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Titolo:
Presynaptic function is altered in snake K+-depolarized motor nerve terminals containing compromised mitochondria
Autore:
Calupca, MA; Prior, C; Merriam, LA; Hendricks, GM; Parsons, RL;
Indirizzi:
Univ Vermont, Coll Med, Dept Anat & Neurobiol, Burlington, VT 05405 USA Univ Vermont Burlington VT USA 05405 Neurobiol, Burlington, VT 05405 USA Univ Strathclyde, Dept Physiol & Pharmacol, Strathclyde Inst Biomed Sci, Glasgow G4 0NR, Lanark, Scotland Univ Strathclyde Glasgow Lanark Scotland G4 0NR G4 0NR, Lanark, Scotland
Titolo Testata:
JOURNAL OF PHYSIOLOGY-LONDON
fascicolo: 1, volume: 532, anno: 2001,
pagine: 217 - 227
SICI:
0022-3751(20010401)532:1<217:PFIAIS>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
FROG NEUROMUSCULAR-JUNCTION; TRANSVERSUS ABDOMINIS MUSCLE; QUANTAL TRANSMITTER RELEASE; CEREBELLAR GRANULE CELLS; ADRENAL CHROMAFFIN CELLS; GARTER SNAKE; CA2+ LOADS; GLUTAMATE EXCITOTOXICITY; SYNAPTIC VESICLES; CYTOSOLIC CA2+;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Parsons, RL Univ Vermont, Coll Med, Dept Anat & Neurobiol, Burlington, VT 05405 USA Univ Vermont Burlington VT USA 05405 Burlington, VT 05405 USA
Citazione:
M.A. Calupca et al., "Presynaptic function is altered in snake K+-depolarized motor nerve terminals containing compromised mitochondria", J PHYSL LON, 532(1), 2001, pp. 217-227

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)) orCCCP 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 byelevated K+ (35 mM), MEPC frequencies initially increased to values > 350 s(-1), hut then declined. The decline occurred more rapidly in preparationstreated 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.

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Documento generato il 01/12/20 alle ore 21:48:14