Desensitization of AMPA receptors upon multiquantal neurotransmitter release

Trussell, Laurence O.; Zhang, Su; Ramant, Indira M.

doi:10.1016/0896-6273(93)90066-z

Cited by 439 publications

(498 citation statements)

References 50 publications

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“…We typically evoked release from tens of synapses simultaneously for our experiments, however. Although there is no indication that transmitter released at the same time from multiple synapses interacts with the AMPA type of glutamate receptors in a nonlinear way at Schaffer collateral synapses (Asztely et al, 1997), cross talk between calycealtype synapses has been reported to result in postsynaptic forms of short-term depression (Trussell et al, 1993;Neher and Sakaba, 2001). Such a phenomenon, if operative at Schaffer collateral synapses, might have led to an overestimate of the actual amount of presynaptic depression in our experiments.…”

Section: Intersynaptic Cross Talkcontrasting

confidence: 40%

“…At some types of synapses, postsynaptic receptor desensitization contributes to short-term depression (Trussell et al, 1993). To confirm that receptor desensitization did not contribute to the rapid decrease in synaptic strength that occurred during stimulation frequencies of 20 and 40 Hz, or when the stimulating frequency was increased during stimulation, experiments similar to those documented in Figures 1 A and 4 B were conducted in the presence and absence of 100 M CTZ, a drug that blocks glutamate receptor desensitization (Patneau et al, 1993;Yamada and Tang, 1993).…”

Section: Receptor Desensitizationmentioning

confidence: 99%

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Limit on the Role of Activity in Controlling the Release-Ready Supply of Synaptic Vesicles

Wesseling

2002

J. Neurosci.

190

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Typical fast chemical synapses in the brain weaken transiently during normal high-frequency use after expending their presynaptic supply of release-ready vesicles. Although it takes several seconds for the readily releasable pool (RRP) to refill during periods of rest, it has been suggested that the replenishment process may be orders of magnitude faster when synapses are active. Here, we measure this replenishment rate at active Schaffer collateral terminals by determining the maximum rate of release that can still be elicited when the RRP is almost completely exhausted. On average, we find that spent vesicles are replaced at a maximum unitary rate of 0.24/sec during periods of intense activity. Because the replenishment rate is similar during subsequent periods of rest, we conclude that no special mechanism accelerates the mobilization of neurotransmitter in active terminals beyond the previously reported, several-fold, residual calcium-driven modulation that persists for several seconds after bouts of intense synaptic activity. In the course of this analysis, we provide new evidence supporting the hypothesis that a simple enzymatic step limits the rate at which reserve synaptic vesicles become ready to undergo exocytosis.

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Section: Intersynaptic Cross Talkcontrasting

confidence: 40%

Section: Receptor Desensitizationmentioning

confidence: 99%

Limit on the Role of Activity in Controlling the Release-Ready Supply of Synaptic Vesicles

Wesseling

2002

J. Neurosci.

190

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“…Synaptic currents did not decay completely between pulses at stimulation frequencies higher than 50 Hz, and a significant shift of the baseline current developed. This introduced series resistance errors, and it might also have signaled the prolonged presence of glutamate in the synaptic cleft, which could lead to postsynaptic receptor desensitization (Trussell and Fischbach, 1989;Trussell et al, 1993). Therefore, we did not stimulate at frequencies higher than 50 Hz.…”

Section: Methodsmentioning

confidence: 99%

Modulation of Transmission during Trains at a Cerebellar Synapse

Kreitzer

Regehr

2000

J. Neurosci.

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Activity-dependent processes dynamically regulate synapses on the time scale of milliseconds to seconds. Here, we examine the factors governing synaptic strength during repetitive stimulation, both in control conditions and during presynaptic inhibition. Field recordings of presynaptic volleys, optical measurements of presynaptic calcium, and voltage-clamp recordings of postsynaptic currents were used to examine parallel fiber to Purkinje cell synapses in cerebellar brain slices at 34°C. In control conditions, regular stimulus trains (1-50 Hz) evoked up to a 250% peak synaptic enhancement, whereas during irregular stimulation, a threefold variability in EPSC amplitude was observed. When initial EPSC amplitudes were reduced by 50%, either by lowering external calcium or by activating adenosine A 1 or GABA B receptors, the peak enhancement during regular trains was 500%, and synaptic variability during irregular trains was nearly sixfold. By contrast, changes in fiber excitability and calcium influx per pulse were small during trains. Presynaptic calcium measurements indicated that by pulse 10, stimulusevoked calcium influx had increased by ϳ15%, which on the basis of the measured relationship between calcium influx and release corresponds to an EPSC enhancement of 50%. This enhancement was the same in all experimental conditions, even in the presence of N 6 -cyclopentyladenosine or baclofen, suggesting that repetitive stimulation does not relieve the G-protein inhibition of calcium channels by these modulators. Therefore, for our experimental conditions, changes in synaptic strength during trains are primarily attributable to residual calcium (Ca res )-dependent short-term plasticities, and the actions of neuromodulators during repetitive stimulation result from their inhibition of initial calcium influx and the resulting effects on Ca res and calcium-driven processes.

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“…Depletion-independent mechanisms of depression were also reported (Hsu et al 1996;Kraushaar and Jonas 2000;Waldeck et al 2000;Gover et al 2002;Kirischuk et al 2002;Pedroarena and Schwarz 2003;Fuhrmann et al 2004). Furthermore, post-synaptic mechanisms (e.g., the desensitization of AMPA receptors) are potential contributors to synaptic depression (Trussell and Fischbach 1989;Trussell et al 1993;Jones and Westbrook 1996).…”

Section: Introductionmentioning

confidence: 99%

Parametric and non-parametric modeling of short-term synaptic plasticity. Part I: computational study

2008

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Parametric and non-parametric modeling methods are combined to study the short-term plasticity (STP) of synapses in the central nervous system (CNS). The nonlinear dynamics of STP are modeled by means: (1) previously proposed parametric models based on mechanistic hypotheses and/or specific dynamical processes, and (2) non-parametric models (in the form of Volterra kernels) that transforms the presynaptic signals into postsynaptic signals. In order to synergistically use the two approaches, we estimate the Volterra kernels of the parametric models of STP for four types of synapses using synthetic broadband input-output data. Results show that the non-parametric models accurately and efficiently replicate the input-output transformations of the parametric models. Volterra kernels provide a general and quantitative representation of the STP.

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Desensitization of AMPA receptors upon multiquantal neurotransmitter release

Cited by 439 publications

References 50 publications

Limit on the Role of Activity in Controlling the Release-Ready Supply of Synaptic Vesicles

Limit on the Role of Activity in Controlling the Release-Ready Supply of Synaptic Vesicles

Modulation of Transmission during Trains at a Cerebellar Synapse

Parametric and non-parametric modeling of short-term synaptic plasticity. Part I: computational study

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