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1 7 Hz elevated the amount released per event (quantal size).
2 ts of transmitter per vesicle (i.e., reduced quantal size).
3 ion with pHoenix only slightly increased the quantal size.
4 quantal size and are potential regulators of quantal size.
5 by decreases in both release probability and quantal size.
6 pa, a catecholamine precursor that increases quantal size.
7 reas occupancy levels were only dependent on quantal size.
8 ause a small, but reproducible, reduction in quantal size.
9 tamate and GABA in synaptic vesicles reduces quantal size.
10 mechanism of release controls both rate and quantal size.
11 subunit (inhibiting PKA activity) increases quantal size.
12 vation results in a compensatory increase in quantal size.
13 of a receptor-mediated mechanism that alters quantal size.
14 ave an estimate of histogram peak spacing or quantal size.
15 an increase and a decrease, respectively, in quantal size.
16 ncentration and thus controlled postsynaptic quantal size.
17 ine reduces synaptic vesicle transmitter and quantal size.
18 ent with a change in quantal content but not quantal size.
19 eases in release probability or postsynaptic quantal size.
20 oorly understood but are key determinants of quantal size.
21 ontent and a PKC-independent increase of the quantal size.
22 distinct, presynaptic mechanism to regulate quantal size.
23 uestions about the presynaptic regulation of quantal size.
24 esicle filling also contribute to changes in quantal size.
25 t this synapse, involves a reduction in EPSC quantal size.
26 pontaneous quantal release with no change in quantal size.
27 that intracellular Ca2+ stores can regulate quantal size.
28 amplitude miniature IPSCs and larger BC-->GC quantal size.
29 role of postsynaptic activity in controlling quantal size.
30 PC12 cells produced a unimodal population of quantal sizes.
31 pe vs CaSR(-/-) pairs) with little change in quantal size (23 +/- 4 pA vs 22 +/- 4 pA) or number of r
32 asticity expression components, reduction in quantal size (a postsynaptic property) contributing to L
33 examined the mechanism underlying increased quantal size after block of synaptic activity at the mam
34 it appears likely that the site of increased quantal size after chronic block of activity is presynap
35 rometric spike half-widths without change in quantal size after either myosin II inhibition or actin
36 % increase) of elementary synaptic currents (quantal size) after kindling results directly from a 75%
39 ry synapses, in terms of larger postsynaptic quantal size amplitudes, in part because they likely con
41 logical analysis demonstrated an increase in quantal size and a concomitant decrease in quantal conte
42 unction (NMJ): a PKA-dependent modulation of quantal size and a retrograde regulation of presynaptic
43 ns suggest that RYRs are essential to normal quantal size and are potential regulators of quantal siz
45 on in small synaptic vesicles increased both quantal size and frequency, consistent with the recruitm
48 ase in striatal slices and reductions in the quantal size and release frequency of catecholamine in d
49 These data demonstrate that ACh controls the quantal size and release frequency of glutamate at haben
51 ocytosis modes and their roles in regulating quantal size and synaptic strength, generating synaptic
52 sary for the developmental increase in AMPAR quantal size and that metabotropic glutamate receptor ac
53 in synaptic vesicles determines postsynaptic quantal size and thus the strength of synaptic transmiss
56 increases in either total receptor number or quantal size, and differences between the variability of
57 learance and little delayed release, a large quantal size, and fast AMPA-type glutamate receptors.
58 f functional release sites, relatively large quantal size, and unusual dynamics of transmitter releas
60 olecular determinants of vesicle filling and quantal size are regulated by neuronal activity in an op
61 t the receptor subunit composition regulates quantal size, Argiotoxin sensitivity, and receptor desen
64 onsolidation resulting in a normalization of quantal size at the few remaining functional synapses.
65 propose that presynaptic activity modulates quantal size at the neuromuscular junction by modulating
70 whereas for mGluR-LTD there was no change in quantal size, but a large decrease in the frequency of e
71 tely 50-fold, in part through an increase in quantal size, but primarily through an increase in the n
73 bility fluctuation analysis revealed similar quantal sizes, but 4-times more functional release sites
74 turation in turn makes it possible to modify quantal size by altering the flux of transmitter through
77 ion of a putative VAChT and demonstrate that quantal size can be regulated by changes in vesicular tr
78 s established that, for dense-core granules, quantal size can be varied by stimulation frequency, cha
79 ionally, extracellular osmolarity influences quantal size, causing quantal size increases under hypot
80 itional quantal analysis that attributes the quantal size change to a postsynaptic mechanism, the pre
82 and show a dramatic increase in presynaptic quantal size consistent with defects in synaptic vesicle
84 nt GABAergic neurons show reduced inhibitory quantal size, consistent with a presynaptic reduction in
88 when the combined variances of the noise and quantal-size distributions were reduced, increasing the
89 lysis of miniature EPSCs revealed that AMPAR quantal size doubled over time in vitro whereas NMDAR qu
90 analysis revealed a gradual augmentation in quantal size during trains of EPSCs, and application of
91 roM) reduced both the evoked current and the quantal size (estimated with MPF analysis) to a similar
93 sed on large numbers of trials, and that the quantal size estimates from the binomial method with N h
95 auses a transient reduction in AMPA receptor quantal size followed by synaptic consolidation resultin
96 ssion, expressed as a compensatory change in quantal size following chronic activity perturbation, is
98 a2+ produces a reduction in the postsynaptic quantal size in addition to its known effect on release
99 examined the mechanism underlying increased quantal size in ClC mice and found that it also appeared
101 e fusion, parallels PTP, suggesting that the quantal size increase also contributes to the PTP genera
105 e of our previous studies, suggests that the quantal size increase is caused by a presynaptic mechani
106 osmolarity influences quantal size, causing quantal size increases under hypotonic conditions, presu
107 to enhanced transmitter release and a larger quantal size, indicating enhanced responsiveness to indi
108 along axons had a distribution with the same quantal size, indicating that a vesicle releases all the
109 c K(+) at a glutamatergic synapse influenced quantal size, indicating that synaptic vesicle K(+)/H(+)
112 sicle volume, our results indicate that when quantal size is altered via the vesicular monoamine tran
114 ecent studies suggest that the modulation of quantal size is associated with corresponding changes in
116 DGluRIIA, since PKA-dependent modulation of quantal size is lost in homozygous viable DGluRIIA- muta
117 the calcium-dependent effect on postsynaptic quantal size is mediated by group 1 metabotropic glutama
119 Moreover, although elevated K+ can increase quantal size it acts by a pathway that does not involve
120 tentiates dopamine (DA) release by elevating quantal size, longer term exposure to L-DOPA (48 hr) pro
122 lease (quantal content), without a change in quantal size (mEPSC amplitude), compensates for altered
124 one could produce an appreciable increase in quantal size, normally attributed to either the presence
125 s release, yielded distributions with a mean quantal size of 0.55 +/- 0.01 nS and a CV of 0.37 +/- 0.
126 transport is the limiting factor determining quantal size of 5-HT and histamine release, intragranula
128 ms: an increase in the frequency but not the quantal size of Ca2+ syntillas, which are brief, focal C
135 f AMPAR miniature events and compromised the quantal sizes of both AMPAR and NMDAR currents evoked at
137 ntent of the TS-eEPSCs without affecting the quantal size or release probability, suggesting a reduct
138 r monoamine transport blocker that decreases quantal size, or l-dopa, a catecholamine precursor that
141 creased amplitude reflects a decrease in the quantal size per mf-CA3 synapse and in the number of act
143 analysis to compare the release probability, quantal size (q) and number of release sites (n) at moss
144 r of release sites (N) kept constant but the quantal size (Q) and the release probability (Pr) allowe
147 bility of neurotransmitter release (Pr), the quantal size (q), and the so-called potency, which is de
152 , then, likely a reflection of the increased quantal size rather than any direct effect on exocytosis
159 At a single set of synapses, the increase in quantal size seen with long-term potentiation was comple
161 CIH also produced no changes in TS-eEPSC quantal size, since the amplitudes of both low calcium-e
162 oic acid (NPPB) antagonized the increases in quantal size, so it seems likely that Cl(-) follows H(+)
163 naptic transmission as a result of increased quantal size, suggesting that the loss of Caz in animals
164 synaptic currents at any synapse and a large quantal size that facilitates the resolution of spontane
165 VGLUT in motoneurons leads to an increase in quantal size that is accompanied by an increase in synap
167 While elevated VGLUT expression increases quantal size, the minimum number of transporters require
168 of all AP-3 produces a dramatic increase in quantal size; these changes were correlated with alterat
169 perometric events, indicating an increase in quantal size: this reflects either an increase in vesicu
177 ver, previous measurements showed that after quantal size was increased the vesicles in the terminal
178 letely blocked in both control and ClC mice, quantal size was large in both groups despite the higher
180 amine was quantal and calcium-dependent, but quantal size was much less than expected for large dense
185 m granules in VMAT2(+/-) cells revealed 5-HT quantal size was reduced more than that of histamine.
188 By using miniature IPSC amplitudes to infer quantal size, we estimated that unitary IPSCs associated
189 the correction procedure is that changes in quantal size were a major factor in obscuring peaks in h
190 influx, readily releasable SV pool size, and quantal size were unaltered, the reduced synaptic streng
191 otransmitter content of individual vesicles (quantal size), whereas deletion of all AP-3 produces a d
192 ively active PKA catalytic subunit decreases quantal size, whereas overexpression of a mutant PKA reg
193 d, exocytosis of compound vesicles increases quantal size, which increases synaptic strength and cont
195 there was a significant decrease in unitary quantal size, which was not due to postsynaptic receptor
196 one dimensions correlate with an increase in quantal size without a change in presynaptic vesicle siz
197 econd, GDNF elicited a small increase in the quantal size, without affecting the average rise and dec
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