on mitochondria may make motor terminals especially vulnerable to stresses and diseases that impair mitochondrial function.
ASJC Scopus subject areas