Space and time characteristics of transmitter release at the nerve‐electroplaque junction of Torpedo.

Abstract

MEPPs. 6. Composite MEPPs with multiple peaks as well as bursts of small MEPPs were often encountered, even during periods of low frequency. They were suggestive of a complete disorganization of quantal events.7. Fast, slow and composite MEPPs were analysed using the computer model. To simulate the entire variety of signals we had to assume that the MEPPs were generated by either synchronized or desynchronized emission of small quantities of transmitter. The typical relationship observed between amplitude and time course in the population of fast MEPPs suggested that the different amounts of transmitter composing a quantum were delivered synchronously close to each other (either at the same spot or at less than 200 nm apart); it is proposed that they acted on overlapping fields of receptors and that their responses summed up in a superadditive manner.8. Computer analysis of the slow-rising MEPPs was of particular interest since their rapid decay phase indicated that the postsynaptic links (cholinesterase and receptors kinetics) were apparently not altered in this subpopulation. More probably their slow and often irregular rate of rise arose from some desynchronization of the release process.9. It is concluded that at the nerve-electroplaque junction evoked transmitter release operates in the form of quanta containing ca 10000 acetylcholine molecules; the quanta activate independent but closely adjacent postsynaptic fields. Each quantum is apparently composed of a preferential number of subunits emitted at the same point, or very close to each other. The subunits are delivered synchronously in the majority of events (fast MEPPs) but subunit desynchronization occasionally occurs (slow-rising and composite MEPPs).

Control of neurotransmitter release by an internal gel matrix in synaptic vesicles

“…The intravesicular matrix makes possible the postfusion control of neurotransmitter release (58,59) and opens the possibility that a quantum does not correspond exactly to the content of one synaptic vesicle, but rather would match a fixed number of molecules displaced by the activity of ionic channels or ionic transporters placed in the vesicle membrane. A single vesicle of Torpedo electric organ contains Ϸ200,000 ACh molecules (60), whereas the number of ACh molecules that generate a miniature end-plate current is 10,000 (61). The fact that neurotransmitters are adsorbed to an internal matrix indicates that unknown molecular mechanisms regulate, with high precision, the number of molecules released immediately after the fusion of a synaptic vesicle.…”

Quantal transmitter release by glioma cells: quantification of intramembrane particle changes

“…1, the size of the quantal steps was close to 100 pA. Knowing that (i) opening of one Xenopus embryonic nicotinic receptor under the present conditions will generate a current of 1^2 pA (Kidokoro and Rohrbough, 1990), (ii) two ACh molecules are needed to activate one receptor, (iii) presumably more than half of the molecules are wasted in the process, the quanta recorded here should result from the synchronous release of at least 400 ACh molecules. This is much less than the 6000^10 000 molecules estimated for the full quantum in adult neuromuscular or nerve^electroplaque junctions (Ku¥er and Yoshikami, 1975;Girod et al, 1993), but compares well with the values reported in embryonic endplates (Evers et al, 1989), sympathetic ganglia (Bennett, 1995), or in the population of small miniature currents which is believed to be the substructure of the classical quantum (Kriebel and Gross, 1974;Girod et al, 1993). A slightly larger value (200 pA) was obtained using neuroblastoma N18-TG-2 cells after transfection with the mediatophore, a proteolipid present in the presynaptic membrane cholinergic nerve terminals (Falk-Vairant et al, 1996a).…”

Neuromuscular transmission at an active zone: the secretosome hypothesis

“…A major problem with the idea that the peaks in the histogram of spontaneous potentials are due to subunits that make up the quantum is that the variance of the individual peaks does not increase much as the number of subunits increases (Bevan, 1976;Katz, 1977). A further possible difficulty with the idea that the peaks are indicative of subunits is that if these are secreted from the same site on the nerve terminal then considerable potentiation of the effects of one subunit due the preceding subunit might be expected; this would then result in the peaks spreading out at increasing intervals in the histograms of spontaneous potentials and an increase in their variance (Girod et al, 1993). A different approach to the idea that subunits must exist is provided by an analysis of the time course of the spontaneous potentials (Chek-Vakil et al, 1995).…”

“…Some of these possess rise times that are very long compared with that of the normal spontaneous potentials and may even show infections on their rising phases. Such different shapes may be due to different patterns of ascynhronous secretion of subunits (Girod et al, 1993;Vautrin et al, 1993), although another explanation is that they arise as a consequence of the method of recording with extracellular electrodes (see van der Kloot, 1996).…”

“…The existence of substantial gradients relating the rise time and the decay time of the MEPC to its amplitude are not then conditional on potentiating effects. Their existence cannot be used to argue for the presence of subunits in the MEPC as has sometimes been done (Girod et al, 1993).…”