Transmitter release: prepackaging and random mechanism or dynamic and deterministic process

Kriebel, Mahlon E.; Vautrin, Jean; Holsapple, James

doi:10.1016/0165-0173(90)90017-i

Cited by 40 publications

(26 citation statements)

References 61 publications

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“…As shown here, when a bothropstoxin-I concentration (0.35 mM) lower than that used in the above studies was applied to neuromuscular preparations, a population of miniature end-plate potentials with an amplitude at least two-times greater than that of other miniature end-plate potentials was observed before there was any change in the resting potential. Additional evidence for a presynaptic action of bothropstoxin-I was the alteration in the quantal content which was based on the well-established relationship between end-plate potentials and miniature end-plate potentials (Fatt & Katz 1951& 1952Kriebel et al 1990).…”

Section: Discussionmentioning

confidence: 99%

The Presynaptic Activity of Bothropstoxin‐I, a Myotoxin from Bothrops jararacussu Snake Venom

Oshima-Franco¹,

Leite²,

Belo³

et al. 2004

Basic Clin Pharma Tox

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Bothropstoxin-I from Bothrops jararacussu snake venom is a lysine-49 phospholipase A 2 with myotoxic and neurotoxic activities. In this study, we used mouse phrenic nerve-diaphragm preparations in the absence and presence of manganese (Mn 2π ), a presynaptic blocker, to investigate a possible presynaptic action of bothropstoxin-I. At concentrations of 0.9 mM and 1.8 mM, Mn 2π produced 50% neuromuscular blockade in less than 4 min., which was spontaneously reversible at the lower concentration. Bothropstoxin-I (1.4 mM) irreversibly inhibited neuromuscular blockade by 50% in 31∫4 min. (mean∫S.E.M., nΩ9). Pretreating preparations with 0.9 mM Mn 2π prevented the blockade by bothropstoxin-I. When added after bothropstoxin-I, Mn 2π produced its characteristic blockade and, after washing, the twitch tension returned to pre-Mn 2π levels, indicating that bothropstoxin-I caused irreversible damage before the addition of Mn 2π . Electrophysiological measurements showed that a concentration of bothropstoxin-I (0.35 mM), which did not produce neuromuscular blockade, caused the appearance of giant miniature end-plate potentials with no change in the membrane resting potential but increased the quantal content. Preparations preincubated with Mn 2π (0.9 mM, 30 min.) were protected against the depolarizing action of bothropstoxin-I (0.7 mM). These results show that, in addition to its well-known myotoxic effect, bothropstoxin-I also has a presynaptic action.

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Section: Discussionmentioning

confidence: 99%

The Presynaptic Activity of Bothropstoxin‐I, a Myotoxin from Bothrops jararacussu Snake Venom

Oshima-Franco¹,

Leite²,

Belo³

et al. 2004

Basic Clin Pharma Tox

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“…5B). This reveals the deterministic nature of the process that releases bursts of transmitter packets (see also Vautrin, 1988;Kriebel et al, 1990;Vautrin and Kriebel, 1991).…”

Section: Rise Time (Msmentioning

confidence: 97%

“…time courses are observed and cannot be incorporated into the quantal theory (Kriebel et al, 1990). These MEPPs have neither a defined amplitude nor a defined rise time (Vautrin and Kriebel, 1991).…”

Section: Introductionmentioning

confidence: 99%

Focal, extracellular recording of slow miniature junctional potentials at the mouse neuromuscular junction

Vautrin

Kriebel

1992

J of Neuroscience Research

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Miniature endplate potentials (MEPPs) with slow rising phase can be attributed either to burst of transmitter releases or to distortion of conduction from remote releasing sites. The spontaneous activity of neuromuscular junctions recorded extracellularly at mouse diaphragms using sharp electrodes was analyzed to test these two hypotheses. The miniature junctional potentials (MEJPs) frequencies observed intracellularly as compared to MEPP frequency measured intracellularly in controls indicate that most events recorded extracellularly are induced by the presence of the electrode. All types of MEPPs (bell-MEPPs, skew-MEPPs, slow-, and giant MEPPs) previously described with intracellular recording methods (Vautrin and Kriebel, Neuroscience 41:71-88, 1991) were observed extracellularly and showed similar characteristics. This means that the presynaptic and postsynaptic zones that generate these synaptic events are restricted within areas of a few micrometers squared of synaptic contact. Long rise times of extracellularly recorded synaptic spontaneous events may be explained by multiple transmitter releases at intervals shorter than the rise time of individual events, which postsynaptic responses fuse into a single peak.

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“…For example, dynamic changes in the properties of miniature postsynaptic signals (Kriebel et al, 1990;Vautrin, 1992) challenge the idea that transmitter quanta are preformed. Elmqvist and Quastel (1965) found that when the choline supply to motor terminal is blocked there is no run-down of the number of all-or-none acetylcholine (ACh) quanta, but rather a progressive decrease in quantal size.…”

Section: Absence Of Preformation Of Quantamentioning

confidence: 99%

“…The composite nature of miniature postsynaptic signals is not readily explained in terms of dumping of all the content of a single vesicle (Kriebel et al, 1990;Vautrin and Barker, 1995;Auger et al, 1998). The interaction between subminiature discharges of transmitter may actually reflect calcium dynamics comparable to those found in muscle cells Berridge, 1997;Coop et al, 1998).…”

Section: On the Formation Of Quantamentioning

confidence: 99%

Surface-accessible GABA supports tonic and quantal synaptic transmission

Vautrin

Maric

Sukhareva

et al. 2000

Synapse

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Exocytosis is commonly viewed as the only secretory process able to account for quantal forms of fast synaptic transmission. However, the demonstrated variability and composite properties of miniature postsynaptic signals are not easily explained by all-or-none exocytotic discharge of transmitter in solution from inside vesicles. Recent studies of endocrine secretion have shown that hormone release does not coincide with exocytosis due to its trapping in the core matrix of the granule. Thus, we tested whether the synaptic transmitter GABA could also be held in a matrix before being released. Using confocal microscopy and flow cytometry of embryonic rat hippocampal neurons, we found a GABA immunoreaction at the surface of live cell bodies and growth cones that coincided spatially and quantitatively with the binding of tetanus toxin fragment C (TTFC). TTFC binds predominantly at membrane sites containing the trisialoglycosphingolipid GT1b. Using flow cytometry, GT1b-containing liposomes preincubated in 100 nM GABA exhibited the same relationship between GABA and TTFC surface binding as found on neurons and growth cones. Embryonic neurons differentiated in culture expressed initially a tonic, and after 3-5 days, transient, postsynaptic signals mediated by GABA acting at GABA(A) receptor/Cl(-) channels. A stream of saline applied to the neuronal surface rapidly and reversibly suppressed both tonic and transient signals. A brief application of the GABAmimetic isoguvacine immediately transformed both tonic and transient GABAergic signals into tonic and transient isoguvacinergic signals. These results and those in the literature are consistent with an immediately releasable compartment of transmitter accessible from the presynaptic surface.

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Transmitter release: prepackaging and random mechanism or dynamic and deterministic process

Cited by 40 publications

References 61 publications

The Presynaptic Activity of Bothropstoxin‐I, a Myotoxin from Bothrops jararacussu Snake Venom

The Presynaptic Activity of Bothropstoxin‐I, a Myotoxin from Bothrops jararacussu Snake Venom

Focal, extracellular recording of slow miniature junctional potentials at the mouse neuromuscular junction

Surface-accessible GABA supports tonic and quantal synaptic transmission

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