Real-time detection of mitochondrial inhibition at frog motor nerve terminals using increases in the spatial variance in probability of transmitter release

Provan, Spencer D.; Miyamoto, Michael D.

doi:10.1016/0304-3940(95)91365-o

Cited by 5 publications

(2 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results suggest that p is associated with [Ca 2+ ] at the active zones, since the calcium ionophore A23187 causes an increase in p but no increase in n or var s p (Brailoiu et al ., 2001). Our results also suggest that var s p is associated with variations in [Ca 2+ ] at the active zones, as might occur with release of Ca 2+ from distal organelles, since agents that promote Ca 2+ release from mitochondria cause increases in var s p (Provan & Miyamoto, 1993; 1995).…”

Section: Methodssupporting

confidence: 57%

Calmodulin increases transmitter release by mobilizing quanta at the frog motor nerve terminal

Brǎiloiu

Miyamoto

Dun

2002

British J Pharmacology

View full text Add to dashboard Cite

1 The role of calmodulin (CaM) in transmitter release was investigated using liposomes to deliver CaM and monoclonal antibodies against CaM (antiCaM) directly into the frog motor nerve terminal. 2 Miniature endplate potentials (MEPPs) were recorded in a high K + solution, and e ects on transmitter release were monitored using estimates of the quantal release parameters m (number of quanta released), n (number of functional transmitter release sites), p (mean probability of release), and var s p (spatial variance in p). 3 Administration of CaM, but not heat-inactivated CaM, encapsulated in liposomes (1000 units ml 71 ) produced an increase in m (25%) that was due to an increase in n. MEPP amplitude was not altered by CaM. 4 Administration of antiCaM, but not heat-inactivated antiCaM, in liposomes (50 ml ml 71 ) produced a progressive decrease in m (40%) that was associated with decreases in n and p. MEPP amplitude was decreased (15%) after a 25 min lag time, suggesting a separation in time between the decreases in quantal release and quantal size. 5 Bath application of the membrane-permeable CaM antagonist W7 (28 mM) produced a gradual decrease in m (25%) that was associated with a decrease in n. W7 also produced a decrease in MEPP amplitude that paralleled the decrease in m. The decreases in MEPP size and m produced by W7 were both reversed by addition of CaM. 6 Our results suggest that CaM increases transmitter release by mobilizing synaptic vesicles at the frog motor nerve terminal.

show abstract

Section: Methodssupporting

confidence: 57%

Calmodulin increases transmitter release by mobilizing quanta at the frog motor nerve terminal

Brǎiloiu

Miyamoto

Dun

2002

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Agents that inhibit mitochondria under nonstimulated conditions produce an increase in var s p, presumably by inhibiting the uptake or promoting the release of mitochondrial Ca 2ϩ (Provan and Miyamoto 1995). Under normal conditions, the uptake of cytoplasmic Ca 2ϩ by these organelles is intensified during tetanic stimulation (David et al 1998), conceivably because the increase in Ca influx leads to more available Ca 2ϩ (increased [Ca 2ϩ ] i ).…”

Section: Discussionmentioning

confidence: 99%

Effect of Hypertonicity on Augmentation and Potentiation and on Corresponding Quantal Parameters of Transmitter Release

Cheng

Miyamoto

1999

Journal of Neurophysiology

Self Cite

View full text Add to dashboard Cite

Augmentation and (posttetanic) potentiation are two of the four components comprising the enhanced release of transmitter following repetitive nerve stimulation. To examine the quantal basis of these components under isotonic and hypertonic conditions, we recorded miniature endplate potentials (MEPPs) from isolated frog (Rana pipiens) cutaneous pectoris muscles, before and after repetitive nerve stimulation (40 s at 80 Hz). Continuous recordings were made in low Ca2+ high Mg2+ isotonic Ringer solution, in Ringer that was made hypertonic with 100 mM sucrose, and in wash solution. Estimates were obtained of m (no. of quanta released), n (no. of functional release sites), p (mean probability of release), and vars p (spatial variance in p), using a method that employed MEPP counts. Hypertonicity abolished augmentation without affecting potentiation. There were prolonged poststimulation increases in m, n, and p and a marked but transient increase in vars p in the hypertonic solution. All effects were completely reversed with wash. The time constants of decay for potentiation and for vars p were virtually identical. The results are consistent with the notion that augmentation is caused by Ca2+ influx through voltage-gated calcium channels and that potentiation is due to Na+-induced Ca2+ release from mitochondria. The results also demonstrate the utility of this approach for analyzing the dynamics of quantal transmitter release.

show abstract

Niflumic acid-induced increase in potassium currents in frog motor nerve terminals: effects on transmitter release

et al. 1996

View full text Add to dashboard Cite

Real-time detection of mitochondrial inhibition at frog motor nerve terminals using increases in the spatial variance in probability of transmitter release

Cited by 5 publications

References 17 publications

Calmodulin increases transmitter release by mobilizing quanta at the frog motor nerve terminal

Calmodulin increases transmitter release by mobilizing quanta at the frog motor nerve terminal

Effect of Hypertonicity on Augmentation and Potentiation and on Corresponding Quantal Parameters of Transmitter Release

Niflumic acid-induced increase in potassium currents in frog motor nerve terminals: effects on transmitter release

Contact Info

Product

Resources

About