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1 endent, indicating that the action of RBO is use dependent.
2                The activity of PD-307243 was use-dependent.
3 (V)1.7 by BPBTS was found to be voltage- and use-dependent.
4 rature sensitivity can be highly dynamic and use-dependent.
5                                              Use-dependent accumulating channel blockade progressivel
6 icantly different from WT-IKs and attenuated use-dependent accumulation of the current.
7 s property enables Kv1.2 channels to exhibit use-dependent activation during trains of very brief dep
8                 Our findings illustrate that use-dependent activation is a unique property of Kv1.2 t
9                                          The use-dependent activation of presynaptic mGluRs that we d
10 suggest that this strategic placement allows use-dependent activation of these synaptic modulators.
11  that other Kv1 channel types do not exhibit use-dependent activation, but this property is conferred
12 e kinetics of recovery from inactivation and use-dependent activity of the channel in both the presen
13 ceptors (NMDARs)-which play key roles in the use-dependent adaptation of glutamatergic synapses-along
14 the constraint, followed by a longer-lasting use-dependent aftereffect in the direction of the constr
15        It is widely thought that persistent, use-dependent alterations in synaptic strength such as l
16 after a small uIPSC1, suggesting that PPD is use dependent and due to a decrease in the quantal conte
17 f NMDAR currents (current run-down) that was use dependent and not readily reversible.
18 bition of 5-HT(3A)Rs and 5-HT(3AB)Rs was non-use dependent and voltage independent, suggesting buprop
19 e receptors (GlyRs) has been shown to be non-use-dependent and nonselective between the picrotoxin co
20 bryonic alpha2 homomeric GlyR is known to be use-dependent and reflects a channel-blocking mechanism,
21 d His-880 in Na(V)1.5 are proton sensors for use-dependent and slow inactivation and have implication
22 ivalent cation-pi interaction underlies both use-dependent and tonic block by TTX.
23 arative studies of chimeric channels between use-dependent and use-independent homologs, we have dete
24 Here, we identify the molecular basis of the use-dependent and voltage-independent inhibitory effect
25    Inhibition of Na+ currents by 8,9-EET was use dependent, and channel recovery was slowed.
26  signaling pathways, is neither voltage- nor use-dependent, and does not affect channel gating.
27 emporally-stable processes that are strictly use-dependent, and dynamically-evolving and context-depe
28             We then examined the action of a use-dependent antagonist of GluA2-containing AMPARs, phi
29 of synaptic NMDARs with a slowly reversible, use-dependent antagonist protected nearly fully against
30 uration in either chamber but induced potent use-dependent atrial-selective depression of the sodium
31 ted recombinant CPI-17 into cells produced a use-dependent attenuation of glutamate-evoked responses
32                 The overgrowth appears to be use-dependent because it can be prevented by restricting
33 chain (Me12), leads to a further increase of use-dependent behavior versus the phenyl Mex derivative
34 noxy-propranol-amine moiety, with consequent use-dependent behavior.
35   To understand the neural substrate for the use-dependent behavioral improvement, we studied the den
36                This effect is similar to the use-dependent biases observed for other movement paramet
37                               38 also showed use dependent block of Na(v)1.6 in HEK cells.
38 cell types but did not affect the frequency (use)-dependent block of Na(+) currents.
39                                              Use-dependent block (10 ms pulses to -10 mV, at 20 Hz) i
40       Flecainide (1-300 mM) caused tonic and use-dependent block (UDB) of I(Na) in a concentration-de
41  frequency-dependent manner, consistent with use-dependent block (UDB).
42 a frequency-dependent manner consistent with use-dependent block (UDB).
43            The terfenadine-induced tonic and use-dependent block and the steady state inhibition of I
44               The qualitative differences in use-dependent block appear to be the result of differenc
45 brane and cytoplasmic regions of IVS5 in the use-dependent block by diltiazem and verapamil.
46 panied by a reduced or by a complete loss of use-dependent block by diltiazem.
47 -fold, and mutations I409A and N418A reduced use-dependent block by etidocaine.
48 e paths should affect the characteristics of use-dependent block by influencing drug on- and off-rate
49                                 However, the use-dependent block by isradipine was retained by these
50 rane segments, shifted activation gating and use-dependent block by lidocaine toward that seen in hH1
51                                              Use-dependent block by mexiletine was greater in inactiv
52 tween inactivation gating of the channel and use-dependent block by phenylalkylamines and benzothiaze
53 ptor transmission is rendered sensitive to a use-dependent block by polyamine compounds.
54 udied affected inactivated-state affinity or use-dependent block by the neuroprotective drug sipatrig
55 mulated infrequently and produces additional use-dependent block during repetitive pulses.
56  the vastly different rates of recovery from use-dependent block for bupivacaine and lidocaine.
57 y slowed inactivation and a complete loss of use-dependent block for mutations in the cytoplasmic con
58 soform specificity can be attained, the huge use-dependent block may help in the development of new s
59 izing shift in activation curves and greater use-dependent block of Ca(V)3.2 channels.
60 ressed channels; (2) suggest that flecainide use-dependent block of DG channels underlies its therape
61                             The reduction in use-dependent block of F430C was consistent with alterat
62 onstrate that prenylamine has both tonic and use-dependent block of hNav1.5 channels similar to that
63 ntials, and (3) elicited a tonic block and a use-dependent block of ICa,L.
64                                 There was no use-dependent block of IFM/QQQ mutant channels with trai
65      Model simulations show that the reduced use-dependent block of IVS6 mutants derives primarily fr
66                                              Use-dependent block of Na(+) channel isoforms by ranolaz
67 issociates too fast to accumulate sufficient use-dependent block of Na+ currents.
68 lse ratio at L4-L2/3 synapses and slowed the use-dependent block of NMDA receptor currents by MK-801
69            We now characterize the tonic and use-dependent block of prenylamine on wild-type human ca
70 vity for the action of ranolazine to produce use-dependent block of sodium channels, leading to suppr
71 erpolarized potentials, whereas the enhanced use-dependent block of the IS6 mutant was due to a highe
72 assumes Class IC characteristics with potent use-dependent block of the sodium channel.
73 e effects of anticonvulsant drugs acting via use-dependent block of voltage-gated Na(+) channels on G
74 ilic drug of clinical relevance, by studying use-dependent block using a two-electrode voltage clamp
75 ry component with intermediate kinetics, and use-dependent block was attenuated in both W402A and W40
76                                              Use-dependent block was best explained by a significant
77 mutations in IIS6 (S804F) and IIIS6 (V1293I) use-dependent block was not statistically different from
78                                Recovery from use-dependent block was slowed when cardiac isoform-spec
79 F1236C mutant channels reduced recovery from use-dependent block, indicating an allosteric effect of
80  F1586C mutation only partially impaired the use-dependent block, suggesting that additional amino ac
81 d moderate unbinding kinetics explain potent use-dependent block, which we propose contributes to the
82 n I and F1236C in domain III exhibit reduced use-dependent block.
83  also markedly accelerated the recovery from use-dependent block.
84 nto the slow inactivated state, resulting in use-dependent block.
85 e conditions, and also induced resistance to use-dependent block.
86  the amino function enhance both potency and use-dependent block.
87 h greatly enhances high-affinity binding and use-dependent block.
88 icity and optimal alkyl chain length enhance use-dependent block.
89 rsal root ganglion (DRG) neurons indicated a use-dependent blockade of sodium channels.
90 imine maleate (MK-801), a well characterized use-dependent blocker of NMDA receptors.
91        Flecainide and RAD-243 retained their use-dependent blocking action and accelerated macroscopi
92 ticonvulsant drugs are known to exert potent use-dependent blocking effects on voltage-gated Na(+) ch
93 te of macroscopic inactivation and exhibit a use-dependent blocking phenomenon reminiscent of the act
94                               Both tonic and use-dependent blocks of ICa,L by terfenadine at -40 mV w
95 onal principles that govern the induction of use-dependent change in excitatory synaptic efficacy als
96    However, to date, evidence for persistent use-dependent change in the strength of this synapse has
97                                          All use-dependent changes appeared in the order NaV 1.8 KO >
98              However, animal studies showing use-dependent changes in motor cortex organization sugge
99 compound action potential (AP), we evaluated use-dependent changes in mouse peripheral nerves, and th
100 , providing an unexpected mechanism by which use-dependent changes in slow afterhyperpolarizations mi
101 ry to invoke such a mechanism to account for use-dependent changes in synaptic release probability.
102                                              Use-dependent changes in the behavior of potassium chann
103 Knocking out TTXr sodium channels influences use-dependent changes of conductive properties (action p
104 velopment and whether this is accompanied by use-dependent changes of inhibitory synaptic strength.
105                                              Use-dependent changes of latency, AP amplitude, and dura
106 activity is not the underlying mechanism for use-dependent changes of neural conduction.
107  of the functional alleles exhibited reduced use-dependent channel inhibition.
108 inly closed-state channels, although a small use-dependent component was observed in Ca(V)3.1 channel
109 ne promotes slow monomorphic VT, probably by use-dependent conduction slowing and wavelength shorteni
110 fast inactivation, which produced a profound use-dependent current attenuation not seen in the wild t
111 tions > or =60 micromol/L, the difference in use-dependent current reduction between IZs and NZs was
112     This potentiation was in contrast to the use-dependent decrease in current for Nav1.2 with beta1.
113                                          The use-dependent decrease in paired-pulse facilitation occu
114 naptic depression at these synapses and this use-dependent decrease in paired-pulse facilitation occu
115 This suggests that biases are not based on a use-dependent decrease in response strength but involve
116              Long-term depression (LTD) is a use-dependent decrease in synaptic efficacy widely recog
117                                  We observed use-dependent decreases of single fibre and compound act
118 mpounds produced concentration-dependent and use-dependent decrements in CAP amplitude, but cocaethyl
119 ciated GTPase Rab35 are key elements of this use-dependent degradative pathway.
120 ite morphology, indicating an upper limit of use-dependent dendrite growth.
121                                              Use-dependent depression at the fast-spiking interneuron
122                  Both EPSCs and IPSCs showed use-dependent depression during trains.
123  large changes in [Cl-]i that could underlie use-dependent depression of GABA-dependent synaptic tran
124                 Ranolazine produced a marked use-dependent depression of sodium channel parameters, i
125 ells led to an initial summation followed by use-dependent depression of the averaged postsynaptic re
126 has either been physiologically exhausted by use-dependent depression, or has been artificially deple
127 regulates recovery of synaptic vesicles from use-dependent depression, probably by a direct interacti
128 and vestibular synapses exhibit conventional use-dependent depression, weakening to a greater extent
129 gonists, the mechanisms responsible for this use-dependent down-regulation remain unclear.
130 in the therapeutically desirable property of use-dependent drug action.
131 below the selectivity filter, is critical in use-dependent drug block.
132 ng in neuronal networks is determined by the use-dependent dynamics of synaptic transmission.
133 nitric oxide cascade generates a short-term, use-dependent enhancement of release.
134  synaptic enhancement when combined with the use-dependent facilitation of MF synapses.
135  and blockade of this enzyme can enhance the use-dependent facilitation of neurohypophysial secretion
136 age-gated sodium and potassium currents in a use-dependent fashion, but had only a small effect on th
137 cking voltage-activated sodium channels in a use-dependent fashion.
138                                              Use-dependent fatigue accompanies many neuromuscular mya
139                                         This use-dependent fatigue is shown to be a consequence of a
140 neral muscle weakness is also accompanied by use-dependent fatigue.
141 on potential generation, thus accounting for use-dependent fatigue.
142  weakness, but is not solely responsible for use-dependent fatigue.
143 ociated contraction failures are manifest as use-dependent fatigue.
144 e, at the cortical level sleep has local and use-dependent features suggesting that it is a property
145 vation, with a 4-fold delay in recovery from use-dependent flecainide block.
146  suggests that neuroligins contribute to the use-dependent formation of neural circuits.
147                                              Use-dependent forms of synaptic plasticity have been ext
148                                  Substantial use-dependent functional upregulation was found for muta
149 tion of a subthreshold dose of picrotoxin, a use-dependent gamma-aminobutyric acid receptor antagonis
150 uromuscular junction, in the presence of the use-dependent glutamate receptor (GluR) blocker philanth
151 le residue that is apparently missing in the use-dependent homologs could largely eliminate the use d
152 ificantly reduced the maximum probability of use-dependent inactivation and slow inactivation, relati
153  terminated primarily by a highly localized, use-dependent inactivation of RyRs but not by the stocha
154 close to the resting potential, and enhanced use-dependent inactivation on high-frequency stimulation
155 proton block, abolished proton modulation of use-dependent inactivation, and altered pH modulation of
156 d slower recovery from inactivation, greater use-dependent inactivation, and reduced action potential
157 ery high threshold of activation and lack of use-dependent inactivation.
158  activation and deactivation kinetics and no use-dependent inactivation.
159 4)(=) influx, indicating that Sul2p exhibits use-dependent inactivation; the transport process itself
160    Recently, it has been demonstrated that a use-dependent increase in the density of dendritic spine
161 ivation processes and by inducing frequency (use)-dependent inhibition of Na(+) currents.
162 y cyclohexane, for example, strongly reduces use-dependent inhibition and speeds recovery of lidocain
163 cific inhibitor of cationic MSCs, showed the use-dependent inhibition characteristic of open channel
164  any of the substituted sites, high-affinity use-dependent inhibition displays substantial cation-pi
165 sting channels but induced a characteristic, use-dependent inhibition during rapid, repetitive stimul
166 under resting conditions but causes a potent use-dependent inhibition during repetitive depolarizatio
167 ceptors, which is a prevailing mechanism for use-dependent inhibition in the nucleus accumbens core a
168 agus nerve recordings, QX-314 induced marked use-dependent inhibition of C-spike amplitude, with IC50
169                             TROX-1 displayed use-dependent inhibition of Ca(V)2.2 with a 10-fold IC(5
170                  ACh also contributes to the use-dependent inhibition of DA release through muscarini
171                           Interestingly, the use-dependent inhibition of hippocampal neurons was depe
172                  Compound 4 exhibited strong use-dependent inhibition of hNa(v)1.5 with pIC50 values
173 F and wild-type sodium currents at baseline, use-dependent inhibition of I(Na) by lidocaine was more
174 he N395K mutation also significantly reduced use-dependent inhibition of lidocaine on Nav1.7 current.
175 diverging effects, we examined the effect of use-dependent inhibition of NMDA receptors on the sponta
176 ays enhanced slow inactivation and exhibited use-dependent inhibition of peak Na(+) currents during r
177 tivation of voltage-gated Ca(2+) channels or use-dependent inhibition of release machinery by presyna
178 akalant and ranolazine were characterized by use-dependent inhibition of sodium channel-mediated para
179                            Cocaine induced a use-dependent inhibition of the non-inactivating mutant
180 , these rapidly reversible blockers produced use-dependent inhibition through an unusual mechanism--t
181 ast and slow inactivation and enhancement of use-dependent inhibition.
182  Like the endogenous blocking protein, these use-dependent inhibitors bind most effectively at depola
183                                              Use-dependent inhibitors of voltage-gated sodium channel
184 philanthotoxins (PhTXs), and argiotoxins are use-dependent ion channel blockers of AMPARs widely empl
185  slow inactivation gating track the distinct use-dependent kinetic properties of diverse LA compounds
186 -redundant dimension, we were able to induce use-dependent learning by passively guiding movements in
187 a second study, we show that error-based and use-dependent learning can change motor behavior simulta
188       Here, we show that a second mechanism, use-dependent learning, simultaneously changes movements
189                   These mutations eliminated use-dependent lidocaine block with no effect on tonic/re
190 ) and in II-S6 (I782C and V786C) reduced the use-dependent lidocaine block.
191 esults show that lowering [Na+]o potentiates use-dependent lidocaine block.
192  direction of depolarization and antagonized use-dependent lidocaine inhibition of fast-inactivated s
193 mechanistic basis of depolarization-induced 'use-dependent' lidocaine block remains uncertain.
194 uronal pathway-dependent mechanism involving use-dependent, local sleep may be the main driver of res
195 f learning and memory are thought to involve use-dependent long-term changes in synaptic function, in
196             Thus, occurrence and polarity of use-dependent long-term changes of cortical response pro
197                                              Use-dependent long-term changes of neuronal response pro
198                      Block was enhanced in a use-dependent manner at higher stimulation rates.
199 )R antagonist, blocks neurotransmission in a use-dependent manner at rat hippocampal synapses and the
200 pyramidal neurons is reliably inhibited in a use-dependent manner by the prototypical Na(+) channel b
201 ynaptic NMDA receptors can be modulated in a use-dependent manner even when the postsynaptic membrane
202 acosamide, which blocks sodium channels in a use-dependent manner, attenuates pain in some patients w
203 apses can change their strength rapidly in a use-dependent manner, but the mechanisms of such short-t
204 sulfonanilide block is known to develop in a use-dependent manner, suggesting a potential role for in
205 xybutoxy)psoralen (PAP-1), blocks Kv1.3 in a use-dependent manner, with a Hill coefficient of 2 and a
206 y and inhibitory inputs into the muscle in a use-dependent manner.
207 tially decreased by MK-801 within 2 min in a use-dependent manner.
208 ase neurotransmitters and neuropeptides in a use-dependent manner.
209 a spark is less than unity and declines in a use-dependent manner.
210 ugs blocked the wild-type Na(+) channel in a use-dependent manner.
211 aptic strength is dynamically regulated in a use-dependent manner.
212 s AMPA receptors lacking GluR2 subunits in a use-dependent manner.
213 ents, sotalol prolonged the APD in a reverse use-dependent manner; such an effect was not seen with e
214 nel may undergo a physical modification in a use-dependent manner; thus, a model that closely simulat
215 nhibitory interneurons is weakened through a use-dependent mechanism involving group II metabotropic
216 hat reorganization is driven by passive, not use-dependent mechanisms.
217          Previously identified potent and/or use-dependent mexiletine (Mex) analogs were used as temp
218                                          The use-dependent model of paired-pulse responsiveness holds
219            However, the applicability of the use-dependent model to inhibitory synapses is controvers
220                                          The use-dependent modification of synapses is strongly influ
221 iable and that SRF plays a prominent role in use-dependent modification of synaptic strength in the a
222 val of retinal input on neural activity- and use-dependent modifications of cortical AChE activity.
223                                              Use-dependent modifications of synapses have been well d
224                                              Use-dependent modifications, such as long-term potentiat
225 NMDAR-dependent mechanisms and contribute to use-dependent modulation of circuit properties.
226 l TGF-beta signaling pathway is critical for use-dependent modulation of GABA(A) synaptic transmissio
227 onstrate that baclofen selectively maintains use-dependent modulation of largely subcortical but not
228                                  Persistent, use-dependent modulation of synaptic strength has been d
229 d change in cone-AC voltage gain exemplifies use-dependent modulations of synaptic transmission in th
230                                              Use-dependent movement therapies can lead to partial rec
231 two physiological processes is causal to the use-dependent muscle fatigue.
232 current may therefore be less susceptible to use-dependent Na channel inhibitors used as local anesth
233                                  619C89 is a use-dependent Na+ channel antagonist that decreases the
234 (LA) that elicits depolarization-dependent ('use-dependent') Na+ channel block, does not slow recover
235                         Our results reveal a use-dependent neural correlate for wearable technology a
236 srupted OFC activity in behaving rats with a use-dependent NMDA antagonist to model the NMDA hypofunc
237 facilitation and the rate of blockade by the use-dependent NMDA receptor blocker (+)-5-methyl-10,11-d
238                 Third, experiments using the use-dependent NMDAR blocker MK-801 show that these indir
239                         Experiments with the use-dependent NMDAR blocker, MK-801, indicate that poten
240 extrasynaptic receptors of a neuroprotective use-dependent NMDAR channel blocker, memantine.
241 s, different developmental strategies may be used, dependent on when in the year conception takes pla
242 is study, we reveal the existence of a novel use-dependent phenomenon in potassium channels, which we
243          In this study, we have examined the use-dependent phenomenon of three benzocaine homologs: e
244 a potential therapeutic target for promoting use-dependent plasticity after spinal cord injury.
245 ses that can be characterized as model-free: use-dependent plasticity and operant reinforcement.
246 tergic synapses shows a remarkable degree of use-dependent plasticity and such modifications may repr
247 hort-term depression is a widespread form of use-dependent plasticity found in the peripheral and cen
248 entify the underlying mechanisms, we studied use-dependent plasticity in human subjects premedicated
249 Aergic inhibition as mechanisms operating in use-dependent plasticity in intact human motor cortex an
250                          Tests were made for use-dependent plasticity in the cholinergic projections
251                            In humans, spinal use-dependent plasticity is inferred from modifications
252 dritic spines are now known to be subject to use-dependent plasticity that affects both their structu
253 r development and longer lasting duration of use-dependent plasticity under d-amphetamine compared to
254                                              Use-dependent plasticity was reduced substantially by de
255 nt a facilitatory effect of d-amphetamine on use-dependent plasticity, a possible mechanism mediating
256           The spinal cord is able to express use-dependent plasticity, as demonstrated in spinalized
257 een implicated in mediating several forms of use-dependent plasticity, but the mechanisms by which it
258                                              Use-dependent plasticity, thought to contribute to funct
259 n the mature cortex are subject to continual use-dependent plasticity.
260 facilitates the effects of motor training on use-dependent plasticity.
261 ulate the function of a pathway may underlie use-dependent plasticity.
262 uronal activity, potentially contributing to use-dependent plasticity.
263 ortex and probed the dynamical properties of use-dependent plasticity.
264 tiarrhythmic effect of sotalol has a reverse use-dependent positive inotropic effect in the intact he
265     Together, our experiments reveal a novel use-dependent, potent, and local mode of Abeta-mediated
266          The ACh concentration dependence of use-dependent potentiation and the delay in the rising p
267 h Nav1.6 coexpressed with beta1 demonstrated use-dependent potentiation during a rapid train of depol
268                                              Use-dependent potentiation of the mutant response during
269                           First, they caused use-dependent potentiation of the response during a trai
270 tor cortex (FL-SMC) in adult rats results in use-dependent proliferation of dendritic processes, foll
271                                  The reverse use-dependent prolongation of APD by sotalol is associat
272                                          The use-dependent properties of synaptic transmission could
273                   We compared the state- and use-dependent ranolazine block of Na(+) currents carried
274 in recovery from inactivation, and increased use-dependent reduction in amplitude during rapid (1- to
275 layed enhanced slow inactivation and greater use-dependent reduction in peak current at fast pulsing
276 ostsynaptic spiral ganglion neurons showed a use-dependent reduction in sound-evoked spiking, corrobo
277 very from availability, inducing significant use-dependent reduction of INa.
278                                         This use-dependent reduction was the result of the entry of T
279                             Here, we studied use-dependent regulation of bipolar cell synaptic transm
280 ese receptors but arises from a voltage- and use-dependent relief of block by internal polyamines.
281 espond to stimuli presented at the PRL (the "use-dependent reorganization" hypothesis), then foveal c
282 ptor alpha1 subunits is subject to a delayed use-dependent repression that was observed after, rather
283       The period of run-up was followed by a use-dependent run-down phase.
284 rth membrane segment, a region implicated in use-dependent rundown and NMDA channel inactivation.
285 ROS and whole-cell recordings to measure the use-dependent rundown of ACh-evoked currents.
286                                              Use-dependent selection of optimal connections is a key
287 g to GluN2 renders these compounds nominally use-dependent, since inhibition will rely on synaptic re
288 that drugs with rapid recovery kinetics from use-dependent sodium channel block could promote oscilla
289 ion in neurite length was ameliorated by the use-dependent sodium channel blocker carbamazepine and b
290 ore distal sites, limiting the expression of use-dependent spike broadening to the most proximal axon
291                                              Use-dependent synapse remodeling is thought to provide a
292 Deletion of synapsins, however, did increase use-dependent synaptic depression induced by a high-freq
293       In the last five years, a new class of use-dependent synaptic plasticity that requires retrogra
294 ence the possibility of their involvement in use-dependent synaptic plasticity, is not known.
295 c cells, which in turn influence release via use-dependent synaptic plasticity.
296 -term synaptic enhancement of both basal and use-dependent synaptic transmission via specific changes
297 ic AMPAR function - inward rectification and use-dependent unblock (UDU), with the latter assayed by
298                      They demonstrate that a use-dependent unblock by internal polyamines potentially
299 ple cleanup before analysis, with the method used dependent upon the sample matrix.
300   Logistic regression analyses of medication use (dependent variable) vs. metabolic equivalent hours

 
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