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 priming contribute to the long recovery from paired-pulse depression.

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

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

5 n evoked synaptic responses, and in synaptic paired-pulse depression.

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

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

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

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

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

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

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

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

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

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

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

17 2.6 and 5.9 ms, respectively, and exhibited paired-pulse depression (50-ms interval).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 of vesicles nearly doubles with cAMP, while paired-pulse depression experiments suggest that release

48 only becomes rate-limiting for recovery from paired-pulse depression for interstimulus intervals shor

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

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

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

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

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

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

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

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

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

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

59 4 of S2 responded with Class 1A properties (paired-pulse depression, large initial EPSPs, an all-or-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 Paired-pulse depression of ONL-evoked synaptic responses

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

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

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

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

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

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

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

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

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

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

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

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

97 2+) regulates the recovery from long-lasting paired-pulse depression, possibly thourgh a Ca(2+)-sensi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 01 had no effect on the potentiation of late paired-pulse depression recorded from kindled animals.

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

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

115 Paired-pulse depression results from the activation of i

116 suggest that multiple factors contribute to paired-pulse depression.SIGNIFICANCE STATEMENT Synaptic

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

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

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

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

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

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

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

124 Paired-pulse depression, the frequency of spontaneous mi

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

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

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

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

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

130 Early paired pulse depression was measured by inserting paired

131 Late paired pulse depression was measured by sequential chang

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

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

134 Yet, ribbon synapses suffer from profound paired-pulse depression, which takes seconds to subside.