Release of LHRH is linearly related to the time integral of presynaptic Ca+ elevation above a threshold level in bullfrog sympathetic ganglia

Peng, Yan-Yi; Zucker, Robert S.

doi:10.1016/0896-6273(93)90334-n

Cited by 101 publications

(70 citation statements)

References 35 publications

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“…Thus, it is likely that the intraterminal channels also have a very fast activation time constant (which was 1.4 msec for the isolated cardiac channels; Gyorke et al, 1994). The small size of a typical nerve terminal (quasispheres with diameters of 0.5-5 M) allows the Ca 2ϩ entering through the plasma membrane channels to equilibrate within 10 msec (Peng and Zucker, 1993) and, therefore, can increase the rate of Ca 2ϩ release from the smooth endoplasmic reticulum within this time. If the intraterminal ryanodine channels can be activated as fast as the isolated channels, then Ca 2ϩ -dependent phenomena that occur at the terminals with a delay of Ն10 msec after the initial Ca 2ϩ influx through the plasma membrane channels can potentially be affected by the intraterminal Ca 2ϩ release through the ryanodine channels.…”

Section: Discussionmentioning

confidence: 99%

“…For the rest of the units, Ca 2ϩ release through the ryanodine channels increased the peak amplitude and the duration of the Ca 2ϩ elevation. The resultant increase of the time integral of Ca 2ϩ elevation above the threshold level for LHRH release is likely to enhance the release because this time integral has been shown to be proportional to LHRH release (Peng and Zucker, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…The fura-2 emission from either a group of terminals on a given cell or one of these terminals was selectively measured by adjusting a field diaphragm that was interposed between the barrier filler for fura-2 emission and the photomultiplier tube. The Ca 2ϩ concentration was calculated as described previously (Peng and Zucker, 1993). The fluorimetric data were digitized at 0.2-1 kHz.…”

Section: Methodsmentioning

confidence: 99%

“…Intraterminal [Ca 2ϩ ] i was studied in a group of boutons contacting a cell (i.e., a unit) instead of individual boutons for three reasons. First, like all other synapses, the preganglionic fiber(s) innervates a ganglionic cell through tens of synaptic boutons (Jan and Jan, 1982;Baluk, 1986;Peng and Zucker, 1993), and the amount of release recorded postsynaptically is the summation of release from all of these presynaptic sites. Second, synaptic transmission for any given terminal is a stochastic event.…”

Section: Effects Of Ryanodine On Intraterminal [Ca 2؉ ] Transients Evmentioning

confidence: 99%

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Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Peng

1996

J. Neurosci.

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Whether Ca 2ϩ released from stores within the presynaptic nerve terminals also contributes to the Ca 2ϩ elevation evoked by action potentials was tested in intact bullfrog sympathetic ganglia. Intraterminal Ca 2ϩ transients (⌬[Ca 2ϩ ] i ) were evoked by electrical shocks to the presynaptic nerves at 20 Hz and were monitored by fura-2 fluorimetry. Ca 2ϩ released through intraterminal ryanodine-sensitive channels accounted for 46% of the peak Ca 2ϩ elevation. Moreover, in half of the terminals when intraterminal release was blocked by ryanodine, ⌬[Ca 2ϩ ] i reached a plateau at 200 Ϯ 24 nM. Because 20 Hz is a frequency favorable for the release of a neuropeptide, luteinizing hormone releasing hormone (LHRH) from these presynaptic nerve terminals, and because the threshold level for LHRH release is 186 nM, intraterminal Ca 2ϩ release during nerve firing is likely to play a major role in regulating LHRH release. The intraterminal ryanodine channels were facilitated by caffeine as in other tissue. The releasable ryanodine-sensitive store could elevate the intraterminal [Ca 2ϩ ] by an amount as high as 1.6 M at a rate as fast as 250 nM/sec. The store could be refilled within 100 sec after a maximal discharge of its content by 20 Hz firing. Oscillation of [Ca 2ϩ ] i evoked by 20 Hz nerve firing occurred in normal Ringer solution, in ryanodine, and in caffeine with a periodicity of ϳ10 sec. Besides the facilitatory effects on the ryanodine-sensitive channels, caffeine also had inhibitory effects on ⌬[Ca 2ϩ ] i via its action on a different process.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Effects Of Ryanodine On Intraterminal [Ca 2؉ ] Transients Evmentioning

confidence: 99%

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Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Peng

1996

J. Neurosci.

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“…Fluorescence ratio imaging techniques were used to measure average intracellular free Ca 2ϩ in motor nerve terminals during and after repetitive stimulation (Almers and Neher, 1985;Delaney et al, 1989;Suzuki et al, 2000). Ca 2ϩ indicators were loaded into frog motor nerve terminals by backfilling the nerves (Peng and Zucker, 1993;Wu and Betz, 1996). The motor nerve was cut a few millimeters proximal to where it branched into the cutaneous pectoris muscle.…”

Section: Methodsmentioning

confidence: 99%

Augmentation Increases Vesicular Release Probability in the Presence of Masking Depression at the Frog Neuromuscular Junction

Kalkstein

Magleby

2004

J. Neurosci.

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Synaptic augmentation is a short-term component of synaptic plasticity that increases transmitter release during repetitive stimulation and decays thereafter with a time constant of ϳ7 sec. Augmentation has typically been observed under conditions where there is little or no depression because of depletion of synaptic vesicles from the readily releasable pool (RRP) of transmitter. We now study augmentation under conditions of pronounced depression at the frog neuromuscular junction to gain additional insight into mechanism. If augmentation reflects an increase in the size of the RRP of transmitter, then augmentation should not be present with depression. Our findings using four different experimental approaches suggested that augmentation was still present in the presence of pronounced depression: mathematical extraction of augmentation from the changes in transmitter release after repetitive stimulation, identification of augmentation with Ba 2ϩ , correction of the data for the measured depletion of the RRP, and identification of an augmentation component of residual Ca 2ϩ . We conclude that the augmentation machinery still acts to increase transmitter release when depression reduces the RRP sufficiently to mask obvious augmentation. The masked augmentation was found to increase transmitter release by increasing the probability of releasing individual vesicles from the depressed RRP, countering the effects of depression. Because augmentation and depression have similar time courses, either process can mask the other, depending on their relative magnitudes. Consequently, the apparent absence of one of the processes does not exclude that it is still contributing to short-term synaptic plasticity.

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Dense-cored vesicles, smooth endoplasmic reticulum, and mitochondria are closely associated with non-specialized parts of plasma membrane of nerve terminals: Implications for exocytosis and calcium buffering by intraterminal organelles

et al. 1999

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Release of LHRH is linearly related to the time integral of presynaptic Ca+ elevation above a threshold level in bullfrog sympathetic ganglia

Cited by 101 publications

References 35 publications

Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Augmentation Increases Vesicular Release Probability in the Presence of Masking Depression at the Frog Neuromuscular Junction

Dense-cored vesicles, smooth endoplasmic reticulum, and mitochondria are closely associated with non-specialized parts of plasma membrane of nerve terminals: Implications for exocytosis and calcium buffering by intraterminal organelles

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