ライフサイエンスコーパス: population spike

1 ese events can be initiated by a propagating population spike.

2 contributes to the hypoxic inhibition of the population spike.

3 ired-pulse depression of the hippocampal CA1 population spike.

4 viral reproduction and resulting in a virus population spike.

5 evoked a greater [K+]o increase and a larger population spike.

6 d 80%, respectively, in the amplitude of the population spike.

7 tes simultaneously, and were associated with population spikes.

8 er area but had no effect on large amplitude population spikes.

9 y activity and in their possible origin from population spikes.

10 the absence of glutamine, suppressed evoked population spikes.

11 and glutamine (0.5 mM) similarly suppressed population spikes.

12 mM, in the absence of glutamine, attenuated population spikes.

13 feedback inhibition of perforant path-evoked population spikes.

14 only quinine reduced the frequency of field population spiking.

15 ent, only a fraction of rats showed multiple population spikes (35%), prolonged field postsynaptic po

16 ificantly reduced paired-pulse inhibition of population spike, a measure of poly-synaptic inhibitory

17 ing was better correlated with the spread of population spikes across the CA1 subfield than with freq

18 lance between oscillatory coupling and local population spiking activity and that these two levels of

19 first was observed as large amplitude field population spiking activity and the second manifested wi

20 o record ongoing and whisker stimulus-evoked population spiking activity in somatosensory cortex of u

21 We provide novel evidence that population spiking activity in the MTG forms distinct re

22 We statistically characterize the population spiking activity obtained from simultaneous r

23 rdings, a measure that is closely related to population spiking activity.

24 when determining long-timescale, persistent population spiking activity.

25 degrees C there was only 7% recovery of the population spike after 3 min of hypoxia.

26 of neuronal function (an electrically evoked population spike) after hypoxia was significantly dimini

27 Population spikes also propagated past microknife cuts w

28 Low-level stimulation, subthreshold for population spikes, also revealed changes in paired-pulse

29 bility were computed, namely, PPI using both population spike amplitude (PSA) and EPSP slope measures

30 ntal cage was associated with a reduction in population spike amplitude and an enhancement in paired-

31 ayed enhanced long-term potentiation of both population spike amplitude and excitatory post-synaptic

32 tory postsynaptic potential slope versus the population spike amplitude showed no difference between

33 in Ca influx directly affect the decline in population spike amplitude, consistent with electrophysi

34 rfused with 10 mM of glucose did not enhance population spike amplitude.

35 , which account for the rapid decline in the population spike amplitude.

36 ic potentials (EPSPs), long-term decrease of population spike amplitudes (PSAs) and EPSP-spike (E-S)

37 icantly larger maximal evoked EPSP slope and population spike amplitudes compared to the other strain

38 Synaptic activity was indicated by population spike amplitudes in the CA1 pyramidal cell su

39 nmol), enhanced the amplitude of the dentate population spike and also increased paired-pulse facilit

40 oxide, decreased the amplitude of the evoked population spike and increased paired-pulse facilitation

41 stress-specific effect on the fEPSP slope or population spike and no effect on paired-pulse plasticit

42 Hz, 15 mT) applied for 30 min amplified the population spike and the slope of EPSP recorded from str

43 inopyridine (4-AP) to induce large amplitude population spikes and 4-12Hz oscillatory activity within

44 ersible concentration-dependent increases in population spikes and decreases in IPSPs.

45 thway stimulation for 24 hours, which evoked population spikes and epileptiform discharges in both de

46 PFF can attenuate the effects of morphine on population spikes and IPSPs in the hippocampus, and sugg

47 G such that the frequency of large amplitude population spikes and the power of 4-12Hz oscillatory ac

48 lnikov homoclinic bifurcation, the number of population spikes and their precise timing are unpredict

49 ose that FOs may be produced by synchronized population spikes and their subthreshold sequelas in cor

50 es of pilocarpine-treated rats showed larger population spikes and weaker paired-pulse inhibition in

51 iminished and abolished, respectively, field population spiking and both antagonists reduced the powe

52 -2,3-dione (CNQX, 10 microM) abolished field population spiking and disrupted 4-12 Hz rhythmic oscill

53 dal cell spikes occurred in phase with local population spikes, as did the first spike of the interne

54 The nature of population spikes associated with seizure initiation (pr

55 o, occurring as a brief series of repetitive population spikes at 150-200 Hz in all hippocampal princ

56 ive hilar stimuli frequently evoked multiple population spikes at proestrus and estrus but only rarel

57 in both strains and was composed of a single population spike before and after bicuculline exposure.

58 tion of the conduction delay for the primary population spike, but typically was less, and approached

59 ents, NPFF (1 microM) alone had no effect on population spikes, but significantly and concentration-d

60 as possible to evoke a normal (>/=10 mV) CA1 population spike by orthodromic stimulation of the Schaf

61 1 was a potentiation of the amplitude of the population spike by up to 20%, but higher intensity fiel

62 fficiently with a nonlinear model based on a population spike code.

63 Antidromic population spikes confirmed projections from superficial

64 ch information about visual motion than does population spike count, even when the neurons respond in

65 Sporadic coherence events between neuronal population spike counts and LFPs were observed during SW

66 rast, temporal dispersion and latency of the population spike do increase with distance from the stim

67 chs of gamma-frequency activity which follow population spikes evoked by low frequency repetitive ext

68 The evoked population spike following the second stimulus was compa

69 The number of population spikes following 1 Hz stimulation increased s

70 Potentiation of EPSP and population spike, following tetanic stimulation of the p

71 re affected following FPI: (1) threshold for population spike generation was increased suggesting tha

72 on in stratum radiatum consisted of a single population spike in PrP gene knockout mice similar to th

73 ion as indicated by inhibition of the evoked population spike in the region CA1 of the hippocampus.

74 izure-like behavior, high stimulus intensity population spikes in the absence of long-term potentiati

75 ompletely dependent upon the total number of population spikes in the read-out window for this system

76 e MR also facilitated PP-evoked granule cell population spikes, in a dose-dependent manner.

77 bserved decreased paired-pulse inhibition of population spikes indicating a decrease in network inhib

78 ls, as well as the elevated amplitude of the population spike induced by HFS, both declined gradually

79 he results suggest that in slices with large population spikes, inhibitory responses to nucleotides a

80 The source of the fast population spikes is limited in space and moving at appr

81 rimary motor cortex of PD patients, neuronal population spiking is excessively synchronized to the ph

82 c plasticity, paired-pulse depression of the population spike, is also abnormal in the dentate gyrus

83 re applied to rat hippocampal slices showing population spikes larger than 5 mV peak-to-peak amplitud

84 ly activate granular cells, so variations in population spike latencies reflect changes in their intr

85 protocol caused an increase in the recorded population spike latency.

86 ate the ability to induce and maintain a CA1 population spike long-term potentiation (PS-LTP) in room

87 Estrogen decreased both population spike LTP and EPSP-spike potentiation at perf

88 In contrast, LTP of the population spike measure was paradoxically enhanced.

89 PILO decreased the amplitude of evoked population spikes measured in CA3.

90 ased the magnitude of PP-evoked granule cell population spikes (median increase = 78%) without affect

91 ularly recorded, orthodromically evoked, CA1 population spikes (neuronal function) was quantified.

92 Multiple population spikes occurred during both phases of the res

93 ethane anesthesia, kainate induced epileptic population spikes occurring at 30-40 Hz.

94 ed rats exhibited LTP of the fEPSP slope and population spike of similar magnitude and time course as

95 These results suggest that population spike patterns are drawn from a limited "voca

96 Across the nervous system, certain population spiking patterns are observed far more freque

97 Population spikes propagated past microknife cuts which

98 on was measured by sequential changes in the population spike (PS) amplitude during 5 Hz stimulation

99 Peak decrease in the population spike (PS) amplitude was by 72+/-17% of contr

100 Population spike (PS) amplitude was increased maximally

101 Population spike (PS) amplitudes from CA1 pyramidal cell

102 Following incubation, CA1 pyramidal cell population spike (PS) amplitudes were measured before an

103 No differences in baseline synaptic population spike (PS) and minor effects on excitatory po

104 , and threshold currents required to evoke a population spike (PS) did not differ for control and Pb-

105 Hydrogen peroxide (H(2)O(2)) inhibits the population spike (PS) evoked by Schaffer collateral stim

106 have shown that one form of neuroplasticity, population spike (PS) potentiation, can be established i

107 after trauma injury, improved CA1 antidromic population spike (PS) recovery to 91 +/- 2%, compared to

108 When 5 Hz stimulation triggered an AD, the population spike (PS) was initially depressed and then i

109 evaluated by measuring the amplitude of the population spikes (PS) in response to paired-pulse ortho

110 hippocampus, fast ripples (>200 Hz) reflect population spikes (PSs) from clusters of bursting cells,

111 citatory postsynaptic potentials (fEPSPs) or population spikes (PSs) were recorded from the CA1 hippo

112 ncrease in amplitude with increases in local population spike rate and synchrony.

113 eversed the hypoxic depression of the evoked population spike recorded from CA1 region of rat hippoca

114 The postsynaptic population spike recorded from the CA1 pyramidal cell re

115 Interictal population spikes recorded from principal neurons betwee

116 is preparation had no effect on the multiple population spikes recorded in Mg2+-free medium, and, in

117 were qualitatively similar to the effects on population spikes recorded in the CA1 cell layer followi

118 od was shortened to 3 min (37 degrees C) the population spike recovered to 94%.

119 ostsynaptic potential (pEPSP)] and cellular (population spike) responses and a suppression of GABA-me

120 By recording population spikes simultaneously throughout the unfolded

121 lation of the granule cells evoked bursts of population spikes superimposed on long-lasting negative

122 ogenous adenosine (100 microM) inhibited the population spike that had been partially resuscitated by

123 an be inferred by building isochrone maps of population spikes that the source generates.

124 1 receptor-mediated inhibition of the evoked population spike, the fEPSP and the intracellularly reco

125 Population spike time patterns were broadly conserved ac

126 therefore permit non-invasive assessment of population spike timing in human cortex.

127 gate the utility of tensor factorizations of population spike trains along space and time.

128 izations decompose a dataset of single-trial population spike trains into spatial firing patterns (co

129 We find that, as a population, spike trains of single units in primary vibr

130 included layer IV, horizontal propagation of population spikes was blocked.

131 ession of perforant path-evoked granule cell population spikes was lost in SE-experienced rats.

132 At 2 days following TBI, inhibition of population spikes was significantly reduced in the CA3 c

133 The percent recovery of population spikes was the measure of neuroprotection.

134 activated pyramidal cells represented by the population spike were modified by EM fields.

135 was applied to the Schaffer collaterals and population spikes were monitored in the CA1 pyramidal la

136 Population spikes were not found to propagate more than

137 Furthermore, population spikes were significantly increased in BACE1-

138 t as an increase in extracellularly recorded population spikes, while the reduction in synaptic GABA

139 rauma occurred in association with a greater population spike with shorter response latency.

140 Pyramidal cells fired exclusively during population spikes with an average probability of 0.34 on

141 Population bursts consist of 2 or more population spikes with peak to peak intervals of approxi

142 rm discharge, but increased the amplitude of population spikes within the evoked burst.

143 persynchronized action potentials (bursts of population spikes) within small discrete neuronal cluste