Post‐tetanic potentiation at the neuromuscular junction of the frog

Rosenthal, Jean

doi:10.1113/jphysiol.1969.sp008854

Cited by 165 publications

(129 citation statements)

References 17 publications

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“…However, in contrast to the greatly increased testing EPPs measured 1 sec after the train at low quantal content, at normal quantal content, the EPP amplitudes dropped to a level that was below the control level, indicating that depression was present. From this depressed value, the testing EPP amplitudes then rose above the control level over time, suggesting that one or more of the slower decaying process that increase transmitter release during the train were obscured by depression immediately after the train, giving rise to classical posttetanic potentiation (Rosenthal, 1969;Magleby, 1973b;Zucker and Regehr, 2002). The depression may reflect a depletion of the RRP of synaptic vesicles during the train with recovery thereafter and perhaps also a decrease in the number of release sites (Takeuchi, 1958;Thies, 1965;Lass et al, 1973;Regehr and Stevens, 2001;Zucker and Regehr, 2002).…”

Section: Depression Dominates the Response Immediately After The Condmentioning

confidence: 99%

“…Such short-term synaptic plasticity has been divided into processes of synaptic enhancement that increase transmitter release and synaptic depression (D) that decrease release. Components of enhancement include facilitation, augmentation (A), and potentiation (P), with time constants of Ͻ1 sec, ϳ7 sec, and tens of seconds to minutes, respectively (Mallart and Martin, 1967;Rosenthal, 1969;Magleby and Zengel, 1976a;McNaughton, 1982;Poage and Zengel, 1993). Components of depression include very fast, fast, and slow components with time constants of recovery of Ͻ0.5 sec, ϳ6 sec, and tens of seconds to minutes, respectively (Takeuchi, 1958;Magleby, 1973b;Dittman and Regehr, 1998;Wu and Betz, 1998;Stevens and Wesseling, 1999b;Wesseling and Lo, 2002) In this report, we study the interaction between augmentation and the fast (ϳ6 sec) component of depression to determine whether augmentation continues to enhance transmitter release when depression dominates the response.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Depression Dominates the Response Immediately After The Condmentioning

confidence: 99%

Section: Introductionmentioning

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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“…Depletion of the releasable transmitter store explains many of the features of short-term depression at several synapses (Liley and North, 1953;Elmqvist and Quastel, 1965;Rosenthal, 1969;Kusano and Landau, 1975), however, at other synapses, changes in the presynaptic spike waveform (Dunlap and Fischbach, 1978;Klein and Kandel, 1980;Augustine, 1990;Sabatini and Regehr, 1997), inactivation of the presynaptic calcium current (Forsythe et al, 1998;Patil et al, 1998), or the inhibitory action of neuromodulators on presynaptic calcium channels (Yawo and Chuhma, 1993;Scanziani et al, 1997) may all contribute to the observed depression.…”

Section: Mechanisms Underlying Depression and Recovery At The Feti-flmentioning

confidence: 99%

Spike Width Reduction Modifies the Dynamics of Short-Term Depression at a Central Synapse in the Locust

Niven

Burrows

2003

J. Neurosci.

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Short-term synaptic depression is an important component of computation within neural networks, but little is known of its contribution to information processing during synaptically generated spike trains. We analyzed short-term synaptic depression at a synapse between two identified motoneurons innervating the hind leg of the locust: the FETi-FlTi synapse (fast extensor tibiae-flexor tibiae). Brief electrical stimulation of a single hind leg proprioceptor, the lump receptor (LR), led to prolonged sequences of spikes in FETi, similar in number and frequency to those during natural kicking movements. Depression at the FETi-FlTi synapse during LR-evoked spike bursts was compared quantitatively to that during antidromic spike trains evoked by electrical stimulation of FETi in the extensor tibiae muscle, and by modeling. The magnitude of the short-term depression was significantly greater during LR-evoked spike trains. On the basis of the model parameters required to fit the depression, the FETi-FlTi synapse is predominantly used for transmitting the timing of the onset of FETi spiking rather than its spike rate. During LR-evoked spike trains, there was a rapid reduction in presynaptic spike width that did not occur during antidromic spike trains under physiological calcium concentrations. This produced a concomitant reduction in the amplitude of the FlTi EPSP, suggesting that it contributed to the differences between the two stimulation regimes. Differences in the short-term depression between synaptically evoked and antidromic spike trains emphasize that the properties of synaptic information transfer are dependent on the in vivo conditions at the synapse and may not be reproduced by in vitro spike trains.

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“…The most clearly established of these is, of course, transmitter release (Katz & Miledi 1967, Douglas 1968. The biosynthesis of certain neurotransmitters is also regulated by calcium ion (Patrick & Barchas 1974), as is the number of quanta of transmitter released per nerve impulse (Rosenthal 1969, Klein & Kandel 1980.…”

Section: Synapsin Imentioning

confidence: 99%

Experimental Approaches to Understanding the Role of Protein Phosphorylation in the Regulation of Neuronal Function

Kennedy¹

1983

Annu. Rev. Neurosci.

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Post‐tetanic potentiation at the neuromuscular junction of the frog

Cited by 165 publications

References 17 publications

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

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

Spike Width Reduction Modifies the Dynamics of Short-Term Depression at a Central Synapse in the Locust

Experimental Approaches to Understanding the Role of Protein Phosphorylation in the Regulation of Neuronal Function

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