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1 de insight as to the mechanisms underpinning short term plasticity.
2 ion, as well as for modeling the dynamics of short-term plasticity.
3 naptic conductance waveform and postsynaptic short-term plasticity.
4 e to maintain a fixed EPSC-IPSC ratio during short-term plasticity.
5  differentially poised for exocytosis shapes short-term plasticity.
6 c facilitation, and protracted maturation in short-term plasticity.
7 gs at CA3/CA1 synapses revealed a deficit in short-term plasticity.
8 hout altering basal synaptic transmission or short-term plasticity.
9 ograde way, resulting in altered presynaptic short-term plasticity.
10 r contributing significantly to this form of short-term plasticity.
11  in more detail and identifies its impact on short-term plasticity.
12 (iii) cbl-b null mice show an enhancement in short-term plasticity.
13 r collateral axons have target-cell specific short-term plasticity.
14 T1 at distinct synaptic sites with different short-term plasticity.
15  for determining basal synaptic strength and short-term plasticity.
16  recruitment determines basal SV priming and short-term plasticity.
17 n mean amplitude, failure rate, kinetics and short-term plasticity.
18 ion of EPSP slope, a measure of pre-synaptic short-term plasticity.
19 us trains, varying 2-fold or more because of short-term plasticity.
20  cycle, modulating synaptic transmission and short-term plasticity.
21 scharged them after induction of presynaptic short-term plasticity.
22 ng-term synaptic plasticity without altering short-term plasticity.
23 ential-evoked release probability and alters short-term plasticity.
24 c, continuously changing because of synaptic short-term plasticity.
25 hips between initial release probability and short-term plasticity.
26 nsmitter release, synaptic transmission, and short-term plasticity.
27 e into functional circuits and show enhanced short-term plasticity.
28 pletion of synaptic vesicles determined this short-term plasticity.
29 TD without a change in basal transmission or short-term plasticity.
30 lly contributes to both the excitability and short-term plasticity alterations that we observed.
31 n and suggest that, in addition to effecting short-term plasticity, AMPA receptors regulate genes inv
32                                 Furthermore, short-term plasticity and calcium sensitivity of neurotr
33 tion to identify the quantal determinants of short-term plasticity and combine these with a short-ter
34     In the current paper it is proposed that short-term plasticity and dynamic changes in the balance
35                      Whereas both inhibitory short-term plasticity and miniature IPSC frequency and a
36 nnels by CaS proteins is required for normal short-term plasticity and normal encoding of information
37 tsynaptic inactivation of presenilins alters short-term plasticity and synaptic facilitation.
38 for the first time how the interplay between short-term plasticity and temporal summation mediates th
39  Nxph1 plays an instructive role in synaptic short-term plasticity and the configuration with GABA re
40 naptic and ectopic sites in the magnitude of short-term plasticity and the proportions of Ca2+ channe
41 nc13-2-mediate opposite forms of presynaptic short-term plasticity and thus differentially affect neu
42                        Rapid cold hardening (short-term plasticity) and developmental acclimation (lo
43 able to residual calcium (Ca(res))-dependent short-term plasticities, and the actions of neuromodulat
44  readily releasable pool of vesicles, alters short-term plasticity, and changes the properties of evo
45 e showed normal basal synaptic transmission, short-term plasticity, and decremental long-term potenti
46 ase probability, Ca2+ dependence of release, short-term plasticity, and fusion pore kinetics.
47 ces in some but not all forms of presynaptic short-term plasticity, and heterogeneity in the short te
48               Thus, basal synaptic strength, short-term plasticity, and homeostasis are determined in
49 synapses with appropriate receptor kinetics, short-term plasticity, and long-term dendritic spike-tim
50 ngstanding debate about a widespread form of short-term plasticity, and will enable future studies th
51     Here we show that, although a variety of short-term plasticities are normal, LTP at mossy fibre s
52                             Several forms of short-term plasticity are caused largely by changes in t
53 in presynaptic release probability (Pr ) and short-term plasticity are intriguing features of cortica
54 est that alterations in presynaptic forms of short-term plasticity are linked to alterations in prepu
55 ngs suggest that basal synaptic strength and short-term plasticity are regulated at the level of rele
56  investigated whether specific mechanisms of short-term plasticity are regulated in a target-dependen
57                 Our results identify altered short-term plasticity as a neural substrate underlying t
58 surable change in basal synaptic strength or short-term plasticity as analyzed in cultured cortical n
59 evoked release, they differentially affected short-term plasticity as assessed by the paired-pulse ra
60 nstrating the dominant role of timing in the short-term plasticity as well as the immediate response
61 pocampus are distinctive for their prominent short-term plasticity, as studied in slices.
62  We show how the differential recruitment of short-term plasticity at breathing versus sniffing frequ
63 ed a method of quantitatively characterizing short-term plasticity at cortical synapses that permits
64 t ultrastructural abnormalities and impaired short-term plasticity at dentate gyrus-CA3 excitatory sy
65 ere a progressive derailment of both LTD and short-term plasticity at perirhinal synapses.
66 d a novel mechanism for target cell-specific short-term plasticity at Schaffer collateral synapses in
67  This property presumably reflects the ample short-term plasticity at the corticogeniculate synapse.
68  targeting and are accompanied by changes in short-term plasticity at the mossy fiber/CA3 circuit.
69                             Here, we studied short-term plasticity at the reciprocal synapse between
70 els can account for the Ca(2+) dependence of short-term plasticity at these synapses.
71 ere, we report that these receptors regulate short-term plasticity at two loci in the corticothalamic
72 reduced paired-pulse facilitation, a form of short term plasticity attributed to presynaptic mechanis
73   The model predicts that the differences in short-term plasticity between synapses onto CA1 pyramida
74 ein receptor (SNARE) proteins play a role in short-term plasticity, Botulinum toxins A, E, and F, wer
75  a stimulus train and does not contribute to short-term plasticity, but induces a steady-state, async
76   Cortical synapses exhibit several forms of short-term plasticity, but the contribution of this plas
77  excitatory synaptic transmission and effect short-term plasticity, but they do not directly regulate
78 gest that NCS-1 acts as a calcium sensor for short-term plasticity by facilitating neurotransmitter o
79       Hyperpolarization may effect a form of short-term plasticity by promoting recovery from sodium
80 lease of 0, 1 or multiple vesicles), P(RRV), short-term plasticity, calcium transients and the requis
81 hat interactions between multiple sources of short-term plasticity can account for the complex kineti
82                                     However, short-term plasticity causes synapses to act as temporal
83 supply to variable demand and thus influence short-term plasticity characteristics and synaptic funct
84 display unique time- and frequency-dependent short-term plasticity characteristics in response to spi
85 synaptic kainate receptors contribute to the short-term plasticity characteristics of mossy fiber syn
86 ned this hypothesis by investigating whether short-term plasticity contributes to the temporal filter
87                                 The observed short-term plasticity could enable mitral cells to overc
88 locker CNQX, and displayed multiple forms of short-term plasticity (depression in approximately 70% t
89                                              Short-term plasticity differentially alters responses fr
90                         Here we compared the short-term plasticity displayed by a neocortical and a h
91 cilitation, suggesting that any differential short-term plasticity does not reflect differences in th
92               At most synapses in the brain, short-term plasticity dynamically modulates synaptic str
93                                              Short-term plasticity endows synapses with nonlinear tra
94 itation and temporal summation, two forms of short-term plasticity essential for working memory.
95             Synaptic depression is a form of short-term plasticity exhibited by many synapses.
96                                 All forms of short-term plasticity failed to significantly affect ong
97                     Together, they determine short-term plasticity features that are superficially si
98  may thus be useful tools for characterizing short-term plasticity from multi-electrode spike recordi
99 proaches for estimating synaptic weights and short-term plasticity from pre- and postsynaptic spike o
100 on rapid timescales, but no suitable form of short-term plasticity has been identified that is both a
101                  Although it is presynaptic, short-term plasticity has been shown at some synapses to
102                                         Thus short-term plasticity has real, important functional con
103          Target cell-specific differences in short-term plasticity have been attributed to difference
104 e smaller global Ca(2+) increases to produce short-term plasticity have remained elusive.
105  of both normal channel protein turnover and short-term plasticity, how is the balance of membrane co
106 riven by one instruction for learning causes short-term plasticity in a Purkinje cell's mossy fiber/p
107  of presynaptic terminals that can influence short-term plasticity in a stimulus-dependent manner.
108  in weaker synapses that are less capable of short-term plasticity in aged individuals, and therefore
109                          Previous studies of short-term plasticity in central nervous systems synapse
110 abbits is divided into two opposing forms of short-term plasticity in different cell classes.
111 riments that elucidate how facilitation, and short-term plasticity in general, contributes to circuit
112 osensitivity, the discovery of long-term and short-term plasticity in hypoxic ventilatory regulation,
113  described "augmenting responses," a form of short-term plasticity in some thalamocortical pathways t
114 wo interconnected neurons exhibited enhanced short-term plasticity in terms of paired pulse ratio (PP
115  on itself exhibited a trend toward enhanced short-term plasticity in terms of PPR and Pr.
116  and altered basal synaptic transmission and short-term plasticity in the CA1 region of the hippocamp
117          Here we looked for the signature of short-term plasticity in the fine-timescale spiking rela
118 therefore play a critical role in regulating short-term plasticity in the olfactory system.
119 putative monosynaptic interactions reflected short-term plasticity in their dynamic and predictable m
120 ) regulate glutamate release probability and short-term plasticity in various areas of the brain.
121 MKII promoter led to deficits in presynaptic short-term plasticity including paired-pulse facilitatio
122 rst discharge >14 Hz and showed considerable short-term plasticity, including paired-pulse depression
123 nt species and is considered to be a form of short-term plasticity inherent to the processing of sens
124 eedback pathway, the different components of short-term plasticity interacted to increase EPSC amplit
125                                     Synaptic short-term plasticity is a key regulator of neuronal com
126                                              Short-term plasticity is a pervasive feature of synapses
127 ar and tufted neurons, and that this form of short-term plasticity is attributable to a reduction of
128                                     Although short-term plasticity is believed to play a fundamental
129 ven the polarity, of that activity-dependent short-term plasticity is changed.
130 tion of synaptic vesicle fusion kinetics and short-term plasticity is critical for rapid encoding and
131 , indicating that the uniquely robust mf-CA3 short-term plasticity is KAR independent.
132 short-term changes in the state of synapses, short-term plasticity is often thought of as a mechanist
133  transmit a range of frequencies in spite of short-term plasticity is poorly understood.
134 owever, paired-pulse facilitation, a form of short-term plasticity, is significantly decreased in BDN
135 the normal maturation of synaptic inhibitory short-term plasticity (iSTP) in the auditory cortex, and
136 entiation (PTP) is a widely observed form of short-term plasticity lasting for tens of seconds after
137                                              Short-term plasticity may contribute, therefore, to temp
138 ibition (DSI) is an endocannabinoid-mediated short-term plasticity mechanism that couples postsynapti
139                                         Such short-term plasticity might also contribute to spatio-te
140 ort-term plasticity and combine these with a short-term plasticity model and cumulative excitatory po
141                  The molecular mechanisms of short-term plasticity observed during synaptic transmiss
142 rt-term plasticity, and heterogeneity in the short term plasticity of synapses onto interneurones.
143 ed-pulse and tetanic depression, whereas the short-term plasticity of asynchronous release has not be
144  the properties and underlying mechanisms of short-term plasticity of asynchronous release.
145                          We investigated the short-term plasticity of both the mitral-to-granule exci
146                   These results suggest that short-term plasticity of cortical synapses could shape t
147 hus demonstrating spiking activity-dependent short-term plasticity of electrical synapses.
148 atory and inhibitory neuron and incorporated short-term plasticity of EPSPs and IPSPs and slow IPSPs.
149                                              Short-term plasticity of EPSPs with increasing frequency
150                       We show that, in vivo, short-term plasticity of excitatory inputs to CA3 pyrami
151 (KO) of Rab3B does not alter the strength or short-term plasticity of excitatory or inhibitory synaps
152  GABAB receptors, modulate the amplitude and short-term plasticity of excitatory synapses, a result n
153  stimulation, we isolated and quantified the short-term plasticity of GABAergic lateral IPSCs (L-IPSC
154                              Therefore, this short-term plasticity of GABAergic synaptic inputs is li
155  pyramidal cells and interneurones including short-term plasticity of inhibitory and excitatory synap
156                                              Short-term plasticity of L-IPSCs may thus influence the
157  amplitude, kinetics, voltage dependence and short-term plasticity of mossy fibre-mediated EPSCs.
158                                              Short-term plasticity of On- and Off-EPSPs, and its pote
159 rtex (V1) show pronounced adaptation-induced short-term plasticity of orientation tuning primarily at
160 he synchronization, temporal patterning, and short-term plasticity of spiking in projection neurons,
161            Surprisingly, the time course and short-term plasticity of synaptic signaling were nearly
162                                        Thus, short-term plasticity of the intracortical circuit can m
163 thermore, domain specific differences in the short-term plasticity of the postsynaptic response indic
164 ores the contributions to different forms of short-term plasticity of the readily releasable vesicle
165 , demonstrating that they are concerned with short-term plasticity of the synapse.
166 th differences in intrinsic excitability and short-term plasticity of their inputs.
167          Induction of LTP or LTD altered the short-term plasticity of transmission onto both pyramida
168 synthesis is required for long-term, but not short-term, plasticity of GABA release from type 1 canna
169 ptual framework for analyzing the effects of short-term plasticity on the I/E balance in disease mode
170 ges in the size of evoked synaptic currents, short-term plasticity, or apparent calcium dependence of
171 ad no effect on basal synaptic transmission, short-term plasticity, or LTP induced by several trains
172 tracellular Ca(2+) requirement for a form of short-term plasticity, post-tetanic potentiation (PTP) a
173 NMDAR) activation can trigger both long- and short-term plasticity, promote cell survival, and initia
174 ate of inhibitory inputs combined with their short-term plasticity properties, regardless of the actu
175  the reciprocal impact of different forms of short-term plasticity (reactivations) on a persistent fo
176 ic facilitation (SF) is a ubiquitous form of short-term plasticity, regulating synaptic dynamics on f
177 dependent manner, but the mechanisms of such short-term plasticity remain unknown.
178 nprimary auditory cortices, attention-driven short-term plasticity retunes neurons to segregate relev
179                                           In short-term plasticity, RIM1 accelerates the priming of s
180 ggest new mechanisms by which inhibition and short term plasticity shape neural responses.
181 significant role in three important forms of short-term plasticity: short-term depression, facilitati
182  adapting neurons connected by synapses with short-term plasticity, showing that the observed linear
183 ation that interacts with activity-dependent short-term plasticity so that the magnitude, and sometim
184                                              Short Term Plasticity (STP) has been shown to exist exte
185 ose-dependently (0.5-2 mg/kg, i.p.) impaired short-term plasticity (STP) and long-term potentiation (
186                                  Presynaptic short-term plasticity (STP) dynamically modulates synapt
187                                   Studies of short-term plasticity (STP) in the hippocampus, performe
188 examine how long-term potentiation (LTP) and short-term plasticity (STP) interact in two different ce
189                                         This short-term plasticity (STP) is a key determinant of neur
190 y of the postsynaptic interneuron, while the short-term plasticity (STP) of inhibitory-to-excitatory
191                                              Short-term plasticity (STP) represents a key neuronal me
192 ptic processes give rise to several forms of short-term plasticity (STP), which is believed to contro
193 napses show large variations in strength and short-term plasticity (STP).
194 this synapse reflects its functional role in short-term plasticity (STP).
195  in high-frequency synaptic transmission and short-term plasticity (synaptic depression and potentiat
196  were modeled by incorporating mechanisms of short-term plasticity that are known to be driven by res
197           Here, we examine the mechanisms of short-term plasticity that can influence transmission at
198 nd the ready releasable pool-key elements of short-term plasticity that define the ability of synapse
199 urs in aging, negatively regulated a form of short-term plasticity that enhances synaptic throughput.
200           Synaptic facilitation is a form of short-term plasticity that enhances synaptic transmissio
201  inner plexiform layer of the retina undergo short-term plasticity that may mediate different forms o
202 d here may represent a basic form of in vivo short-term plasticity that modifies neuronal function.
203         Facilitation is an important form of short-term plasticity that occurs in most synapses.
204  from incorporating nonlinear terms, such as short term plasticity, that provide theoretical advances
205 rachidonoylglycerol (2-AG)-dependent form of short-term plasticity, that is, depolarization-induced s
206 xhibit normal fast synaptic transmission and short term plasticity, they are severely impaired in in-
207 r control and an altered endocytosis affects short-term plasticity through quantal size changes.
208 n/secretion coupling, vesicle recycling, and short-term plasticity throughout the CNS.
209  modulate vagal brainstem circuits undergoes short-term plasticity via alterations in cAMP levels sub
210                                 Furthermore, short-term plasticity was disrupted in AC8-/- mice but n
211                    In contrast, this form of short-term plasticity was not further enhanced in RIM1al
212                                              Short-term plasticity was unchanged at CF-PC synapses, s
213 possible mechanisms for these differences in short-term plasticity, we developed a mechanistic mathem
214 lus protocols that invoke different forms of short-term plasticity, we find differences in some but n
215 he experimental basis for a general model of short-term plasticity, we studied three synapses in rat
216  presynaptic proteins, and impaired synaptic short term plasticity were observed in hippocampal neuro
217 nother cell type tend to show characteristic short-term plasticity, which varies from facilitating to
218    These results demonstrate the presence of short-term plasticity within spinal inhibitory circuits.
219                                              Short-term plasticity would allow rapid re-weighting tha

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