ライフサイエンスコーパス: paired-pulse depression

1 ge all-or-none AMPA-mediated EPSP that shows paired pulse depression.

2 NMDA or kindling-induced modulation of late paired-pulse depression.

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

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

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

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

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

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

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

10 ent exocytosis was investigated by measuring paired-pulse depression.

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

12 Late paired-pulse depression (150-500 ms IPI) was significant

13 Paired pulse depression (20 ms ISI) was reduced in cases

14 on the stimulus intensity function for early paired-pulse depression (20-30 ms interpulse intervals,

15 2.6 and 5.9 ms, respectively, and exhibited paired-pulse depression (50-ms interval).

16 ments shown to increase the strength of late paired pulse depression, administration of the N-methyl-

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

18 owing paired pulse potentiation, two showing paired pulse depression and eleven with no significant n

19 rs in field CA1 exhibited a larger degree of paired-pulse depression and a slower recovery rate from

20 identified on the basis of their large size, paired-pulse depression and all-or-none appearance in re

21 tically on the GABA interneurons, attenuated paired-pulse depression and allowed for a normal and sta

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

23 (3) Paired-pulse depression and its regulation by age and se

24 and on the correlation between the degree of paired-pulse depression and the decay rate of the curren

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

26 Paired pulse depression at a 200 ms ISI was not signific

27 repetitive (5-20 Hz) stimulation, as well as paired-pulse depression at both GC and CA3 inputs to int

28 cesses responsible for the reduction in late paired-pulse depression at high stimulus intensities are

29 ibution of NMDA currents to the loss of late paired-pulse depression at high stimulus intensities in

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

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

32 onsiderable short-term plasticity, including paired-pulse depression at intervals <25 ms, intraburst

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

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

35 Pb exposure induced an increase in paired-pulse depression at the 20 ms 1PI and reduced pai

36 y contrast, desensitization plays no role in paired-pulse depression at the cerebellar climbing fiber

37 responses cannot account for its effects on paired-pulse depression, but that volatile anaesthetics

38 pre-train values, indicating a loss of late paired pulse depression by the middle of the train.

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

40 sion, but that volatile anaesthetics enhance paired-pulse depression by prolonging the decay of the s

41 was occluded, and in some cases converted to paired-pulse depression, by picrotoxin.

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

43 In contrast to late paired pulse depression, early paired pulse depression r

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

45 NMDA currents to reduce the strength of late paired-pulse depression in naive animals is altered foll

46 Two pulses of hindpaw stimulation caused paired-pulse depression in the ACC.

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

48 evoked glutamatergic EPSCs and a decrease in paired-pulse depression, indicating a presynaptic action

49 DAMGO decreased the magnitude of paired-pulse depression, indicating that mu receptors we

50 rrents (EPSCs) and decrease the magnitude of paired-pulse depression, indicating that opioid receptor

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

52 (2) Paired-pulse depression is reduced after dark rearing an

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

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

55 4 of S2 responded with Class 1A properties (paired-pulse depression, large initial EPSPs, an all-or-

56 these results suggest that a failure of late paired pulse depression may be a precipitating event in

57 ion, and our results suggest that the strong paired-pulse depression may be a result of activity-depe

58 epletion alone cannot account for the strong paired-pulse depression observed at some cortical synaps

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

60 y, changes in the strength of early and late paired pulse depression of dentate granule cell field po

61 al inhibition, monosynaptic evoked IPSCs and paired pulse depression of evoked EPSCs, were also impai

62 perforant path evoked field potentials or in paired pulse depression of evoked field potentials using

63 The retinogeniculate EPSP exhibited a paired-pulse depression of 60.3 +/- 5.6 % at 10 Hz, whil

64 tial AMPA receptor blockade had no effect on paired-pulse depression of AMPA EPSCs.

65 We have previously demonstrated that late paired-pulse depression of dentate granule cell field po

66 Paired-pulse depression of EPSPNs at 50 Hz was converted

67 At frequencies > 40 Hz it produced paired-pulse depression of EPSPNs, along with marked sum

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

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

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

71 lation of the medial perforant path produced paired-pulse depression of inter-pulse intervals (IPIs)

72 lofen and adenosine reduced the magnitude of paired-pulse depression of IPSCs, and neither blocked cu

73 Control experiments indicated that neither paired-pulse depression of IPSPs nor presynaptically med

74 pses and therefore contributes to short-term paired-pulse depression of minimal responses.

75 EPSPAs, which paralleled the time course of paired-pulse depression of monosynaptic IPSCs, and a pot

76 Partial NMDA receptor blockade reduced paired-pulse depression of NMDA but not of AMPA synaptic

77 tive postsynaptic holding potentials reduced paired-pulse depression of NMDA EPSCs to near that of AM

78 e NMDA channel with depolarization increased paired-pulse depression of NMDA EPSCs.

79 flux through NMDA receptors is important in paired-pulse depression of NMDA responses but has no eff

80 Paired-pulse depression of ONL-evoked synaptic responses

81 ced GABAergic inhibition onto granule cells, paired-pulse depression of perforant path-evoked granule

82 We find that paired-pulse depression of presynaptic release is not ac

83 tics such as halothane, is the prolonging of paired-pulse depression of the hippocampal CA1 populatio

84 AB response, as indicated by no reduction in paired-pulse depression of the monosynaptic GABAA respon

85 re that another form of synaptic plasticity, paired-pulse depression of the population spike, is also

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

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

88 SPNs in control medium whereas it eliminated paired-pulsed depression of EPSPNs in the presence of pi

89 ormal Mg(2+)-containing medium, resulted in 'paired-pulse depression' of EPSPN.

90 A failure of early paired pulse depression often precedes the onset of inte

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

92 se reducing glutamate release with low Ca2+, paired-pulse depression, or weak stimuli shortened the E

93 2+) regulates the recovery from long-lasting paired-pulse depression, possibly thourgh a Ca(2+)-sensi

94 In these thirty-two connections, paired pulse depression (PPD) was apparent (2nd EPSP int

95 Paired-pulse depression (PPD) and facilitation are found

96 Paired-pulse depression (PPD) appeared to be independent

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

98 neurons of ethanol-treated animals exhibited paired-pulse depression (PPD) compared with saline-treat

99 Sr2+ converted paired-pulse depression (PPD) of eIPSCs to a paired-puls

100 We studied paired-pulse depression (PPD) of GABA(A)ergic IPSCs unde

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

102 Paired-pulse depression (PPD) was not predominant in hig

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

104 have a high probability of release and show paired-pulse depression (PPD), whereas parallel fiber (P

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

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

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

108 01 had no effect on the potentiation of late paired-pulse depression recorded from kindled animals.

109 trast to late paired pulse depression, early paired pulse depression remained at maximum strength unt

110 spinal cord slices and enhancing hippocampal paired-pulse depression, respectively.

111 Paired-pulse depression results from the activation of i

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

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

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

115 s accompanied by a decrease in the extent of paired-pulse depression, suggesting that it is presynapt

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

117 hippocampal short- and long-term plasticity (paired-pulse depression, synaptic fatigue, long-term pot

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

119 Paired-pulse depression, the frequency of spontaneous mi

120 ntials resulted in statistically significant paired-pulse depression, the mean of the averaged second

121 neuronal calcium sensor-1 (NCS-1) can switch paired-pulse depression to facilitation without altering

122 -evoked IPSCs, baclofen causes a change from paired-pulse depression to paired-pulse facilitation, su

123 decay 11.2 +/- 0.9 ms, n = 7) IPSCs showing paired-pulse depression (to 68 +/- 5 %, n = 6).

124 Paired pulse depression was apparent at < 10 and 20-60 m

125 Early paired pulse depression was measured by inserting paired

126 Late paired pulse depression was measured by sequential chang

127 A decrease in late paired-pulse depression was observed at high stimulus in

128 A form of short-term presynaptic plasticity, paired-pulse depression, was not altered by retigabine,