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Presynaptic function is altered in snake K+‐depolarized motor nerve terminals containing compromised mitochondria

1 Presynaptic function was investigated at K+‐stimulated motor nerve terminals in snake costocutaneous nerve muscle preparations exposed to carbonyl cyanide m‐chlorophenylhydrazone (CCCP, 2 μm), oligomycin (8 μg ml−1) or CCCP and oligomycin together. 2 Miniature endplate currents (MEPCs) were recorded at ‐150 mV with two‐electrode voltage clamp. With all three drug treatments, during stimulation by elevated K+ (35 mm), MEPC frequencies initially increased to values > 350 s−1, but then declined. The decline occurred more rapidly in preparations treated with CCCP or CCCP and oligomycin together than in those treated with oligomycin alone. 3 Staining with FM1‐43 indicated that synaptic vesicle membrane endocytosis occurred at some CCCP‐ or oligomycin‐treated nerve terminals after 120 or 180 min of K+ stimulation, respectively. 4 The addition of glucose to stimulate production of ATP by glycolysis during sustained K+ stimulation attenuated the decline in MEPC frequency and increased the percentage of terminals stained by FM1‐43 in preparations exposed to either CCCP or oligomycin. 5 We propose that the decline in K+‐stimulated quantal release in preparations treated with CCCP, oligomycin or CCCP and oligomycin together could result from a progressive elevation of intracellular calcium concentration ([Ca2+]i). For oligomycin‐treated nerve terminals, a progressive elevation of [Ca2+]i could occur as the cytoplasmic ATP/ADP ratio decreases, causing energy‐dependent Ca2+ buffering mechanisms to fail. The decline in MEPC frequency could occur more rapidly in preparations treated with CCCP or CCCP and oligomycin together because mitochondrial Ca2+ buffering and ATP production were both inhibited. Therefore, the proposed sustained elevation of [Ca2+]i could occur more rapidly.