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

Calupca, Michelle A. and Prior, Chris and Merriam, Laura A. and Hendricks, Gregory M. and Parsons, Rodney L. (2001) Presynaptic function is altered in snake K+-depolarized motor nerve terminals containing compromised mitochondria. Journal of Physiology, 532 (1). pp. 217-227. ISSN 0022-3751

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Abstract

Presynaptic function was investigated at K+-stimulated motor nerve terminals in snake costocutaneous nerve muscle preparations exposed to carbonyl cyanide m-chlorophenly- hydrazone (CCCP, 2 muM), oligomycin (8 mug ml(-1)) or CCCP and oligomycin together. Miniature endplate currents (MEPCs) R ere 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), hut then declined. The decline occurred more rapidly in preparations treated with CCCP or CCCP and oligomycin together than in those treated with oligomycin alone. 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. The addition of glucose to stimulate production of ATP bp 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. 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+](1)). For oligomycin-treated nerve terminals, a progressive elevation of [Ca2+](1) 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 a ere both inhibited. Therefore, the proposed sustained elevation of [Ca2+](1) could occur more rapidly.