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

1 gh frequency tetanic stimulation, but not by low frequency stimulation.

2 duces qualitatively different sensation than low-frequency stimulation.

3 high probabilities of release in response to low-frequency stimulation.

4 were found in NMDA-dependent LTD induced by low-frequency stimulation.

5 F-PC synaptic transmission is reduced during low-frequency stimulation.

6 imulation or long-term depression induced by low-frequency stimulation.

7 term depression (LTD) was readily induced by low-frequency stimulation.

8 F facilitate long-term depression induced by low-frequency stimulation.

9 th those of sham controls that received only low-frequency stimulation.

10 excitation but is difficult to activate with low-frequency stimulation.

11 scrib synapse behaves relatively normally at low-frequency stimulation.

12 ked inhibitory synaptic currents (34%) after low-frequency stimulation.

13 ffect depotentiation, the reversal of LTP by low-frequency stimulation.

14 eated and untreated slices when initiated by low frequency stimulation (0.2 Hz).

15 rom the iLF, cLF, cIML and DH in response to low-frequency stimulation (0.03-0.1 Hz) were sensitive t

16 m depression (LTD) was elicited by prolonged low frequency stimulation (1 Hz, 15 min).

17 tors (betaARs) enables LTP induction also by low-frequency stimulation (1 Hz) or theta frequencies (~

18 The LTD induced by low-frequency stimulation (1 Hz) protocols was found to

19 Strikingly, low-frequency stimulation (1 Hz, 15 min) of the glutamat

20 ve of synaptic strength induced by prolonged low-frequency stimulation (1-5 Hz) is systematically up-

21 locked cocaine-primed reinstatement, whereas low-frequency stimulation (10 Hz) of this pathway in the

22 Transmitter output during low-frequency stimulation (2-5 Hz) is maintained entirel

23 This LTP required relatively low-frequency stimulation (20 Hz) and simultaneous activ

24 However, low-frequency stimulation (4 Hz) intermitted with fast r

25 rning and corrected forelimb stepping, while low-frequency stimulation (5 and 20 Hz) had no effect.

26 Sustained low-frequency stimulation (5 Hz) of primary afferent fib

27 At low-frequency stimulation, 5-CT markedly reduces charge

28 We show that at low-frequency stimulation, a filamentous-actin cell cort

29 We show that at low-frequency stimulations, a first sub-pool is graduall

30 Here, we report that repetitive low-frequency stimulation activates BK channels through

31 hip14 mutants show exocytic defects at low frequency stimulation and a nearly complete loss of

32 it long-term depression (LTD) in response to low-frequency stimulation and modest depolarization.

33 responses were observed for 56 (25%) of the low-frequency stimulations and for 76 (50%) of the high-

34 strate CA1-region long-term depression after low-frequency stimulation, and AC8 KO mice also fail to

35 1 hour), input-specific, depotentiates with low-frequency stimulation, and is blocked by N-methyl-D-

36 Evoked inhibition was larger under low-frequency stimulation, and, importantly, this change

37 Continuous and intermittent low frequency stimulation at 0.4 mA and 0.2 ms produced

38 ontaneous or evoked synaptic currents during low-frequency stimulation at 0.05 Hz in these Xenopus cu

39 Previous studies in slices have shown that low-frequency stimulation at 5 Hz, i.e., theta pulse sti

40 sion was extremely frequency dependent, with low-frequency stimulation being largely ineffective.

41 on is necessary for effective STN DBS, or if low frequency stimulation can be effective when paired w

42 rium oxide ((2) H(2) O) labeling and chronic low-frequency stimulation (CLFS) in vivo to investigate

43 rm of long-term depression (LTD) produced by low-frequency stimulation combined with glutamate transp

44 Low-frequency stimulation given shortly after LTP induct

45 tetanus [post-tetanic potentiation (PTP)] or low-frequency stimulation [homosynaptic depression (HSD)

46 ontractions at the intermediate length under low-frequency stimulation (i.e., 20 Hz).

47 How such low frequency stimulation in turn elicits sufficient cat

48 Chronic low-frequency stimulation increased the levels of slow-t

49 Chronic low-frequency stimulation increased the myosin heavy cha

50 Low frequency stimulation induced long-term depression (

51 Low-frequency stimulation induced a transient depression

52 Low-frequency stimulation induced LTP of synaptic zinc s

53 tively detect proBDNF or mBDNF, we show that low-frequency stimulation induced predominant proBDNF se

54 e and high levels of PE persistently reduced low-frequency stimulation-induced eCB-LTD.

55 c core, TLR4.KO animals exhibit a deficit in low-frequency stimulation-induced NMDAR-dependent long-t

56 erminals in the VTA in vivo is aversive, and low-frequency stimulation induces long-term depression i

57 ity suppresses epileptiform activity and (2) low frequency stimulation is an effective stimulation pr

58 e induction of long-term depression (LTD) by low-frequency stimulation is accompanied by a marked shr

59 diaphragm fatigue resulting from repetitive low-frequency stimulation is associated with lipid perox

60 sults of this preliminary study suggest that low-frequency stimulation is tolerable and reduces epile

61 Low-frequency stimulation known to induce long-term depr

62 We find that ACh release evoked by low-frequency stimulation leads to biphasic excitatory-i

63 In the presence of dynasore, low-frequency stimulation led to sustained accumulation

64 In control conditions (0.5 mM EGTA) low frequency stimulation (LFS; 200 stimuli) delivered t

65 he induction, but not maintenance, of LTD by low-frequency stimulation (LFS) (1 Hz/15 min) without af

66 Prolonged low-frequency stimulation (LFS) (900 pulses/1 Hz) of the

67 magnitude with that obtained with prolonged low-frequency stimulation (LFS) but requires far fewer s

68 tablished the efficacy of cell type-specific low-frequency stimulation (LFS) in controlling ictogenes

69 d the efficacy of optogenetic and electrical low-frequency stimulation (LFS) in interfering with seiz

70 Low-frequency stimulation (LFS) is an alternative tool f

71 frequencies during inflammatory injury, and low-frequency stimulation (LFS) of HT DRG neurons select

72 Low-frequency stimulation (LFS) of non-nociceptive affer

73 Like LTP, spine expansion was reversed by low-frequency stimulation (LFS) via a phosphatase-depend

74 Here, we use low-frequency stimulation (LFS), a protocol shown to ind

75 le the application of CCK4 induced LTP after low-frequency stimulation (LFS).

76 e in synaptic strength induced by subsequent low-frequency stimulation (LFS).

77 cke solution containing 100 microM choline), low-frequency stimulation (LFS, 3-5 Hz/15 min) of the pr

78 To produce LTD, prolonged low-frequency stimulation (LFS, 900 stimuli at 1 Hz) was

79 s preparation, we have tested the effects of low-frequency stimulation (LFS; 1 Hz for 15 min) on syna

80 In the hippocampal CA1 region, low-frequency stimulation (LFS; 200 pulses at 1 Hz) caus

81 t stimulation [TBS]) or LTD (900-pulse, 1-Hz low-frequency stimulation [LFS]) was induced in the DG o

82 mpus-mPFC-evoked potentials and an augmented low-frequency stimulation LTD of the pathway, suggesting

83 tients with epilepsy and that suppression by low frequency stimulation may be mediated by long-term d

84 LTD was input-specific, i.e., low frequency stimulation of one pathway produced LTD of

85 nerve can elicit or inhibit micturition, and low frequency stimulation of the compound pudendal nerve

86 Low-intensity, low-frequency stimulation of a vagus nerve elicited pauc

87 In conclusion, low-frequency stimulation of C1 neurons activates pontin

88 We previously found that low-frequency stimulation of direct temperoammonic (TA)

89 Prolonged low-frequency stimulation of excitatory afferents to bas

90 ed rapidly and reversibly by brief trains of low-frequency stimulation of mossy fiber axons.

91 Low-frequency stimulation of PAG afferents in vitro unex

92 Low-frequency stimulation of parallel fibers facilitates

93 Here, we report that low-frequency stimulation of PP inputs to CA1 has no las

94 ia gelatinosa neurons that can be induced by low-frequency stimulation of primary afferent Adelta-fib

95 The LTP evoked by low-frequency stimulation of primary afferents in the pr

96 psychiatric illnesses.SIGNIFICANCE STATEMENT Low-frequency stimulation of temperoammonic (TA) inputs

97 Low-frequency stimulation of the cholinergic axons drove

98 Low-frequency stimulation of the fornix activates the hi

99 Low-frequency stimulation of the fornix occurred in 4-ho

100 We tested the hypothesis that low-frequency stimulation of the fornix reduces interict

101 In current-clamp recordings, low-frequency stimulation of the MNTB led to a decline i

102 When LSO neurons were depolarized, low-frequency stimulation of the MNTB produced a signifi

103 This realization has led to low-frequency stimulation of the PPN for treating patien

104 the mechanisms of transmitter release during low-frequency stimulation of the Schaffer collaterals we

105 The differential effects of high- and low-frequency stimulation of this pathway seem most like

106 aintained in culture without or with chronic low frequency stimulation (one 5 s train of 5 Hz pulses

107 lease probability under conditions of either low-frequency stimulation or high-frequency augmentation

108 tion of LTP by high-frequency stimulation or low-frequency stimulation paired with postsynaptic depol

109 We found that low frequency stimulation, paired with greater pulse wid

110 mutant with reduced TrkB by a depolarization-low-frequency stimulation pairing protocol that puts min

111 Low-frequency stimulation produced long-term depression

112 Secondary EPSPs evoked by low-frequency stimulation ranged from 0.5 to 10 mV in am

113 We also found that low-frequency stimulation reduced the amplitude of the p

114 Repetitive low frequency stimulation results in potentiation of twi

115 Moreover, high-frequency, but not low-frequency stimulation selectively induced the secret

116 In contrast, prolonged low-frequency stimulation shifts the equilibrium toward

117 We suggest that repeated low-frequency stimulation simultaneous with LTD inductio

118 Here we show that, during low-frequency stimulation, single-vesicle fusion leads t

119 rimental design independent LTP and control (low-frequency stimulation) sites were examined.

120 , and PP1 in depotentiation of LTP caused by low-frequency stimulation that immediately follows LTP-i

121 ion-related co-firing, a process enhanced by low-frequency stimulation that promotes motor recovery.

122 The stronger the afferent activation during low-frequency stimulation, the greater was the probabili

123 Low frequency stimulation to the 'dominant' cortical swa

124 elicits larger spine calcium transients than low-frequency stimulation under all stimulus conditions,

125 For low-frequency stimulation under normal physiological con

126 np54p, long-term depression (LTD) induced by low-frequency stimulation was blocked in the mouse hippo

127 ause the induction of synaptic plasticity by low-frequency stimulation was enhanced at an unprimed sy

128 long-term depression evoked by paired-pulse low-frequency stimulation was modestly facilitated in th

129 evoked from the iLF, cLF, cIML and DH during low-frequency stimulation were reduced by NMDA receptor

130 ), synaptic strength recovered rapidly after low-frequency stimulation, whereas in another group of n

131 ptor activation, for instance in response to low-frequency stimulation, whereas LTP is induced by the

132 Conversely, low-frequency stimulation, which reduces the number of s

133 ORNs reliably follow low frequency stimulations with high fidelity by generat

134 otentiation was induced, however, by pairing low-frequency stimulation with direct depolarization of

135 est tremor may be significantly entrained by low frequency stimulation without stimulation timing-dep

136 We tested whether non-auditory low-frequency stimulation would increase audience dancin