ライフサイエンスコーパス: high-frequency stimulation

1 ascade is accurate and fast enough to follow high frequency stimulation.

2 and these inputs can be potentiated through high frequency stimulation.

3 current, reducing neuronal ability to follow high frequency stimulation.

4 nt of Ad-LacZ infected cells with periods of high frequency stimulation.

5 ng less than half the energy of conventional high frequency stimulation.

6 facilitated, after strong depolarizations or high frequency stimulation.

7 dergo long-term potentiation (LTP) following high frequency stimulation.

8 long-term increase in latency caused by the high frequency stimulation.

9 polarization and to sustain AP firing during high frequency stimulation.

10 ed before and immediately after cessation of high frequency stimulation.

11 the time period of 30 s after switching off high frequency stimulation.

12 onic movements where it was suppressed after high frequency stimulation.

13 NMDA receptor-independent form of LTP during high frequency stimulation.

14 prevents excessive glutamate release during high-frequency stimulation.

15 of LTP that is BDNF independent, induced by high-frequency stimulation.

16 Loss of FMRP led to enhanced responses to high-frequency stimulation.

17 postsynaptic calcium, and can be reversed by high-frequency stimulation.

18 intensify postsynaptic Ca(2+) signals during high-frequency stimulation.

19 it regulates excitability during periods of high-frequency stimulation.

20 viding constant SV size during long-lasting, high-frequency stimulation.

21 of long-term potentiation by short bursts of high-frequency stimulation.

22 ery near highly active exocytic sites during high-frequency stimulation.

23 fusing fully with the plasma membrane during high-frequency stimulation.

24 e more quickly than wild-type in response to high-frequency stimulation.

25 tral synapses rapidly depress in response to high-frequency stimulation.

26 es of baroreceptor neurons is reduced during high-frequency stimulation.

27 GLUT1 recycles more slowly during prolonged, high-frequency stimulation.

28 charge transfer and current potentiation by high-frequency stimulation.

29 NMDAR-mediated currents induced by bursts of high-frequency stimulation.

30 vous system are transiently depressed during high-frequency stimulation.

31 current and failure of the neurons to follow high-frequency stimulation.

32 release at 15%-20% of the normal rate during high-frequency stimulation.

33 ontent and facilitation of EPP amplitudes at high-frequency stimulation.

34 tentials and NMDA receptor activation during high-frequency stimulation.

35 of synaptic NMDAR currents during bursts of high-frequency stimulation.

36 neurotransmission over prolonged periods of high-frequency stimulation.

37 A3 induced by either brief or long trains of high-frequency stimulation.

38 ired the maintenance of LTP induced by brief high-frequency stimulation.

39 ntiation of neuromuscular transmission after high-frequency stimulation.

40 magnesium-free bathing medium, or following high-frequency stimulation.

41 he stronger activation that occurs following high-frequency stimulation.

42 tiation was lower than 1 hour after the last high-frequency stimulation.

43 , and a reduction in their ability to follow high-frequency stimulation.

44 se excitatory synaptic currents triggered by high-frequency stimulation.

45 ons to sustain SV recycling during trains of high-frequency stimulation.

46 to an increase in Nav1.1 availability during high-frequency stimulation.

47 s exhibit reduced synaptic depression during high-frequency stimulation.

48 city and success rates of APs in response to high-frequency stimulation.

49 a subset of SVs that respond specifically to high-frequency stimulation.

50 t in location toward the AZ periphery during high-frequency stimulation.

51 role comes into play primarily during brief high-frequency stimulation.

52 synaptic depression during brief periods of high-frequency stimulation.

53 reas LTD required low intracellular cAMP and high-frequency stimulation.

54 plasticity lasting for tens of seconds after high-frequency stimulation.

55 had been previously potentiated by repeated high-frequency stimulation.

56 d with all low frequency and/or intermittent high frequency stimulations.

57 equency stimulations and for 76 (50%) of the high-frequency stimulations.

58 The cKO mice were unresponsive to high frequency stimulation (100 Hz), while the NMN-treat

59 High frequency stimulation (100 or 40 Hz) in layer IV in

60 cilitation, and response to a brief train of high-frequency stimulation (100 Hz, 40 pulses) that exha

61 High-frequency stimulation (130 Hz) of the left anterior

62 eceptor-independent LTP: LTP induced by very high-frequency stimulation (200 Hz-LTP), LTP induced by

63 High-frequency stimulations (25-40 Hz) of thalamocortica

64 However, when high frequency stimulation (30 Hz for 10 s) preceded imm

65 lation (depression) of EPSP amplitude during high-frequency stimulation (-39 +/- 4% and -53 +/- 4%, u

66 rminals and increased synaptic fatigue under high-frequency stimulation, accompanied by the developme

67 ning receptors preferentially desensitize at high-frequency stimulation, accounting for the inability

68 prevented this decrease indicating that the high frequency stimulation activated the NMDA receptor a

69 An additional bout of high-frequency stimulation administered under urethane c

70 fact, if LY294002 was withdrawn 5 min after high-frequency stimulation, an LTP of fEPSP was seen.

71 can account for the complex kinetics during high frequency stimulation and cause stimulus-history-de

72 onic features are the quickest to respond to high frequency stimulation and may thus directly relate

73 ated in area CA1 in response to LTP-inducing high frequency stimulation and that this activation requ

74 apid changes in synaptic efficacy induced by high-frequency stimulation and BDNF at central excitator

75 eadily releasable pool of vesicles evoked by high-frequency stimulation and by increasing the fractio

76 blocked all broadening of the AP(syn) during high-frequency stimulation and eliminated synaptic facil

77 ndent protein kinase C (PKC) is activated by high-frequency stimulation and mediates post-tetanic pot

78 napsins boost the release probability during high-frequency stimulation and suggest that this effect

79 stimulus is recruited within milliseconds by high-frequency stimulation and support an ultrafast reco

80 ORNs to better synchronize their output with high-frequency stimulation and to perceive brief stimuli

81 yfish opener muscle is elicited by prolonged high frequency stimulation, and arises from an increase

82 mined depletion at individual synapses using high frequency stimulation, and estimated the size of th

83 long-term potentiation of EPSPs triggered by high frequency stimulation, and prevented the EPSP-spike

84 voked release, responses evoked by sustained high-frequency stimulation, and short-term plasticity we

85 mparable inhibitory efficacy to conventional high-frequency stimulation (ANOVA, F = 5.331, P < 0.001)

86 stioned because endogenous activation during high-frequency stimulation appears to have little impact

87 voked field EPSPs was induced selectively by high-frequency stimulation applied to the outer third of

88 demand and greater specificity than current high frequency stimulation approaches, and may lower the

89 We used high-frequency stimulation as a known activator of Ca(2+

90 Continuous high frequency stimulation at 0.4 mA and 0.2 ms produced

91 The effects of high frequency stimulation at GP sites can be prevented

92 lly designed amplifier allowing simultaneous high frequency stimulation at therapeutic parameter sett

93 Upon high-frequency stimulation at 100 Hz, successive became

94 ction of presynaptic miniature release after high-frequency stimulation at Drosophila neuromuscular j

95 with both binomial statistical analysis and high-frequency stimulation at the amphibian neuromuscula

96 d electrically evoked synaptic responses for high-frequency stimulation at three synapses in the mous

97 ition of firing by 5-CT is diminished during high-frequency stimulation, because relief from synaptic

98 and theoretically, that the neurons support high-frequency stimulation beyond the inverse membrane t

99 Burst high-frequency stimulation (BHFS) (10 stimuli with 100 H

100 Interestingly, after chronic high-frequency stimulation, both the short- and long-ter

101 In response to high-frequency stimulation, both wild-type and mutant ne

102 itation (PPF) was enhanced; (2) responses to high frequency stimulation bursts were distorted; (3) lo

103 ed enhanced LTP in the hippocampal CA1 after high-frequency stimulation, but Ng-/- mice were affected

104 and induction of long-term potentiation with high-frequency stimulation, but not theta burst stimulat

105 o achieve results similar to STN lesions and high-frequency stimulation, but with fewer side effects.

106 sations are an epiphenomenon and explain how high-frequency stimulation can provide analgesia without

107 ression reduced long-term potentiation after high-frequency stimulation compared with WT littermates

108 nced synaptic fatigue at CA1 synapses during high-frequency stimulation, compared with wild-type anim

109 rough astrocyte glutamate transporters under high-frequency stimulation conditions, a feature that su

110 ed after exercise was reversed by repetitive high-frequency stimulation, consistent with enhanced SOC

111 indow limited to the first few minutes after high-frequency stimulation delivery.

112 h stellate cells and Purkinje cells, whereas high-frequency stimulation depresses stellate cell synap

113 onses of mitral and external tufted cells to high frequency stimulation did not originate presyaptica

114 High-frequency stimulation did not increase the overlap

115 maximized, and p alone is decreased, another high-frequency stimulation elicits additional LTP.

116 riggered synaptic transmission; furthermore, high-frequency stimulation elicits synaptic facilitation

117 calcium influx in presynaptic neurons during high-frequency stimulation, enhanced synaptic vesicle re

118 tocol suppresses aggression priming, whereas high-frequency stimulation enhances aggression, mimickin

119 Brief, high-frequency stimulation evoked repetitive postsynapti

120 nhanced synaptic depression during prolonged high-frequency stimulation followed by delayed recovery.

121 During trains of high-frequency stimulation GABAA and GABAB receptors wor

122 It has been hypothesized that during high frequency stimulation glutamate a major neurotransm

123 charge transferred across the synapse during high frequency stimulations (>5 Hz).

124 itors that inhibited LTP when present during high-frequency stimulation had no effect on potentiated

125 blocked the stabilization of LTP induced by high frequency stimulation (HFS) in hippocampal slices.

126 everal laboratories have observed that brief high frequency stimulation (HFS) of cortical afferents i

127 High frequency stimulation (HFS) of nociceptors produced

128 tients, 31 sides) and then separately during high frequency stimulation (HFS) of the STN (16 patients

129 High frequency stimulation (HFS) of the STN improved tre

130 f inhibition of LTPs that were induced using high frequency stimulation (HFS), versus theta burst sti

131 N55212-2 and anandamide, but not cOA blocked high frequency stimulation (HFS)-LTP.

132 and 20 minutes following exposure to visual high-frequency stimulation (HFS) ( approximately 8.8 Hz,

133 In the PL-NAc core pathway, high-frequency stimulation (HFS) had no effect on eLFP i

134 Moreover, the CCKBR antagonists also blocked high-frequency stimulation (HFS) induced LTP formation i

135 High-frequency stimulation (HFS) of BLA and mPFC depress

136 It was recently demonstrated that high-frequency stimulation (HFS) of cortical inputs indu

137 erm changes in synaptic efficacy produced by high-frequency stimulation (HFS) of glutamatergic affere

138 High-frequency stimulation (HFS) of neocortical afferent

139 (LTP) of synaptic strength that results from high-frequency stimulation (HFS) of the afferent pathway

140 e activation of postsynaptic ASIC-1as during high-frequency stimulation (HFS) of the presynaptic nerv

141 glutamate is released within the STN during high-frequency stimulation (HFS) of the STN.

142 Our previous study showed that high-frequency stimulation (HFS) of the subthalamic nucl

143 long-term potentiation (LTP) after a single high-frequency stimulation (HFS) or two spaced HFSs at 1

144 Surprisingly, the same high-frequency stimulation (HFS) protocol induces presyn

145 tentiation (LTP) induced by the same type of high-frequency stimulation (HFS) that induces LTP at MF

146 Moreover, high-frequency stimulation (HFS) that typically triggers

147 mGluR7 activation during high-frequency stimulation (HFS) triggers presynaptic LT

148 /y) and Shank3B(-/-) lines, and administered high-frequency stimulation (HFS) via implanted electrode

149 degrees C (control group) and, 90 min later, high-frequency stimulation (HFS) was applied to the medi

150 synapses exhibited deficits in responses to high-frequency stimulation (HFS), as well as in long-ter

151 undergo long-term depression (LTD) following high-frequency stimulation (HFS), in contrast to MF-pyra

152 e clamping the postsynaptic cell soma during high-frequency stimulation (HFS), intracellular injectio

153 activity induced by K+ depolarization or by high-frequency stimulation (HFS), known to induce synaps

154 r function gain or function loss, transforms high-frequency stimulation (HFS)-induced long-term poten

155 ion (LTP) induced in hippocampal area CA1 by high-frequency stimulation (HFS).

156 enhancement of synaptic transmission during high-frequency stimulation (HFS).

157 tenuation of the synaptic fatigue induced by high-frequency stimulation (HFS).

158 est the Ca2+ dependence of the VOCC, we used high-frequency stimulation (HFS).

159 n induced by theta-burst stimulation but not high-frequency stimulation (HFS).

160 FPL-LTD occludes LTD induced by high-frequency stimulation (HFS-LTD) and requires elevat

161 atrial fibrillation, endocardial continuous high frequency stimulation identified GP sites producing

162 paroxysmal atrial fibrillation, synchronized high frequency stimulation identified sites initiating p

163 CAP area declined more rapidly during high frequency stimulation if monocarboxylate transport

164 ronounced short-term depression (STD) during high-frequency stimulation; (ii) a conversion of that ST

165 der to potentiate with a burst of relatively high frequency stimulation in MeA-trained birds: the cha

166 f PFC responses resulting from vHipp and BLA high-frequency stimulation in adult rats that received r

167 of synaptic vesicle (SV) endocytosis during high-frequency stimulation in central nerve terminals.

168 Furthermore, high-frequency stimulation in Uva simultaneously suppres

169 However, high-frequency stimulation in Uva suppressed auditory-ev

170 Acetylcholine synapses are depressed by high-frequency stimulation, in part due to desensitizati

171 High frequency stimulation increased AP failure rates an

172 o produce SVs that respond preferentially to high-frequency stimulation, independent of their role in

173 in a decrease in transmitter release during high-frequency stimulation, indicating an inhibition of

174 afts contracted when stimulated ex vivo, and high frequency stimulation induced tetanus.

175 In addition, high-frequency stimulation induced a consistent long-ter

176 Prolonged high-frequency stimulation induced NMDA receptor-depende

177 GRF1 can also mediate high frequency stimulation-induced LTP (HFS-LTP) in mice

178 showed that, although the magnitude of both high-frequency stimulation-induced and pairing-induced L

179 cellular cleavage of proBDNF greatly reduced high-frequency stimulation-induced extracellular mBDNF.

180 High-frequency stimulation-induced long-term depression,

181 tm1 haploinsufficiency significantly blocked high-frequency stimulation-induced long-term potentiatio

182 to a priming effect that enhanced subsequent high-frequency stimulation-induced LTP.

183 The facilitatory effects of the high-frequency stimulation-induced priming event itself

184 ease evoked by RGC activation and found that high-frequency stimulation induces a long-lasting subthr

185 High-frequency stimulation induces a transient calcium e

186 ) in CA1 is impaired in Pyk2 KO mice using a high frequency stimulation induction protocol but not wi

187 ibited long-term potentiation in response to high-frequency stimulation instead of the expected depre

188 We used this model to assess whether high frequency stimulation is necessary for effective ST

189 High frequency stimulation is used to identify GP sites

190 We show that actin polymerization induced by high-frequency stimulation is blocked by local inhibitio

191 long-term potentiation (LTP) triggered by a high-frequency stimulation is facilitated in hypocretin

192 Chronic high-frequency stimulation is safe and highly effective

193 , an increase in synaptic efficacy following high-frequency stimulation, is widely considered a mecha

194 High-frequency stimulation leads to a transient increase

195 ABSTRACT: High-frequency stimulation leads to post-tetanic potenti

196 High-frequency stimulation leads to post-tetanic potenti

197 High frequency stimulation led to a significant reductio

198 targeted regional approach through localized high-frequency stimulation (LHFS) using low-amplitude el

199 In contrast to high-frequency stimulation-LTP, such betaAR-LTP requires

200 Our findings suggest that high frequency stimulation may suppress pathologically e

201 ies have investigated how activity evoked by high-frequency stimulation may interact with the existin

202 that chronic ventromedial prefrontal cortex high-frequency stimulation may serve as a novel effectiv

203 Subsequently, the high frequency stimulation-mediated synaptic potentiatio

204 imal LG-S EPSP amplitude and the response to high-frequency stimulation (modulation) recorded in untr

205 High-frequency stimulation, multivesicular release (MVR)

206 ibited neither reliable phase-locking during high-frequency stimulation nor sensitivity to stimulus d

207 High frequency stimulation of mouse hippocampal slices r

208 High frequency stimulation of the afferents in vivo lead

209 High frequency stimulation of the cZI results in greater

210 d by action potential-evoked release (during high frequency stimulation of the mossy fibres), tonic i

211 synapses that are inactive, normally during high-frequency stimulation of a converging synaptic inpu

212 We examined the effect of high-frequency stimulation of a crucial component of the

213 We found that high-frequency stimulation of afferent fibers elicits sy

214 During high-frequency stimulation of both motifs, some connecti

215 h to preserve stable AP waveforms, even upon high-frequency stimulation of chromaffin cells during st

216 of potentiation induced in vivo by repeated high-frequency stimulation of cortical association fiber

217 duced by either glutamate uptake blockade or high-frequency stimulation of corticostriatal tracts.

218 High-frequency stimulation of DCN parallel fiber synapse

219 s pharmacologically prevented LTP induced by high-frequency stimulation of glutamatergic axons, or by

220 ause its activation usually requires strong, high-frequency stimulation of inputs.

221 High-frequency stimulation of mossy fibers induced long-

222 Here we demonstrate that high-frequency stimulation of mossy fibres in rat hippoc

223 ngs from dentate granule cells revealed that high-frequency stimulation of perforant path afferents i

224 iated synaptic depression, induced either by high-frequency stimulation of PF or mGluR1 agonist DHPG,

225 slices, we now demonstrate that conditioning high-frequency stimulation of primary afferents activate

226 -CA1 EPSPs, ADX71743 reversed the ability of high-frequency stimulation of SC afferents to reduce IPS

227 a manner that can be reversed by subsequent high-frequency stimulation of SC inputs.

228 on of long-term potentiation (LTP) evoked by high-frequency stimulation of Schaffer collaterals, and

229 High-frequency stimulation of thalamic inputs led to a l

230 nced the magnitude of dentate LTP induced by high-frequency stimulation of the angular bundle.

231 classes of neural progenitors, we found that high-frequency stimulation of the ATN increases symmetri

232 l timed postsynaptic action potential during high-frequency stimulation of the auditory nerve.

233 ious research has demonstrated that repeated high-frequency stimulation of the granule cell layer of

234 uces long-term potentiation (LTP) induced by high-frequency stimulation of the intracortical axons in

235 We also found that sustained, high-frequency stimulation of the locus coeruleus at fre

236 LTP was induced by high-frequency stimulation of the medial perforant path

237 Short bursts of high-frequency stimulation of the ML elicited Ca2+ trans

238 resent study aims to delineate the effect of high-frequency stimulation of the MLR (MLR-HFS) on gait

239 High-frequency stimulation of the perforant path project

240 on of their resting membrane potential after high-frequency stimulation of the perforant path.

241 the fidelity of synaptic transmission during high-frequency stimulation of the presynaptic cell.

242 ty (LTP-IE) of jcBNST neurons in response to high-frequency stimulation of the stria terminalis.

243 cal evidence of the therapeutic potential of high-frequency stimulation of the subthalamic nucleus (S

244 tudy, we postulate that clinically effective high-frequency stimulation of the subthalamic nucleus im

245 ery, primarily in the form of the bilateral, high-frequency stimulation of the subthalamic nucleus, i

246 performed a multicenter trial of unilateral high-frequency stimulation of the ventral intermedius nu

247 t, we report here that repeated low-current, high-frequency stimulation of the VTA provoked afterdisc

248 re involved in the mechanism of DBS, and how high-frequency stimulation of these cells may lead to al

249 High-frequency stimulation of these ensembles in the ret

250 High-frequency stimulation of these glutamatergic inputs

251 icostriatal long-term depression (LTD) after high-frequency stimulation of tissue from AC5KO mice.

252 During high-frequency stimulation of vagal afferents, leptin in

253 In a rodent model, DBS-like high-frequency stimulation of VS can either enhance or i

254 ort, we describe the facilitatory effects of high-frequency stimulation on the induction of homosynap

255 on the elimination of vagal reflex evoked by high frequency stimulation or an extensive approach at a

256 (LTP) induction by either single or repeated high frequency stimulation or theta burst stimulation in

257 had no significant effect on LTP induced by high-frequency stimulation or long-term depression induc

258 nhibitors suppressed the induction of LTP by high-frequency stimulation or low-frequency stimulation

259 ctor, a neurotrophin that is released during high-frequency stimulation patterns used to elicit LTP.

260 In contrast, high-frequency stimulation preferentially increased extr

261 High-frequency stimulation produced sustained potentiati

262 al for long-term potentiation induced with a high frequency stimulation protocol (HFS-LTP) in the dor

263 Finally, depressing OFC-DMS pathway with a high frequency stimulation protocol in awake mice over-p

264 Importantly, we found that high-frequency stimulation reduces DC fiber activation t

265 Furthermore, high-frequency stimulation resulted in increased facilit

266 However, high-frequency stimulation revealed greatly elevated pos

267 , and enhanced use-dependent inactivation on high-frequency stimulation; S246L is likely a benign pol

268 DC fiber collaterals cannot reliably follow high-frequency stimulation, strongly affecting the netwo

269 t on potentiated synapses when applied after high-frequency stimulation, suggesting that PI3-kinase i

270 naptic dysfunction increased, while thalamic high-frequency stimulation suppressed tremor-related act

271 These findings suggest that high frequency stimulation suppresses epileptiform activ

272 However, when challenged with sustained high frequency stimulation, synapses in old mice exhibit

273 ced at both sites with either theta burst or high-frequency stimulation (TBS or HFS).

274 ess refractoriness, and improved response to high-frequency stimulation than dysmyelinated counterpar

275 pse presented facilitation during MOC fibers high-frequency stimulation that disappeared at mature st

276 spines, which can be reversed by subsequent high-frequency stimulation that induces LTP.

277 stration was so robust that after repetitive high-frequency stimulation the Ca content of responsive

278 During high-frequency stimulation, the greatest firing rate and

279 During high-frequency stimulation, the synapse undergoes short-

280 In response to high-frequency stimulation, the synaptic-vesicle pool ca

281 tion of late-phase LTP expression induced by high-frequency stimulation; the early phase of LTP is un

282 that express CRH (CrhINs) releases CRH upon high-frequency stimulation to enhance excitability of la

283 Furthermore, analysis of high-frequency stimulation trains suggests an impairment

284 nmol) into area CA3 15 min before delivering high-frequency stimulation (two times at 100 Hz, 1 sec).

285 that chronic ventromedial prefrontal cortex high-frequency stimulation upregulated neurogenesis-asso

286 LTP versus LTD is induced by high-frequency stimulation versus low-frequency, but sti

287 es were achieved by daily amygdala kindling, high frequency stimulation was delivered to the SNr bila

288 Suppression of spontaneous activity by high frequency stimulation was found to be frequency (<

289 LTP was blocked when high-frequency stimulation was applied in the presence o

290 LTP of NMDA and AMPA EPSCs after high-frequency stimulation was reduced by prior inhibiti

291 lation that immediately follows LTP-inducing high-frequency stimulation, we wondered whether NMDAR-in

292 lobe, 111 (27%) low-frequency and 176 (55%) high-frequency stimulations were associated with a clini

293 quency facilitation tests and LTP induced by high-frequency stimulation when compared with untreated

294 itical for long-term potentiation induced by high-frequency stimulation, whereas proBDNF facilitate l

295 High-frequency stimulation, which evoked robust long-ter

296 stered the specific GR agonist RU 28362 that high-frequency stimulation, which normally produces LTP,

297 C2230 inhibited CaV2.2 during high-frequency stimulation, while sparing other voltage-

298 tached recordings, mitral cells responded to high frequency stimulation with sustained responses, whe

299 uch adaptation allows a neuron to respond to high-frequency stimulation with lower-frequency firing t

300 Here we report that high-frequency stimulation with the miniature coil could