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1 ry (n = 56) olfactory bulbs before and after theta burst stimulation.
2 otocol (DePo) consisting of brief continuous theta burst stimulation.
3 ts and 12 healthy subjects, using continuous theta burst stimulation.
4 after the repeated application of continuous theta burst stimulation.
5 d SM-expressing O-LM cells to afferent fiber theta burst stimulation.
6 eled spines produced by a threshold level of theta burst stimulation.
7 tiation (LTP) was induced at both sites with theta burst stimulation.
8 caused loss of long-term potentiation after theta-burst stimulation.
9 ral cell inhibition were also potentiated by theta-burst stimulation.
11 ed from this hypothesis, induction of LTP by theta-burst stimulation activates an actin regulatory pa
12 Ca(2+) influx through L-type channels during theta burst stimulation, an action exerted via 12(S)-HPE
13 mulation need to be further explored such as theta-burst stimulation and the combination of tDCS and
15 stimulation, a protocol that is weaker than theta-burst stimulation and was not sufficient to induce
18 ates long-term potentiation (LTP) induced by theta burst stimulation at Schaffer collateral synapses
19 transmission or on postsynaptic responses to theta burst stimulation, but nonetheless fully restored
20 lectrical stimulation of cortical inputs and theta burst stimulation combined with nicotine exposure
21 l processing in PMd, using either continuous theta burst stimulation (cTBS) at 80% (inhibitory cTBS)
23 s hypothesis, we applied off-line continuous theta burst stimulation (cTBS) over the left inferior fr
24 ed in 30 healthy volunteers after continuous theta burst stimulation (cTBS) over the right cerebellar
34 Long-term potentiation (LTP) in response to theta burst stimulation in the hippocampus was also redu
37 y, we found that hippocampal LTP, induced by theta-burst stimulation in mature (>8-week-old) GluR1 kn
39 Glycine-induced LTP was occluded by previous theta burst stimulation-induced potentiation, indicating
41 lts provide Class I evidence that continuous theta burst stimulation is a viable add-on therapy in ne
42 show that long-term potentiation induced by theta-burst stimulation is decreased after presynaptic b
43 -term potentiation induced in area CA1 using theta-burst stimulation is particularly compromised by t
45 ion with high-frequency stimulation, but not theta burst stimulation, is perturbed in hippocampal CA1
46 In healthy humans, we applied intermittent theta burst stimulation (iTBS) to the vermis lobule VII
51 s underwent long-term depression (LTD) after theta burst stimulation of the accessory olfactory bulb,
52 s with drug-resistant epilepsy suggests that theta burst stimulation of the fornix may be associated
53 th a small group of cases to explore whether theta burst stimulation of the fornix might improve memo
61 of synaptic potentiation (E-LTP) induced by theta-burst stimulation of rat hippocampal CA1 synapses.
63 , explored by means of transcranial magnetic theta burst stimulation over the primary motor cortex, w
66 ed for the induction of LTP in response to a theta burst stimulation protocol that depends on Ca(2+)
68 male, 3 female, mean age 34 +/- 3 years) or theta burst stimulation (TBS) (n = 9, 6 male, 3 female,
69 induction of long-term potentiation (LTP) by theta burst stimulation (TBS) activates beta1 integrins,
71 ent, long-term potentiation (LTP) induced by theta burst stimulation (TBS) at one retinal input sprea
73 adult rats, coincident pre- and postsynaptic theta burst stimulation (TBS) induced LTP and we show th
74 e we report that repetitive light stimuli or theta burst stimulation (TBS) of the optic nerve in the
79 ed in layer II/III, layer V or layer VI with theta burst stimulation (TBS), but was not observed in l
80 enetic deletion of MAGL selectively enhanced theta burst stimulation (TBS)-induced long-term potentia
81 oA antisense oligodeoxynucleotides inhibited theta burst stimulation (TBS)-induced RhoA upregulation
83 s in the synaptic response of SPNs following theta-burst stimulation (TBS) of cortical afferents.
84 ignificant deficits in LTP induced by either theta-burst stimulation (TBS) or "pairing." Slices expos
86 tag." TrkB is transiently activated by weak theta-burst stimulation (TBS) that induces only early-ph
88 h is induced by stimulation at theta rhythm [theta-burst stimulation (TBS)-LTP], but there was no imp
93 recovery period, either LTP (100-pulse, 5-Hz theta-burst stimulation [TBS]) or LTD (900-pulse, 1-Hz l
94 se in corticospinal excitability by applying theta burst stimulation to either the dorsolateral prefr
96 and adult rat hippocampus that had undergone theta-burst stimulation to produce long-term potentiatio
97 before and immediately after TMS (continuous theta burst stimulation) to the left or right AC, and th
98 ether the repeated application of continuous theta burst stimulation trains could ameliorate spatial
100 -D-aspartate receptor (NMDAR) opening during theta burst stimulation was enhanced by M(1) receptor ac
101 explored through intermittent or continuous theta-burst stimulation was also similar in the "G" and
104 ponses and long-term potentiation induced by theta-burst stimulation were decreased in nicastrin cKO
106 ntiation of glutamatergic transmission after theta burst stimulation with or without nicotine only oc
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