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1 ry conductances (i.e. approximately balanced synaptic currents).
2 Ca(2+) permeability and the waveform of the synaptic current.
3 temperature on the decay time constant of a synaptic current.
4 ers under motor neuron endings, and generate synaptic current.
5 c input was followed by a decrease in evoked synaptic current.
6 d a corresponding increase in AMPAR-mediated synaptic current.
7 e the size and the kinetics of the resulting synaptic current.
8 ncy of spontaneous excitatory and inhibitory synaptic currents.
9 re unlikely because Zn(2+) did not block the synaptic currents.
10 l recordings and reductions in NMDA-mediated synaptic currents.
11 in a dramatic acceleration of NMDAR-mediated synaptic currents.
12 5 mM as measured using spontaneous GABAergic synaptic currents.
13 frequency and size of spontaneous miniature synaptic currents.
14 PA glutamate receptor levels, and excitatory synaptic currents.
15 ndent effect on ethanol action in evoked and synaptic currents.
16 defects in activity-dependent regulation of synaptic currents.
17 oducing increased peak-to-peak modulation of synaptic currents.
18 euronal excitability and an increase in NMDA synaptic currents.
19 2 selectively reduced AMPA receptor-mediated synaptic currents.
20 ase without any change in the size of evoked synaptic currents.
21 appreciated, producing saturation effects on synaptic currents.
22 not preclude sensory-induced enhancement of synaptic currents.
23 decreases the strength of evoked excitatory synaptic currents.
24 had reduced inhibitory, but not excitatory, synaptic currents.
25 , leaving only "feedforward" thalamocortical synaptic currents.
26 mulation led to a 67% increase in inhibitory synaptic currents.
27 hroidine had no effect on VTA- or PPN-evoked synaptic currents.
28 AMPA-mediated over NMDA-mediated excitatory synaptic currents.
29 clamp, but had no effects on fast inhibitory synaptic currents.
30 apted despite essentially no gain control in synaptic currents.
31 pleting terminals of GABA slowed glycinergic synaptic currents.
32 at lowers input resistance increases unitary synaptic currents.
33 2+) transients amplify inspiratory-modulated synaptic currents.
34 of the A-type channel subunit Kv4.2 enhances synaptic currents.
35 y regulates spine growth and potentiation of synaptic currents.
36 kely accounting for the changes in miniature synaptic currents.
37 dent long-term depression of NMDA-R-mediated synaptic currents.
38 creases in the frequency of spontaneous mini-synaptic currents.
39 ithout blockade of inhibitory and excitatory synaptic currents.
40 mately 6x) and longer duration of inhibitory synaptic currents.
41 R spines and reduced rectification of MF-PYR synaptic currents.
42 litude and frequency of miniature inhibitory synaptic currents.
43 l model, and its regulation by intrinsic and synaptic currents.
44 in BCs was correlated with rapidly decaying synaptic currents.
45 rdings can be used to forecast modulation of synaptic currents.
46 ntrum through an increase in inhibitory post-synaptic currents.
47 ted a long-lasting increase in GABA-mediated synaptic currents.
48 o IMI responses, we found CCAP modulation of synaptic currents.
49 resent at synapses they contribute little to synaptic currents.
50 etermine both the shape and the amplitude of synaptic currents.
51 o able to prolong artificial excitatory post synaptic currents.
52 are correlated with a decrease in GABAergic synaptic currents.
54 receptor pool, as we observe no recovery of synaptic current after MK-801 synaptic blockade and wash
55 prefrontal cortex, miniature excitatory post synaptic current amplitude was slightly reduced, miniatu
59 creasing and increasing miniature excitatory synaptic currents amplitude/frequency, respectively.
60 TP was characterized by measuring inhibitory synaptic current amplitudes in response to repetitive st
61 for a link between Abeta-induced effects on synaptic currents and AD-relevant neuronal network oscil
62 is condition, they receive fewer spontaneous synaptic currents and are more prone to die during the c
64 tely increase NMDA receptor (NMDAR)-mediated synaptic currents and decrease AMPA receptor (AMPAR)/NMD
67 h, before the behavioral phenotype develops, synaptic currents and glutamate release were increased.
68 with a shift toward inward rectification of synaptic currents and increased expression of GluR1, but
72 ipulation is compensated for at the level of synaptic currents and receptive fields (RFs) in the soma
73 enuates GABA(A) receptor-mediated inhibitory synaptic currents and reduces sensitivity to exogenously
75 differential effects in elevating excitatory synaptic currents and surface GluA2 levels compared with
76 CREB activity increases both NMDAR-mediated synaptic currents and surface level of NMDARs, while inh
78 of the altered muscle membrane properties on synaptic currents and thus provides hitherto the most de
79 ties of neurons are also altered: inhibitory synaptic currents and vesicular gamma-aminobutyric acid
80 R-16/alpha7 AChRs, a consequent reduction in synaptic current, and predictable behavioral defects.
81 ent potentiation of NMDAR Ca(2+) permeation, synaptic currents, and Ca(2+) rises in dendritic spines.
82 These findings reveal a central role for synaptic currents, and especially inhibition, in the rel
83 olved both AMPA receptor-mediated changes in synaptic currents, and faster decay rates of NMDA recept
84 413L displays deficits in NMDAR trafficking, synaptic currents, and spine density, raising the possib
85 uration, level of background noise, ratio of synaptic currents, and strengths of short-term depressio
87 computational models, approximately balanced synaptic currents are also more energy efficient than ot
89 that significantly more frequent and larger synaptic currents are likely due to more numerous, large
93 ificant reduction of NMDAR-mediated ionic or synaptic current, as well as the surface expression of N
95 ncy of both miniature (mini) and spontaneous synaptic currents at excitatory and inhibitory synapses.
96 es on newborn GCs in adult mice, we examined synaptic currents at the developmental stage when NMDA r
99 itude of spontaneous excitatory postsynaptic synaptic currents between preterm and term MNTB neurons.
100 cytes significantly accelerated the onset of synaptic currents but did not alter action potential gen
101 sed propagation of GABA(A) receptor-mediated synaptic currents, but did not change significantly dire
102 reduction of PPN-evoked, and not VTA-evoked, synaptic currents by the alpha7-nAChR antagonist methyll
104 aptic NMDARs induces a lasting change in the synaptic current, by changing the subunit composition of
107 s exhibited prolonged NMDA receptor-mediated synaptic currents, caused by a deficit in glutamate upta
109 ides remained constant, the first changes in synaptic currents, compared to wild-type mice could be d
110 rticular, the slow decay of kainate receptor synaptic currents contrasts with the rapid deactivation
113 nd the presence or absence of EtOH-sensitive synaptic currents correlated with cell surface peptide l
114 ABA(A) receptor subunit mRNAs, and GABAergic synaptic current decay in the medial preoptic area (mPOA
116 le abolishing GABAA receptor-mediated phasic synaptic currents, did not reveal a tonic GABAA receptor
117 t clusters, spontaneous and evoked GABAergic synaptic currents disappeared in thalamocortical cells w
119 exhibiting electrically excitable membranes, synaptic currents, dopamine release, and substantial red
122 -4-isoxazolepropionic acid receptor-mediated synaptic current (eEPSC) amplitude in both lamina I and
123 Interestingly, the NMDA/AMPA ratio of the synaptic current elicited in mPFC neurons by afferent fi
125 mportant synaptic behaviors, excitatory post-synaptic current (EPSC), has been updated as a stretched
126 microM) reversibly inhibited excitatory post synaptic currents (EPSCs) recorded from subiculum neuron
127 Using these models, we show that balanced synaptic currents evoke fewer spikes per second than exc
128 ound to account for <3% of the PC inhibitory synaptic currents evoked by electrical stimulation.
129 y, both forms of plasticity uniformly scaled synaptic currents evoked by pulse trains, and these chan
131 siological experiments, larger NMDA-mediated synaptic currents, evoked in CA1 principal cells by Scha
132 effects on spontaneously occurring miniature synaptic currents, except that there is a decrease in re
133 g-lasting increases in sharp wave-associated synaptic currents, exhibits enhanced excitatory synaptic
135 ion ([Ca(2+)](i)) and changes in spontaneous synaptic current frequency caused by the neurotoxicant m
136 amacrine cells and by recording RB-mediated synaptic currents from AII amacrine cells in mouse retin
139 lish sharply delimited spatial domains where synaptic currents from one or another input appear to be
140 e a faster time constant of decay and evoked synaptic currents have a smaller NMDA/AMPA ratio than th
141 for the postsynaptic clustering of GABAARs, synaptic currents have been detected in neurons obtained
142 ulate brain function by generating tonic and synaptic currents; however, it remains unknown whether H
148 potentials, as well as action potentials and synaptic currents in anatomically identified CA1 and CA3
150 on of spontaneous, but not evoked, GABAergic synaptic currents in BLA principal neurons; the effect w
151 ificant reduction in amplitude of inhibitory synaptic currents in both cultured neurons and hippocamp
155 re informative spikes approximately balanced synaptic currents in cortical neurons can promote both c
156 st spiking activity followed by recording of synaptic currents in distinct types of anatomically iden
158 ergic interneurons triggers large inhibitory synaptic currents in dorsal striatal projection neurons,
162 e examined whether BRAG1 and BRAG2 influence synaptic currents in hippocampal CA1 pyramidal neurons u
163 Here we examined excitatory and inhibitory synaptic currents in human tissue samples obtained from
164 of D1/D5 receptors increased auditory-evoked synaptic currents in infragranular layers, prolonging lo
168 MDAR) antagonists, we demonstrate that NMDAR synaptic currents in NRG2 KOs are augmented at hippocamp
169 regulation of AMPA receptor (AMPAR)-mediated synaptic currents in pyramidal neurons of prefrontal cor
170 uency and amplitude of spontaneous miniature synaptic currents in rat hippocampal neurons in culture.
172 ture and amplitude of evoked excitatory post-synaptic currents in second-order neurons as well as inc
173 us pain, inward currents in DRG neurons, and synaptic currents in spinal cord neurons are all reduced
177 tion, with decreased amplitude of excitatory synaptic currents in the developing hippocampus and redu
178 educed the amplitude of evoked glutamatergic synaptic currents in the NAcore in an mGluR2/3-dependent
179 synapses in spinal cord slices by recording synaptic currents in the presence of a low-affinity comp
180 naptic currents, indicating a major role for synaptic currents in the relationship between cortical L
181 currents relative to AMPA receptor-mediated synaptic currents in the remaining transfected neurons w
184 We investigated in rat cerebellar slices synaptic currents in Unipolar Brush Cells (UBCs), which
185 whereas 100 mum Thio-THIP did not affect the synaptic currents in ventrobasal thalamus neurons or str
188 res exhibited potentiation of AMPAR-mediated synaptic currents, including an increase in the amplitud
189 redicted membrane potential as accurately as synaptic currents, indicating a major role for synaptic
190 en mGluRs were activated by trains of evoked synaptic currents instead of direct application of agoni
192 ent integration of excitatory and inhibitory synaptic currents is an important process for shaping th
193 he decay time course of GABAergic inhibitory synaptic currents is considerably faster when recorded w
194 t unitary amplitude of spontaneous miniature synaptic currents is decreased dramatically in FUS-ALS f
196 ileptic DGCs, the neurosteroid modulation of synaptic currents is diminished and alpha4 subunit-conta
197 with depression, direct proof for changes in synaptic currents is lacking in large brain areas such a
199 A balance between excitatory and inhibitory synaptic currents is thought to be important for several
201 , associated with higher-frequency miniature synaptic currents, larger long-term potentiation, and de
202 otostimulation with whole-cell recordings of synaptic currents makes it possible to map circuits betw
203 fluence of these subunits on GABAAR-mediated synaptic currents may help in identifying the roles and
204 e impact of nanomolar zinc concentrations on synaptic currents mediated by 2A-type NMDA receptors.
206 curs via the PKA pathway and does not affect synaptic currents mediated by AMPA or NMDA receptors.
207 tion also increased the amplitude of quantal synaptic currents mediated by AMPA- and NMDA-type glutam
208 ectrical synapses, and evoke slow inhibitory synaptic currents mediated by GABA(A) and GABA(B) recept
210 ferentially blocks extrasynaptic rather than synaptic currents mediated by NMDARs in the same neuron.
211 significantly inhibited evoked and miniature synaptic currents mediated by non-NMDA receptors through
212 of glutamate are voltage-independent, as are synaptic currents mediated by the electrically neutral n
213 DR neurons exhibit inhibitory 'phasic' post-synaptic currents mediated primarily by synaptic GABAA r
214 mice frequency of miniature excitatory post-synaptic currents (mEPSC) and inhibitory post-synaptic c
215 e exhibited normal miniature excitatory post-synaptic currents (mEPSC), suggesting that action-potent
216 e loss and smaller miniature excitatory post-synaptic currents (mEPSCs) in granule cells of the DG.
217 channels enhances miniature excitatory post-synaptic currents (mEPSCs) onto EC layer III pyramidal n
218 ynaptic currents (mEPSC) and inhibitory post-synaptic currents (mIPSC) are elevated at 2 weeks and, m
219 ked IPSCs (eIPSCs) and spontaneous miniature synaptic currents (mIPSCs) of visualized nRT cells in yo
220 (increased frequency of miniature excitatory synaptic currents, modestly enhanced long-term potentiat
221 he amplitude and duration of excitatory post synaptic currents near the action potential threshold.
222 We found that the amplitude of excitatory synaptic currents necessary to fire rodent pyramidal cel
224 hough field potentials (FPs) may reflect the synaptic currents of neurons near the recording electrod
226 es and the frequency of miniature excitatory synaptic currents onto CRH neurons were reduced in "care
227 passive integration of inspiratory-modulated synaptic currents or do active processes modulate these
228 There were no differences in the excitatory synaptic currents or the passive and active properties o
229 ariability in pyramidal cells as a result of synaptic current- or conductance-mediated membrane fluct
230 nism of GluN1a, reversibly blocks excitatory synaptic currents, prevents the induction of long-term p
237 the development of glycine-receptor-mediated synaptic currents recorded from the interneurons of the
238 of H2O2 on GABAA receptor-mediated tonic and synaptic currents recorded in cultured mouse hippocampal
241 and significantly reduced GABA(A)R-mediated synaptic currents relative to AMPA receptor-mediated syn
244 or kinetics, of spontaneous excitatory post-synaptic currents (sEPSC) in Dyt1 DeltaGAG heterozygous
245 We found no changes in the size of evoked synaptic currents, short-term plasticity, or apparent ca
248 lyses revealed an LTP-associated increase of synaptic current sinks in layer IV/lower layer II/III at
249 SC-CM increased the frequency of spontaneous synaptic currents (SSCs) within 3-15 min by an average o
251 es drove IN activity despite small amplitude synaptic currents, suggesting an active role in IN infor
252 ate (NMDA) receptor-mediated excitatory post-synaptic currents, suggesting intact excitatory transmis
253 examining the dopamine D2 receptor-mediated synaptic current that resulted from somatodendritic rele
254 he well described primary rod pathway, evoke synaptic currents that are preferentially mediated by CP
256 of serotype 1, 5, and 8 led to light-evoked synaptic currents that depressed much more than electric
257 also predicts accurately the faster decay of synaptic currents that is observed in spasmodic mice.
262 cells in the guinea pig retina and monitored synaptic currents that were evoked by visual stimulation
263 results to generate simulated M/T population synaptic currents that were injected into real cortical
265 nd depression, which modify the amplitude of synaptic currents, this activity-induced change in AMPA
268 in the significant reduction of disinhibited synaptic currents to healthy control levels, suggesting
269 ral interaction of excitatory and inhibitory synaptic currents to shape the firing pattern of the neu
270 s the amplitude of excitatory and inhibitory synaptic currents to the MSO and, moreover, show that th
271 activity reduced the LTP of these excitatory synaptic currents triggered by high-frequency stimulatio
272 ma receptor isoform produces slowly decaying synaptic currents typical of SCS that transit to a much
274 ng potentiation of NMDAR- and AMPAR-mediated synaptic currents via glucocorticoid receptors (GRs) sel
275 peak of the population discharge, the inward synaptic current was essentially mediated by glutamate r
284 s (PC-->DCN), light- and electrically evoked synaptic currents were remarkably similar for ChR2 expre
286 slightly reduced, miniature inhibitory post synaptic currents were unaffected, and intrinsic membran
288 a TH(+) neuron evoked a brief GABA-mediated synaptic current, whereas evoked dopamine release was as
289 apses selectively prolongs the decay time of synaptic currents, whereas a switch from GluR2-lacking t
290 n in AMPA- and NMDA-mediated excitatory post-synaptic currents, whereas the control peptide, TAT-myc,
291 ic responses as detected in larger miniature synaptic currents which are caused by enlarged presynapt
292 h other, generating negative correlations in synaptic currents which cancel the effect of shared inpu
293 ne receptor-mediated inhibitory postsynaptic synaptic currents, which were prevalent in preterm MNTB
295 tch-clamp recordings demonstrated excitatory synaptic currents with strikingly long duration and epil
296 ng-term plasticity of NMDA receptor-mediated synaptic currents with the polarity of plasticity determ
297 lockade of Cl- currents (including tonic and synaptic currents) with picrotoxin reduced interspike in
298 stsynaptic apparatus and generate functional synaptic currents within 4-6 h when cocultured with matu
299 s may provide a powerful means of amplifying synaptic currents without incurring plateau potentials o
300 in gene dramatically increased NR2A-mediated synaptic currents, without affecting AMPA receptor curre
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