ライフサイエンスコーパス: population spike

1 on of "neuronal avalanches" (i.e., spurts of population spiking).

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

3 contributes to the hypoxic inhibition of the population spike.

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

5 viral reproduction and resulting in a virus population spike.

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

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

8 tes simultaneously, and were associated with population spikes.

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

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

11 the absence of glutamine, suppressed evoked population spikes.

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

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

14 feedback inhibition of perforant path-evoked population spikes.

15 only quinine reduced the frequency of field population spiking.

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

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

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

19 urons transition from aperiodic uncorrelated population spike activity to become increasingly synchro

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

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

22 This work demonstrates the utility of population spiking activity for isolating neural rhythms

23 Finally, population spiking activity further increased in respons

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

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

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

27 viously been shown to correspond to neuronal population spiking activity of the first excitatory feed

28 We find that population spiking activity organizes into bursts during

29 Population spiking activity preceded actual movement, an

30 memory function involves patterns of neural population spiking activity, shaped by experience and re

31 provide a biomarker for bursts of underlying population spiking activity, we suggest that examining t

32 uronal coupling of LGN and MT cells to local population spiking activity.

33 coherence with corresponding rhythms in the population spiking activity.

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

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

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

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

38 Population spikes also propagated past microknife cuts w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 eptic networks (i.e., spontaneous interictal population spikes and seizures), the network structure i

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

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

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

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

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

64 -2,3-dione (CNQX, 10 microM) abolished field population spiking and disrupted 4-12 Hz rhythmic oscill

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

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

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

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

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

70 Our findings revealed that the delays in population spiking between brain regions vary depending

71 ve single-trial portrayal of evoked cortical population spike bursts in healthy human subjects.

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

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

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

75 1 was a potentiation of the amplitude of the population spike by up to 20%, but higher intensity fiel

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

77 sive single-trial analyses of human cortical population spikes concurrent with low-frequency mass pos

78 Antidromic population spikes confirmed projections from superficial

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

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

81 suggested that HFAbs reflect transitions to population spiking, denoting temporal windows for networ

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

83 show that abDGCs promote sparser hippocampal population spiking during mnemonic processing of novel s

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

85 duration in vivo and increased dentate gyrus population spikes ex vivo.

86 The evoked population spike following the second stimulus was compa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 icantly larger and spatially triggered local population spikes locked to the trough of the theta osci

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

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

107 known as "ping-ponging", in which different populations spike maximally in alternating time bins, ca

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

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

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

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

112 Multiple population spikes occurred during both phases of the res

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

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

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

116 retrieved target object can be decoded from population spike patterns in adjacent entorhinal cortex

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

118 Distributed neural population spiking patterns in macaque inferior temporal

119 Machine learning decoding revealed that dCA1 population spikes predicted BLA assembly firing rate, su

120 on of precise timing of feedforward thalamic population spiking, presenting a highly sensitive, timin

121 Population spikes propagated past microknife cuts which

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

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

124 Population spike (PS) amplitude was increased maximally

125 Population spike (PS) amplitudes from CA1 pyramidal cell

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

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

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

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

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

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

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

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

134 ynchronous neuronal firing phenomenon called Population Spikes (PS).

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

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

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

138 mma responses are primarily generated by the population spike rate of pyramidal neurons in layers V a

139 ocation: encoding perceived location through population spike rate relative to baseline.

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

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

142 Interictal population spikes recorded from principal neurons betwee

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

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

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

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

147 By recording population spikes simultaneously throughout the unfolded

148 ker trajectory endpoints could be decoded by population spiking, suggesting that PPC is involved in m

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

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

151 Full synaptic recovery engendered interictal population spikes that spread via long-distance synapses

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

153 1 receptor-mediated inhibition of the evoked population spike, the fEPSP and the intracellularly reco

154 Population spike time patterns were broadly conserved ac

155 opes in the brainstem, and for a distributed population spike-time code for which synchrony to the en

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

157 ed on the neuronal sequence within bursts of population spiking to represent information.

158 he previously observed mesoscale (fMRI, LFP, population spiking) to the microscale, namely, V (m) flu

159 We show that the pattern of population spike train coactivity carries stimulus-speci

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

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

162 n of these energy bursts into time-sequenced population spike trains may generate temporally unique "

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

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

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

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

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

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

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

170 Population spikes were not found to propagate more than

171 Furthermore, population spikes were significantly increased in BACE1-

172 sensory EEG/MEG responses that can represent population spikes when averaged over hundreds of trials

173 ntion-associated high-gamma oscillations and population spiking while abolishing slow waves in sleep-

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

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

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

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

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

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