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2 glutamate by vesicular fusion, which induces quantal AMPA receptor-mediated currents in NG2(+) glial
3 ombined depolarizing effect enables the fast quantal AMPAR component to trigger action potentials at
4 of spontaneous release without any change in quantal amplitude (miniature endplate current), (2) redu
6 was mediated by a decrease in both synaptic quantal amplitude and quantal content, the latter inferr
7 mitral and external tufted cells had similar quantal amplitude and release probability, suggesting th
9 s that the sensors triggering changes in the quantal amplitude and vesicle release exist at different
11 ot additive; whereas TNFalpha increased AMPA quantal amplitude at control synapses, TNFalpha reduced
13 litude at control synapses, TNFalpha reduced quantal amplitude at prescaled synapses, demonstrating s
14 (AMPARs), and results from a fourfold larger quantal amplitude compared with the thalamic inputs onto
15 two different mechanisms underlie changes in quantal amplitude during homeostatic synaptic plasticity
17 our data suggest that scaling up and down of quantal amplitude is not driven by changes in synaptic a
18 ndings suggest that homeostatic increases in quantal amplitude may normally be triggered by reduced l
19 natal week the quantal frequency but not the quantal amplitude of synaptic events increased more than
21 ns were accompanied by scaling of excitatory quantal amplitude via the postsynaptic, GB(1b)-containin
31 synaptic scaling involves uniform scaling of quantal amplitudes across all synaptic inputs formed on
32 reases the presynaptic vesicle size, reduces quantal amplitudes and evoked synaptic transmission and
33 lysis reveals that AMPA/NMDA ratios and AMPA quantal amplitudes increase during the first postnatal w
34 e was measured directly by comparing unitary quantal amplitudes of paired EPSCs before and during 5-H
40 g in presynaptic axonal boutons with optical quantal analysis in postsynaptic dendritic spines to fin
47 ing protein (CREB) during induction, and (2) quantal analysis to identify synaptic changes during mai
48 ken together, these results expand classical quantal analysis to incorporate endocytic and exocytic p
49 onstruction, combined with a novel method of quantal analysis, showed that the strong inhibitory inpu
52 tion, which verifies the basic assumption of quantal analysis--the same mechanism controls the quanta
55 ometry revealed that release of dopamine was quantal and calcium-dependent, but quantal size was much
59 HT2C) receptor, global analysis of construct quantal brightness was consistent with the predominant f
60 IDA for use in a two-dimensional system with quantal brightnesses, a method was developed to quantify
61 rst and cooperative gating kinetics provided quantal Ca(2+) increases (i.e., steps of fixed amplitude
62 vity with a timescale comparable to that for quantal Ca2+ release was observed under any steady ligan
63 s of intracellular Ca2+ signaling, including quantal Ca2+ release, by tuning ligand sensitivities of
64 ny schemes have been proposed to account for quantal Ca2+ release, including the presence of heteroge
65 To clarify the molecular mechanisms behind quantal Ca2+ release, the graded Ca2+ release from intra
67 h will enable high-throughput measurement of quantal catecholamine release simultaneously with optica
68 ting persistent presynaptic and postsynaptic quantal changes at excitatory synapses in inhibitory loc
69 nce-dose (ID) models need to account for the quantal characteristics of cellular switches that contri
70 1 degrees Mn) type depresses and has a large quantal content (Qc) and a high release probability (Pr)
71 vesicle refilling prevented upregulation of quantal content (QC), while leaving baseline release rel
72 nerve-muscle preparations revealed that the quantal content (the number of ACh quanta released per n
74 ar junction is unique in having a very small quantal content and a high release probability under con
75 used by both a PKC-dependent increase of the quantal content and a PKC-independent increase of the qu
76 adily releasable pool of vesicles diminishes quantal content and antagonizes the postsynaptic enhance
77 dulation but not binding in vitro, increased quantal content and decreased paired-pulse and tetanic f
78 n 1A-calcium channel interactions, decreased quantal content at these synapses and increased paired-p
79 pha3*-nAChR currents are prolonged at higher quantal content because of ACh spillover and postsynapti
81 C) enhances synaptic release probability and quantal content but reduces the size of the ready-releas
82 alcium concentration, which may increase the quantal content by activation of protein kinase C (PKC).
83 ready showed, respectively, lower and higher quantal content compared with WT mice, before signs of M
84 obability of release of neurotransmitter and quantal content is increased, yet the abundance of the p
87 Cs occurs as a consequence of a low baseline quantal content of evoked IPSCs using whole cell patch-c
88 IH rats we clearly show that CIH reduced the quantal content of the TS-eEPSCs without affecting the q
90 The effect upon EPSC decay time of changing quantal content was 5-10 times more pronounced for alpha
91 Prolongation of EPC decay was reversed when quantal content was lowered by reducing extracellular ca
92 r of vesicles released per action potential (quantal content) in R6/2 muscle, which analysis of eEPC
93 ude of evoked release (endplate current) and quantal content, (3) age-dependent changes in the extent
94 (flx) soleus muscles, one with high (mature) quantal content, and another with low (immature) quantal
95 striking reduction of the endplate potential quantal content, consistent with additional presynaptic
96 n quantal size and a concomitant decrease in quantal content, suggesting functional consequences for
97 rease in both synaptic quantal amplitude and quantal content, the latter inferred from an increase in
103 regulate the biochemical realization of its quantal-count threshold with respect to its Q(count).
105 cal block of desensitization to identify the quantal determinants of short-term plasticity and combin
109 we find that a combination of significantly quantal elements, six of seven atoms being hydrogen, bec
110 se-response relationships for all (including quantal) endpoints can be recast as relating to an under
111 stablishing the magnitude of the fundamental quantal event at this peripheral sensory synapse, we pro
114 f calcium (Ca2+) was applied to study evoked quantal events before and after LTP induction at the sam
115 s and stellate cells by triggering bursts of quantal events either with alpha-latrotoxin or with high
117 c currents and the frequency of asynchronous quantal events, and abolishes the activity-induced recru
118 synapses, have fewer spontaneous inhibitory quantal events, and exhibit reduced expression of inhibi
121 ffers a significant metabolic advantage over quantal excitatory postsynaptic currents--an advantage t
122 evice will enable high-throughput studies of quantal exocytosis and may also find application in rapi
123 alyte ferricyanide and perform recordings of quantal exocytosis from bovine adrenal chromaffin cells
124 indium tin oxide (ITO) electrodes to measure quantal exocytosis from cells in microfluidic channels.
125 scharge their contents during the process of quantal exocytosis, but microfabricated devices offer th
128 by spontaneous photopigment activation or by quantal fluctuations in photon absorption, but was inste
134 ptor agonist (JWH133 or GP1a) for 7-10 days, quantal glutamate release became more frequent and spine
135 and is comparable to the measured exocytotic quantal glutamate release in amperometric glutamate sens
139 how these constraints give rise to adaptive quantal information sampling in time, which maximises in
140 Our main message is that stochasticity in quantal information sampling is less noise and more proc
142 bition of PVN neuronal activity: a synaptic, quantal inhibitory modality (IPSCs, I(phasic)) and a sus
143 uctances allows three modes of transmission: quantal, ion accumulation and resistive coupling to be m
144 s potentiation to an increase in the size of quantal IPSC, suggesting a strengthening of the postsyna
146 mplitude in L2/3 neurons or the amplitude of quantal L4-L2/3 synaptic responses measured in strontium
150 f the connections could be described using a quantal model that assumed simple binomial statistics.
152 ntact vertebrate central nervous system, the quantal nature of synaptic transmission is difficult to
155 ation with green glutamate sensors to relate quantal neurotransmission to presynaptic Ca(2+) kinetics
156 a whole brain with eye attached preparation, quantal neurotransmission was examined in the turtle bra
157 inherent response variability expected from quantal neurotransmitter release, and thereby confers th
162 major determining factor for the slope of a quantal, population concentration-response curve is indi
163 We demonstrate that yolk proteolysis is a quantal process in which a subset of dormant YPs within
164 flash amplitudes suggests they represent the quantal product of one or more polyribosomes, while inte
165 d the release of ATP that directly activated quantal purinergic currents in the pyramidal neurons.
166 ic and postsynaptic sites by increasing both quantal release and expression of AChR subunits and othe
167 eveals largely normal synaptic transmission, quantal release and trans-synaptic homeostatic compensat
169 s accumulate neurotransmitters, enabling the quantal release by exocytosis that underlies synaptic tr
170 ggest why each active zone averages only one quantal release event during every other action potentia
171 that a change in the efficacy of spontaneous quantal release events is sufficient to trigger the indu
172 icotinic acetylcholine receptors (nAChRs) by quantal release of acetylcholine (ACh) from motoneurons
175 Kinetic analysis of miniature EPSCs revealed quantal release of mixed events associating AMPARs and N
176 bending or direct application of JA caused a quantal release of oxidizable material from gland cells
179 h components reflect variations in hair-cell quantal release rates and are eliminated by pharmacologi
180 ipophylic dye FM1-43 and focal recordings of quantal release to investigate how synapsin affects vesi
182 nals reduced vesicular docking and inhibited quantal release, indicating a direct and selective synap
183 of presynaptic syt-IV increased spontaneous quantal release, whereas a loss of postsynaptic syt-IV i
189 nd production predicted by Nash Equilibrium, Quantal Response Equilibrium, level-k cognition, fictiti
194 ic photoreceptor responses, governed by four quantal sampling factors (limitations): (i) the number o
195 s of exocytotic events, and (iii) monitoring quantal secretory events from thin slices of the adrenal
197 pe vs CaSR(-/-) pairs) with little change in quantal size (23 +/- 4 pA vs 22 +/- 4 pA) or number of r
198 asticity expression components, reduction in quantal size (a postsynaptic property) contributing to L
203 rometric spike half-widths without change in quantal size after either myosin II inhibition or actin
204 logical analysis demonstrated an increase in quantal size and a concomitant decrease in quantal conte
205 nfirmed by estimates of release probability, quantal size and contact number at the AOB-to-ACP synaps
207 ase in striatal slices and reductions in the quantal size and release frequency of catecholamine in d
208 These data demonstrate that ACh controls the quantal size and release frequency of glutamate at haben
210 ocytosis modes and their roles in regulating quantal size and synaptic strength, generating synaptic
211 in synaptic vesicles determines postsynaptic quantal size and thus the strength of synaptic transmiss
212 olecular determinants of vesicle filling and quantal size are regulated by neuronal activity in an op
214 onsolidation resulting in a normalization of quantal size at the few remaining functional synapses.
217 itional quantal analysis that attributes the quantal size change to a postsynaptic mechanism, the pre
220 analysis revealed a gradual augmentation in quantal size during trains of EPSCs, and application of
221 auses a transient reduction in AMPA receptor quantal size followed by synaptic consolidation resultin
222 ssion, expressed as a compensatory change in quantal size following chronic activity perturbation, is
223 a2+ produces a reduction in the postsynaptic quantal size in addition to its known effect on release
224 e fusion, parallels PTP, suggesting that the quantal size increase also contributes to the PTP genera
228 e of our previous studies, suggests that the quantal size increase is caused by a presynaptic mechani
229 osmolarity influences quantal size, causing quantal size increases under hypotonic conditions, presu
231 the calcium-dependent effect on postsynaptic quantal size is mediated by group 1 metabotropic glutama
233 oading into synaptic vesicles, and increased quantal size of asynchronous released vesicles but did n
234 ms: an increase in the frequency but not the quantal size of Ca2+ syntillas, which are brief, focal C
237 ntent of the TS-eEPSCs without affecting the quantal size or release probability, suggesting a reduct
238 creased amplitude reflects a decrease in the quantal size per mf-CA3 synapse and in the number of act
240 , then, likely a reflection of the increased quantal size rather than any direct effect on exocytosis
248 amine was quantal and calcium-dependent, but quantal size was much less than expected for large dense
252 influx, readily releasable SV pool size, and quantal size were unaltered, the reduced synaptic streng
253 one dimensions correlate with an increase in quantal size without a change in presynaptic vesicle siz
254 otransmitter content of individual vesicles (quantal size), whereas deletion of all AP-3 produces a d
257 learance and little delayed release, a large quantal size, and fast AMPA-type glutamate receptors.
258 ionally, extracellular osmolarity influences quantal size, causing quantal size increases under hypot
260 nt GABAergic neurons show reduced inhibitory quantal size, consistent with a presynaptic reduction in
261 to enhanced transmitter release and a larger quantal size, indicating enhanced responsiveness to indi
262 along axons had a distribution with the same quantal size, indicating that a vesicle releases all the
263 c K(+) at a glutamatergic synapse influenced quantal size, indicating that synaptic vesicle K(+)/H(+)
265 CIH also produced no changes in TS-eEPSC quantal size, since the amplitudes of both low calcium-e
266 naptic transmission as a result of increased quantal size, suggesting that the loss of Caz in animals
267 While elevated VGLUT expression increases quantal size, the minimum number of transporters require
268 ic strength onto PNs as a result of a larger quantal size, whereas autaptic and heterosynaptic PV-PV
269 d, exocytosis of compound vesicles increases quantal size, which increases synaptic strength and cont
286 of all AP-3 produces a dramatic increase in quantal size; these changes were correlated with alterat
288 f AMPAR miniature events and compromised the quantal sizes of both AMPAR and NMDAR currents evoked at
289 bility fluctuation analysis revealed similar quantal sizes, but 4-times more functional release sites
291 necessary to trigger increases in excitatory quantal strength, few studies have been able to examine
292 Deprivation also increased the amplitude of quantal synaptic currents mediated by AMPA- and NMDA-typ
295 e showed no difference in either spontaneous quantal synaptic transmission or low frequency evoked sy
298 lity with reduced synaptic fidelity, reduced quantal transmission, and more orphaned presynaptic and
300 and strontium, showing that they result from quantal transmitter release at single release sites.