Saturation of postsynaptic glutamate receptors after quantal release of transmitter

Tang, Cha‐Min; Margulis, Michael; Shi, Qing-Yao; Fielding, Alex

doi:10.1016/0896-6273(94)90423-5

Cited by 105 publications

(89 citation statements)

References 33 publications

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“…If the second PSC had been independent of the first, it should have had the same amplitude on average. This suggests that the first release event was occupying a large fraction of postsynaptic receptors, leaving fewer for the second, which is convincing evidence for saturation, provided receptor desensitization was not a factor (116). In addition, at the climbing fiber, two closely spaced PSCs are differentially affected by the low-affinity AMPA receptor antagonist DGG (129).…”

Section: B Postsynaptic Receptor Saturationmentioning

confidence: 69%

Structural Contributions to Short-Term Synaptic Plasticity

Xu‐Friedman

Regehr

2004

Physiological Reviews

152

111

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Xu-Friedman, Matthew A., and Wade G. Regehr. Structural Contributions to Short-Term Synaptic Plasticity. Physiol Rev 84: 69–85, 2004; 10.1152/physrev.00016.2003.—Synaptic ultrastructure is critical to many basic hypotheses about synaptic transmission. Various aspects of synaptic ultrastructure have also been implicated in the mechanisms of short-term plasticity. These forms of plasticity can greatly affect synaptic strength during ongoing activity. We review the evidence for how synaptic ultrastructure may contribute to facilitation, depletion, saturation, and desensitization.

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Section: B Postsynaptic Receptor Saturationmentioning

confidence: 69%

Structural Contributions to Short-Term Synaptic Plasticity

Xu‐Friedman

Regehr

2004

Physiological Reviews

152

111

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“…This apparent mismatch between neuronal and hemodynamic behavior may result from neuronal processes, such as a neurotransmitter release from presynaptic thalamic terminals, undetected by the electrophysiological recording methods used (11)(12)(13). Here we present data showing that the hemodynamic response within a cortical column (a principal barrel in Barrel cortex) increases beyond saturation of the thalamic input to the same column.…”

mentioning

confidence: 60%

Coupling of the cortical hemodynamic response to cortical and thalamic neuronal activity

Devor

Ulbert

Dunn

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

211

180

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Accurate interpretation of functional MRI (fMRI) signals requires knowledge of the relationship between the hemodynamic response and the neuronal activity that underlies it. Here we address the question of coupling between pre-and postsynaptic neuronal activity and the hemodynamic response in rodent somatosensory (Barrel) cortex in response to single-whisker deflection. Using full-field multiwavelength optical imaging of hemoglobin oxygenation and electrophysiological recordings of spiking activity and local field potentials, we demonstrate that a point hemodynamic measure is influenced by neuronal activity across multiple cortical columns. We demonstrate that the hemodynamic response is a spatiotemporal convolution of the neuronal activation. Therefore, positive hemodynamic response in one cortical column might be explained by neuronal activity not only in that column but also in the neighboring columns. Thus, attempts at characterizing the neurovascular relationship based on point measurements of electrophysiology and hemodynamics may yield inconsistent results, depending on the spatial extent of neuronal activation. The finding that the hemodynamic signal observed at a given location is a function of electrophysiological activity over a broad spatial region helps explain a previously observed increase of local vascular response beyond the saturation of local neuronal activity. We also demonstrate that the oxy-and total-hemoglobin hemodynamic responses can be well approximated by space-time separable functions with an antagonistic center-surround spatial pattern extending over several millimeters. The surround ''negative'' hemodynamic activity did not correspond to observable changes in neuronal activity. The complex spatial integration of the hemodynamic response should be considered when interpreting fMRI data.Barrel cortex ͉ blood oxygenation ͉ intrinsic signals ͉ optical imaging T he advent of noninvasive imaging methods such as functional MRI (fMRI) has made it possible to obtain spatial maps of hemodynamic ''activation'' in the human brain under a variety of conditions (1, 2). However, the indirect and poorly understood nature of the coupling between these hemodynamic signals and the underlying neuronal activity has greatly limited the interpretability of neuroimaging results. Recently, several groups have attempted to characterize this coupling in the form of a linear or nonlinear neurovascular ''transfer function '' (3-8). In principle, if such a function could be defined, it would provide a basis for inferring time-averaged local neuronal activity based on hemodynamic measurements. Furthermore, it would permit more accurate integration of hemodynamic imaging methods with noninvasive electrophysiological recordings such as electroencephalography and magnetoencephalography (9, 10).In a previous publication (3), using simultaneous spectroscopic optical imaging and electrophysiological measurements in rodent somatosensory cortex during brief and spatially localized stimuli, we found a strongly nonlinear r...

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“…1 C and E and 3. These are interpreted as progressive saturation of postsynaptic receptors by successive vesicular release events at single synaptic sites (19,23,27). They cannot be explained by dendritic filtering, because the predicted peak current attenuation due to dendritic filtering in MLIs is only 20% at a distance of 50 μm, which is much too weak to explain the observed sublinearity (28).…”

Section: Resultsmentioning

confidence: 88%

Readily releasable pool of synaptic vesicles measured at single synaptic contacts

Trigo

Sakaba

Ogden

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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To distinguish between different models of vesicular release in brain synapses, it is necessary to know the number of vesicles of transmitter that can be released immediately at individual synapses by a high-calcium stimulus, the readily releasable pool (RRP). We used direct stimulation by calcium uncaging at identified, singlesite inhibitory synapses to investigate the statistics of vesicular release and the size of the RRP. Vesicular release, detected as quantal responses in the postsynaptic neuron, showed an unexpected stochastic variation in the number of quanta from stimulus to stimulus at high intracellular calcium, with a mean of 1.9 per stimulus and a maximum of three or four. The results provide direct measurement of the RRP at single synaptic sites. They are consistent with models in which release proceeds from a small number of vesicle docking sites with an average occupancy around 0.7.release site | exocytosis | interneurons | cerebellum

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Saturation of postsynaptic glutamate receptors after quantal release of transmitter

Cited by 105 publications

References 33 publications

Structural Contributions to Short-Term Synaptic Plasticity

Structural Contributions to Short-Term Synaptic Plasticity

Coupling of the cortical hemodynamic response to cortical and thalamic neuronal activity

Readily releasable pool of synaptic vesicles measured at single synaptic contacts

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