ライフサイエンスコーパス: paired-pulse

1 onses (36 taste-responsive) were tested with paired pulses.

2 degrees C, and stimulated mossy fibers with paired pulses.

3 , the CT was electrically stimulated using a paired-pulse (10-2000 ms interpulse interval; blocks of

4 Therefore, paired-pulse adaptation does not reduce the discriminabi

5 At the single neuron level, although paired-pulse adaptation reduces the information about th

6 In concert with these alterations, paired-pulse analyses suggested enhanced synaptic inhibi

7 ince these early studies, the development of paired-pulse and repetitive TMS protocols allowed invest

8 tro, increased quantal content and decreased paired-pulse and tetanic facilitation.

9 ntal content at these synapses and increased paired-pulse and tetanic facilitation.

10 pike-timing-dependent-plasticity (STDP) when paired pulses are repeatedly applied with different timi

11 A bimodal distribution of the peak of paired-pulse attenuation was found with modes at 10 ms a

12 The majority (34; 75.6%) showed paired-pulse attenuation, defined as fewer evoked spikes

13 The paired-pulse behavior is characterized by the second res

14 igin as they showed substantial variation in paired-pulse behaviour.

15 Furthermore, the size of the MEPs evoked by paired pulses decreased up to 30 ms beforehand.

16 We show that marked paired pulse depression is the same in simultaneously re

17 Recovery from paired pulse depression occurs with a time constant of 2

18 reatment and detected only a 20% increase in paired pulse depression suggesting an increase in neurot

19 ation of either rods or cones recovered from paired-pulse depression (PPD) at rates similar to the re

20 We find that this release of GABA undergoes paired-pulse depression (PPD) that recovers in <1 min (s

21 However, during paired-pulse depression (PPD), there was a significant d

22 ed with low-LG mothers, as well as increased paired-pulse depression (PPD).

23 change in amplitude with raised P(r) nor was paired-pulse depression altered.

24 er, evoked synaptic responses displayed less paired-pulse depression and dramatic facilitation in res

25 tral inhibitory synapse invariably exhibited paired-pulse depression at interstimulus intervals of le

26 ON L-IPSCs showed paired-pulse depression at intervals <1 s, whereas OFF L

27 sensitization with cyclothiazide reduced the paired-pulse depression at long-duration interstimulus i

28 reduced synaptic transmission and increased paired-pulse depression at physiological [Ca](o).

29 as ruled out as a mechanism for long-lasting paired-pulse depression by examining the effect of selec

30 In addition, paired-pulse depression did not differ between SACs loca

31 environment increases response strength and paired-pulse depression in the auditory cortex of awake

32 of inhibition of Ca2+ influx, the degree of paired-pulse depression is significantly reduced.

33 t increase in spontaneous EPSC frequency and paired-pulse depression of evoked EPSCs.

34 de of mEPSCs with little effect on mIPSCs or paired-pulse depression of evoked IPSCs.

35 xcitatory synaptic transmission and stronger paired-pulse depression of GABA(A) currents in the hippo

36 atencies, low failure rates, and substantial paired-pulse depression of the ST-evoked EPSCs indicate

37 ow-frequency oscillatory bursts and enhanced paired-pulse depression of visual evoked potentials.

38 Depending on the stimulus, either paired-pulse depression or facilitation could be elicite

39 set of interneurones (approximately 15%) had paired-pulse depression rather than paired-pulse facilit

40 d LTP was associated with an increase in the paired-pulse depression ratio.

41 DA receptor D2R agonist and showed a marked paired-pulse depression that required 2 min for full rec

42 l inhibitory synaptic density, a decrease in paired-pulse depression, and a reexpression of endocanna

43 pyramidal-to-multipolar synapse, which shows paired-pulse depression, elevation of [Ca2+]o from physi

44 d that the mammillothalamic pathway exhibits paired-pulse depression, lack of a metabotropic glutamat

45 4 of S2 responded with Class 1A properties (paired-pulse depression, large initial EPSPs, an all-or-

46 2+) regulates the recovery from long-lasting paired-pulse depression, possibly thourgh a Ca(2+)-sensi

47 piperidine dicarboxylic acid (PDA) increased paired-pulse depression, suggesting that a presynaptic c

48 approximately 3-fold increase in presynaptic paired-pulse depression, suggesting that deletion of Min

49 diated EPSCs to a similar extent and reduced paired-pulse depression, suggestive of an inhibition of

50 er, hair cells held at -60 mV displayed only paired-pulse depression.

51 aptic component also exists for long-lasting paired-pulse depression.

52 and BAPTA-AM, EGTA-AM increased long-lasting paired-pulse depression.

53 ed enhanced responses to tones and increased paired-pulse depression.

54 o a lesser extent, they reduced long-lasting paired-pulse depression.

55 , and this was associated with a decrease in paired-pulse depression.

56 the initial AMPAR-mediated EPSC and enhanced paired-pulse depression.

57 LY354740, but not XA, also reduced DG paired-pulse depression.

58 At a neurophysiological level, the PMv paired-pulse effect (PPE) on M1 corticospinal activity w

59 ced both paired-pulse suppression (n=11) and paired-pulse enhancement (n=4); tetanic stimulation (25

60 Reducing the intensity to 80% AMT increased paired-pulse excitability at an interstimulus interval (

61 sion does not alter facilitation measured in paired-pulse experiments but slows the rate of inactivat

62 initial stimuli, consistent with results of paired-pulse experiments; however, synaptic depression i

63 s of USP14 in ax(J) mice causes a deficit in paired pulse facilitation (PPF) at hippocampal synapses.

64 itatory postsynaptic potentials (fEPSPs) and paired pulse facilitation (PPF) in KO and control hippoc

65 pus, reduced Cyfip1 levels serve to decrease paired pulse facilitation and increase miniature EPSC fr

66 aptic transmission, as measured by decreased paired pulse facilitation and long-term potentiation, an

67 However, adult-like responses that exhibited paired pulse facilitation did not fully emerge until 2 w

68 Acute ethanol also reduced paired pulse facilitation of EPSPs and EPSCs only in CET

69 siological recordings of basal transmission, paired pulse facilitation, and LTP and combined this wit

70 aptic function, assessed by fiber volley and paired pulse facilitation, is unchanged.

71 ether the synaptic strengthening produced by paired-pulse facilitation (PPF) also results in changes

72 nce the amplitude and slowed the recovery of paired-pulse facilitation (PPF) of evoked EPSCs.

73 Paired-pulse facilitation (PPF) was correlated with resi

74 ings, the quantal size did not change during paired-pulse facilitation (PPF), supporting the notion t

75 pairment of the input/output (I/O) curve and paired-pulse facilitation (PPF).

76 nuating PF-EPSCs in leaner mice, we examined paired-pulse facilitation (PPF).

77 ) induction accompanied by a 30% increase in paired-pulse facilitation (PPF).

78 the SC was accompanied by a reduced ratio of paired-pulse facilitation (PPR).

79 es depression, whereas Ca(v)beta(4b) induces paired-pulse facilitation [PPF] followed by synaptic dep

80 These inhibitors also block the changes in paired-pulse facilitation and coefficient of variation t

81 pe in DBA mice, we found significantly lower paired-pulse facilitation and enhanced short term depres

82 presynaptic short-term plasticity including paired-pulse facilitation and frequency facilitation.

83 bnormalities in basal synaptic transmission, paired-pulse facilitation and long-term depression (LTD)

84 m hippocampal neurons, resulting in enhanced paired-pulse facilitation and long-term potentiation.

85 rom AT mice exhibited decreases in degree of paired-pulse facilitation and magnitude of long-term pot

86 Since PMF exposure modified paired-pulse facilitation and paired-pulse inhibition, i

87 Paired-pulse facilitation and synaptic fatigue during pr

88 her hand, the cortical input exhibits graded paired-pulse facilitation and the capacity to activate m

89 presynaptic function, measured by changes in paired-pulse facilitation and the rate of blockade by th

90 ted excitatory synaptic input that undergoes paired-pulse facilitation as well as NMDA receptor and G

91 , which appears to be a central mechanism of paired-pulse facilitation at this synapse.

92 iating vesicle release, effectively restored paired-pulse facilitation deficits back to control level

93 tion, accelerates inactivation, and prevents paired-pulse facilitation in a Ca2+-independent manner.

94 r/NMDA receptor current ratios and increased paired-pulse facilitation in activated GFP-positive but

95 -dependent and associated with a decrease in paired-pulse facilitation in both pathways.

96 ficant changes in the input/output curve and paired-pulse facilitation in CA3-CA1 synapses, which cou

97 r, these mutant mice did show enhancement of paired-pulse facilitation in excitatory synaptic transmi

98 ase, lowered synaptic strength, and enhanced paired-pulse facilitation in Mint-deficient mice, sugges

99 nhibited synaptic transmission and increased paired-pulse facilitation in rat hippocampal slices supp

100 cadienoic acid, but not LA, increase somatic paired-pulse facilitation in rat hippocampus by 80%, sug

101 ce (RIM1alpha(+/+)) SE caused an increase in paired-pulse facilitation in the CA1 region of the hippo

102 ical approaches, we found there was enhanced paired-pulse facilitation in the Schaffer Collateral-CA1

103 in Syb1-deficient NMJs is markedly altered: paired-pulse facilitation is significantly enhanced, sug

104 Paired-pulse facilitation of EPSCs, an index of release

105 ecrease in postsynaptic, polyamine-dependent paired-pulse facilitation of the photolytic currents, in

106 accompanied by a significant decrease in the paired-pulse facilitation ratio during the post-apneic p

107 cting mostly presynaptically as it increased paired-pulse facilitation ratio of IPSCs and decreased m

108 ptic function, as measured by an increase in paired-pulse facilitation ratio.

109 mplitude, and an increase in the evoked EPSC paired-pulse facilitation ratio.

110 IPSP and IPSC amplitudes were increased, and paired-pulse facilitation ratios were lower than in naiv

111 ot NMDA, receptor EPSCs and has no effect on paired-pulse facilitation ratios.

112 itability, evoked synaptic transmission, and paired-pulse facilitation remain unaltered.

113 Furthermore, paired-pulse facilitation revealed that the site of LTP

114 onto the majority of interneurones had less paired-pulse facilitation than synapses onto pyramidal c

115 The switch also abolished the paired-pulse facilitation that arose from an activity an

116 In the MF-CA3 pathway, paired-pulse facilitation was abolished by PKC agonists

117 Paired-pulse facilitation was observed over a wide range

118 tude, but not frequency, of miniature EPSCs; paired-pulse facilitation was unaffected.

119 plitude, input-output relationship and 50 ms paired-pulse facilitation were unchanged following COX10

120 ditionally, elevated O-GlcNAc led to reduced paired-pulse facilitation, a form of short term plastici

121 gp influences basal synaptic transmission or paired-pulse facilitation, a form of short-term synaptic

122 Paired-pulse facilitation, a measure of presynaptic mech

123 increases in excitatory presynaptic release, paired-pulse facilitation, and increased AMPA receptor t

124 rated increased basal synaptic transmission, paired-pulse facilitation, and long-term potentiation co

125 e-timing-dependent plasticity learning rule, paired-pulse facilitation, and ultralow-power consumptio

126 ction in EPSC amplitude and it did not alter paired-pulse facilitation, but in contrast to low Ca(2+)

127 AMPA receptors exhibited well characterized paired-pulse facilitation, frequency facilitation, and N

128 15%) had paired-pulse depression rather than paired-pulse facilitation, showed only depression in res

129 ith what has been termed Class 2 properties (paired-pulse facilitation, small initial excitatory post

130 highest frequencies (> 50 Hz), also reduced paired-pulse facilitation, suggesting a requirement for

131 iniature excitatory postsynaptic currents or paired-pulse facilitation, suggesting a specific effect

132 c LTP was associated with reduced amounts of paired-pulse facilitation, suggesting that it is express

133 ed basal synaptic transmission and decreased paired-pulse facilitation, suggesting that neurotransmit

134 forskolin, elevated extracellular Ca2+, and paired-pulse facilitation.

135 on, whereas unreliable connections underwent paired-pulse facilitation.

136 the synaptotagmin-1 mutation does not affect paired-pulse facilitation.

137 ic sites modulates synaptic transmission and paired-pulse facilitation.

138 frequency of miniature EPSCs, and increased paired-pulse facilitation.

139 n increase in success rate and a decrease in paired-pulse facilitation.

140 d release probability, measured as increased paired-pulse facilitation.

141 o61-8048 increased neuronal excitability and paired-pulse facilitation.

142 us and evoked synaptic activity are reduced; paired pulse-facilitation is impaired, and synaptic tran

143 vels of Ca(v)1.2 result in reduced GABAergic paired-pulse inhibition and increased GABAergic post-tet

144 Moreover, we observed decreased paired-pulse inhibition of population spikes indicating

145 n from hippocampus of PS rats expressed less paired-pulse inhibition than slices from control rats.

146 n Sprague-Dawley rats increased granule cell paired-pulse inhibition, decreased epileptiform afterdis

147 osure modified paired-pulse facilitation and paired-pulse inhibition, it was concluded that it modifi

148 ostsynaptic receptor kinetics with a loss of paired-pulse inhibition.

149 reased inhibition contributed to the reduced paired-pulse inhibition.

150 lation, latencies of ON L-IPSCs increased at paired-pulse intervals (PPIs) of 50 and 300 ms, whereas

151 icited by transcranial magnetic stimulation, paired-pulse intracortical inhibition, spinal motor neur

152 goldfish Mb bipolar cell (BC) terminals with paired-pulse light stimulation, we isolated and quantifi

153 as normal but long-term depression evoked by paired-pulse low-frequency stimulation was modestly faci

154 refore assessed SI excitability by combining paired-pulse median nerve stimulation with recording som

155 e investigate the time course of single- and paired-pulse MEP modulation.

156 Paired-pulse MEPs were facilitated, whilst single-pulse

157 onstration that the LLSR can be modified via paired-pulse methods, and may open up new possibilities

158 ation was delivered as single pulses (n=55), paired-pulses (n=15) and tetanic trains (n=11).

159 of the population spikes (PS) in response to paired-pulse orthodromic stimulation.

160 Using a spatiotemporal paired-pulse paradigm, this study revealed that fundamen

161 neurons after activation of nAChRs during a paired-pulse paradigm.

162 acortical M1 excitability was measured using paired pulse paradigms: short and long interval intracor

163 ally, during a train of depolarizing pulses, paired pulse plasticity was significantly changed by usi

164 mbrane capacitance measurements we find that paired-pulse plasticity at an adult frog auditory hair c

165 We found paired-pulse plasticity at corticostriatal synapses refl

166 Input-output curves and paired-pulse plasticity were not significantly altered i

167 EPSC amplitude and paired-pulse plasticity, however, was influenced by bloc

168 ensitization participates in corticostriatal paired-pulse plasticity.

169 conservatively be 10 mM in order to maximize paired-pulse population responses while the presence of

170 ChRs possess a newly described phenomenon of paired-pulse potentiation that may be involved in regula

171 s observed, a phenomenon referred to here as paired-pulse potentiation.

172 perties of short-term depression elicited by paired-pulse (PP) and train stimulation.

173 transcranial magnetic stimulation (TMS) in a paired pulse protocol to investigate interhemispheric in

174 ic depression at rod and cone synapses using paired-pulse protocols involving two complementary measu

175 We used paired-pulse protocols with intracortical microstimulati

176 Similarly, in response to paired-pulse protocols, short term facilitation occurred

177 d enhanced short-term plasticity in terms of paired pulse ratio (PPR) and release probability (Pr), c

178 wofold by 1.0 mM TEA, with a decrease in the paired pulse ratio (PPR), effects not reproduced by bloc

179 bility (Pr), and the concomitant increase in paired pulse ratio (PPR), which occur in barrel cortex d

180 tic currents (sEPSCs) and an increase in the paired pulse ratio (PPR).

181 Whisker deprivation increased the paired pulse ratio at L4-L2/3 synapses and slowed the us

182 s to 2.4 +/- 0.4 s, P = 0.02), and decreased paired pulse ratio from 1.18 +/- 0.06 to 0.97 +/- 0.03 (

183 d by increased mEPSC frequency and decreased paired pulse ratio in core MSNs.

184 st, increased the amplitude, and reduced the paired pulse ratio of evoked IPSCs.

185 This modulation also shifts the paired pulse ratio of the layer 4 input from depression

186 so decreased the amplitude but increased the paired pulse ratio of the monosynaptic EPSCs in SNr GABA

187 ased the average amplitude and decreased the paired pulse ratio, consistent with a presynaptic site o

188 ased the average amplitude and decreased the paired pulse ratio, consistent with a presynaptic site o

189 lf-amplitude of EPSPs and IPSPs and the EPSP paired pulse ratio.

190 and there was a significant increase in the paired pulse ratio.

191 The paired-pulse ratio (IPSC(2)/IPSC(1)) of the total IPSC w

192 f Munc13-3 (Munc13-3(-/-)) show an increased paired-pulse ratio (PPR), which led to the hypothesis th

193 ffect was associated with an increase in the paired-pulse ratio and a decrease in the frequency of mi

194 Paired-pulse ratio and coefficient of variance analyses

195 4-L2/3 synapses, accompanied by increases in paired-pulse ratio and coefficient of variation, indicat

196 ed inhibitory synapses exhibited increase in paired-pulse ratio and in the coefficient of variation o

197 of LTD is not associated with changes in the paired-pulse ratio and is blocked by loading with a post

198 ression is accompanied by an increase in the paired-pulse ratio and the coefficient of variance, sugg

199 correlated with changes of release indices: paired-pulse ratio and the inverse of the coefficient of

200 CD rats displayed an increase in paired-pulse ratio in both glutamatergic synapses (+48 +

201 CCK reduced the coefficient of variation and paired-pulse ratio of AMPA EPSCs suggesting that CCK fac

202 NE increased the paired-pulse ratio of eEPSCs and reduced the frequency o

203 amplitude of evoked EPSCs, and decreased the paired-pulse ratio of eEPSCs in ten neurons.

204 entiate evoked EPSCs (eEPSCs) and change the paired-pulse ratio of eEPSCs.

205 ally reduced the amplitude and increased the paired-pulse ratio of EPSCs evoked by electrical stimula

206 dition, administration of PrRP decreased the paired-pulse ratio of EPSCs evoked by two identical stim

207 frequent and smaller miniature EPSCs, higher paired-pulse ratio of EPSCs, smaller AMPAR-mediated EPSC

208 f the AMPA component, nor does it affect the paired-pulse ratio of EPSCs.

209 ty, decreased mEPSC amplitude, and increased paired-pulse ratio of evoked EPSCs.

210 istributions of miniature IPSCs, whereas the paired-pulse ratio of evoked IPSCs was unaffected, sugge

211 Changes to the paired-pulse ratio of inputs to the EP suggested that do

212 rter inhibitor reduced the amplitude but not paired-pulse ratio of NMDAR-mediated excitatory postsyna

213 ng the frequency of synaptic events, and the paired-pulse ratio of synaptic inputs to BLA pyramidal n

214 crease was accompanied by an increase in the paired-pulse ratio of two consecutive eEPSCs, and a decr

215 y the mGluR agonist-mediated increase in the paired-pulse ratio of two consecutive eIPSCs in conjunct

216 The toxin effects on the paired-pulse ratio resulted in different phenotypes depe

217 In addition, nicotinic effect on mEPSC or paired-pulse ratio was also prevented by MLA.

218 y after head injury; no concurrent change in paired-pulse ratio was found in granule cells after pair

219 The paired-pulse ratio was increased for IPSCs evoked after

220 re decreased in amplitude by leptin, and the paired-pulse ratio was increased, suggesting effects on

221 cell EPSCs such as kinetics, amplitude, and paired-pulse ratio were similar across cortical subdivis

222 ria, including the coefficient of variation, paired-pulse ratio, AMPA-NMDA receptor activity, and the

223 m) decreased eIPSC amplitudes, increased the paired-pulse ratio, and attenuated isoflurane-induced in

224 s (IC(50) of 240+/-20 microm), increased the paired-pulse ratio, and decreased the frequency of mIPSC

225 Changes in failure rate, in paired-pulse ratio, and in the coefficient of variation

226 nses was accompanied by a marked decrease in paired-pulse ratio, indicating a presynaptic mechanism o

227 associated with changes of release indices: paired-pulse ratio, inverse coefficient of variation and

228 ted short-term plasticity as assessed by the paired-pulse ratio, regardless of the initial release pr

229 ese effects are presynaptic by measuring the paired-pulse ratio, variance of EPSC amplitudes, and res

230 n coefficient of variation with no change in paired-pulse ratio--and depend on GABAB receptor signali

231 ked from the dorsal root with an increase in paired-pulse ratio.

232 t of evoked IPSCs (eIPSCs), and enhanced the paired-pulse ratio.

233 evoked EPSCs (eEPSCs), and reduced the EPSC paired-pulse ratio.

234 (SC) pathway revealed significantly enhanced paired pulse ratios (PPRs) in Dyt1 DeltaGAG heterozygous

235 Interestingly, EPSC paired pulse ratios in the CA1 were enhanced without a c

236 Paired pulse ratios of electrically evoked postsynaptic

237 his enhancement, we estimated the changes in paired-pulse ratios (PPRs) and RRP size during PTP.

238 ed increased sEPSC frequencies and decreased paired-pulse ratios (PPRs) while D2 cells displayed larg

239 NT application increased paired-pulse ratios and decreased extracellular levels o

240 We further observed reductions in both the paired-pulse ratios and the enhanced short-term depressi

241 In contrast, paired-pulse ratios decreased in trained animals as well

242 Additional measurements of paired-pulse ratios showed no significant difference bet

243 Changes in miniature IPSCs and evoked IPSC paired-pulse ratios suggested altered probability of GAB

244 However, IPSP paired-pulse ratios were unchanged by CGRP, and there wa

245 fficient of variation of EPSPs, and increase paired-pulse ratios, consistent with a reduced probabili

246 mEPSCs, but unchanged mEPSC frequencies and paired-pulse ratios, suggesting altered postsynaptic eff

247 ervated synapses, quantified by decreases in paired-pulse ratios.

248 nses, accelerated desensitization and slowed paired pulse response recovery.

249 In accord with this, paired-pulse response ratios, a measure of transmitter r

250 of glutamine (0.5 mM) has minimal effects on paired-pulse responses and high-K+ induced epileptiform

251 tic vesicle release probability, assessed by paired-pulse responses, synapse maturation, assessed by

252 P14/N20, N20/P25 and P25/N33 components) and paired-pulse SSEPs between S1s (interhemispheric inhibit

253 was assessed using motor threshold (MT) and paired pulse stimulation at short (2-15 milliseconds) an

254 Paired pulse stimulation with intervals of 10-100 ms cau

255 tio and CA1 output are partially restored by paired-pulse stimulation at short intervals, indicating

256 Paired-pulse stimulation caused greater depression of fa

257 Paired-pulse stimulation depresses high-probability site

258 1 channels regulate cortical excitability to paired-pulse stimulation in humans.

259 Paired-pulse stimulation of the GP nerve in 13 rats prod

260 In vitro paired-pulse stimulation of the mixed perforant path rev

261 Paired-pulse stimulation of the perforant pathway was us

262 EPSCs were evoked by paired-pulse stimulation or by application of stimulus t

263 function assessed using brief repetitive or paired-pulse stimulation protocols, also revealed signif

264 Bipolar paired-pulse stimulation was applied to the Schaffer col

265 eover, analysis of the effects of ethanol on paired-pulse stimulation, spontaneous IPSC events, and b

266 Paired-pulse stimulation, the application of two stimuli

267 iriform cortical neurons and facilitate with paired-pulse stimulation, whereas distal dendrodendritic

268 ease in cleft glutamate concentration during paired-pulse stimulation.

269 By varying the interpulse interval (IPI), paired-pulse stimulations caused: a depression (20 ms IP

270 Paired-pulse stimuli indicated a postsynaptic site of ac

271 Further Ca2+ influx during paired-pulse stimuli then leads to depression.

272 Furthermore, paired-pulse stimuli with interpulse intervals of 200-40

273 ion of the GP nerve in 13 rats produced both paired-pulse suppression (n=11) and paired-pulse enhance

274 hyper-inhibition, i.e., abnormally increased paired-pulse suppression and an abnormally high resistan

275 post-SE, granule cells exhibited diminished paired-pulse suppression and decreased seizure discharge

276 Paired-pulse suppression and epileptiform discharge thre

277 Our data demonstrate that paired-pulse suppression of human SI is significantly re

278 ate gyrus abolished the abnormally increased paired-pulse suppression recorded in chronically hyper-i

279 We found that paired-pulse suppression was characterized by substantia

280 d participants who showed either low or high paired-pulse suppression.

281 Paired-pulse synaptic depression at TC projections lasts

282 Paired-pulse tactile stimulation revealed a dramatic shi

283 or conditioning pulse over PMd (CS1) using a paired pulse TMS design.

284 We suggest that paired pulse TMS may be capable of investigating propert

285 subjects prepare to grasp a visible object, paired-pulse TMS at a specific interval facilitates moto

286 of glutamate transmission) explored through paired-pulse TMS of the primary motor cortex.

287 Paired-pulse TMS was delivered to the left hemisphere at

288 tracortical facilitation (ICF) produced by a paired-pulse TMS, and forearm flexor H reflexes before a

289 Paired-pulse transcranial magnetic stimulation (ppTMS) w

290 Previous results using paired-pulse transcranial magnetic stimulation (TMS) hav

291 erior or posterior AC areas using MRI-guided paired-pulse transcranial magnetic stimulation (TMS) whi

292 ight play a role in its genesis, single- and paired-pulse transcranial magnetic stimulation (TMS), an

293 tability assessed in MS patients by means of paired-pulse transcranial magnetic stimulation (TMS).

294 Paired-pulse transcranial magnetic stimulation indexed f

295 We used paired-pulse transcranial magnetic stimulation over prim

296 Previous studies have used paired-pulse transcranial magnetic stimulation to show t

297 GABA(A)ergic intracortical inhibition using paired-pulse transcranial magnetic stimulation, and (2)

298 Using paired-pulse transcranial magnetic stimulation, we inves

299 The nAChRs were activated using a paired-pulse uncaging protocol, where the duration of th

300 Eight identical paired pulses were applied during one stimulation train