ライフサイエンスコーパス: spike firing

1 in equal and independent of the frequency of spike firing.

2 non-linear patterns in Purkinje cell simple-spike firing.

3 ose mediated by channelrhodopsins or natural spike firing.

4 y without altering the temporal precision of spike firing.

5 overshoot with robust sustained or transient spike firing.

6 ressions were the only significant change in spike firing.

7 entiation of the hump potential to full Ca2+ spike firing.

8 lic period, but which had little relation to spike firing.

9 on but not D2 receptor activation to enhance spike firing.

10 ession of conditional increases in CS-evoked spike firing.

11 concentration, cells responded with sporadic spike firing.

12 -mediated modulation of spontaneous neuronal spike firing and CB1R-mediated presynaptic inhibition of

13 onship between the learned changes in simple-spike firing and learning in eye velocity suggests an or

14 c HCN channels in pyramidal neurons modulate spike firing and synaptic potential integration by influ

15 reduce spike frequency and curtail sustained spike firing and that these effects entail protein kinas

16 tOH (11-66 mM) also decreased current-evoked spike firing and this was accompanied by a decrease in i

17 ctivity (increased responsiveness, irregular spike firing, and increased burst activity) in SNL rats.

18 eta frequency stimulation, decreased complex spike firing, and reduced the p42/44MAPK-mediated phosph

19 he distinction between synaptic activity and spike firing, and species differences encourage caution

20 evented EtOH's effect on holding current and spike firing, and western blotting revealed the presence

21 With simple-spike firing as observed in vivo, the presentation of a

22 e concentration, reflecting the abolition of spike firing at pre-pulse concentrations which still evo

23 threshold to spike and increases the gain of spike firing by 2- to 3-fold.

24 ata suggest that these pathways may increase spike firing by inhibition of a slow A-type potassium cu

25 ns, demonstrating that the changes in simple spike firing can be independent of climbing fiber input.

26 igated the intrinsic membrane properties and spike firing characteristics of rostral ipsi-lesional MV

27 lation on Kv4 channel control of the gain of spike firing depended on a signaling cascade leading to

28 , I(h); how I(h) influences excitability and spike firing depends primarily on channel distribution i

29 GN and BLA exhibit associative plasticity of spike firing during auditory fear conditioning.

30 h is correlated with the amount of RD-evoked spike firing during the induction protocol.

31 lobe vermis and hemisphere have high simple spike firing frequencies that precede complex spikes wit

32 ts is the modulation of Purkinje cell simple spike firing frequency, which has implications for contr

33 urst firing into physiological tonic, single-spike firing in 6-OHDA rats in vivo.

34 lectrical synapses could promote coordinated spike firing in a cellular assemblage of GnRH1 neurons t

35 Rates of simple spike firing in both on-beam and off-beam Purkinje cell

36 in, a selective SK channel blocker, affected spike firing in hippocampal neurons in different ways.

37 The results demonstrate that simple spike firing in lobules IV-VI is significantly correlate

38 e show that dopamine-mediated enhancement of spike firing in NAcb shell medium spiny neurons was prev

39 The two optoXRs exerted opposing effects on spike firing in nucleus accumbens in vivo, and precisely

40 show that a dopamine-induced enhancement of spike firing in nucleus accumbens neurons in brain slice

41 s of odorant receptors, inhibiting the basal spike firing in olfactory sensory neurons.

42 Synchronous spike firing in previously silent neurones could be driv

43 In this manner, I(h) can enhance spike firing in response to an EPSP when spike threshold

44 cal blockade of I(h) significantly increased spike firing in RTN neurons and large spontaneous IPSC f

45 ransmission and the consequent STN-triggered spike firing in SNr neurons.

46 Contextual modulation of spike firing in the amygdala is a putative mechanism for

47 periments that dissociate auditory CS-evoked spike firing in the lateral amygdala (LA) and both condi

48 d a substantial increase in both CS-elicited spike firing in the MGN and conditional freezing behavio

49 onditioning-related increases in CS-elicited spike firing in the MGN and conditional freezing to the

50 attenuates the ability of the vSub to drive spike firing in the NAc.

51 ppear to mediate dopaminergic enhancement of spike firing in the NAcb shell, and may therefore play a

52 g, and immunohistochemistry, we find that 1) spike firing is inhibited by dopamine and SKF 83959 (an

53 of the cerebellar cortex, changes in simple spike firing likely reflect the contribution of the cere

54 wed modulation of synaptic potentials and/or spike firing locked to the oscillation produced by venti

55 a concise model of the synaptic input driven spike firing mechanism that gives a close quantitative m

56 slices, by combining patch-clamp analysis of spike firing, membrane currents and synaptic inputs with

57 lative physiological importance of different spike-firing modes remains unclear.

58 In contrast, the simple spike firing of 91.0% of the Purkinje cells was not sign

59 Two sets of analyses of the simple spike firing of 97 Purkinje cells examined the effects o

60 r the expression of plasticity in the simple-spike firing of cerebellar Purkinje cells during trial-o

61 ll three monoamines decreased current-evoked spike firing of lOFC neurons and this action required Gi

62 hat ethanol inhibits persistent activity and spike firing of PFC neurons and that the degree of ethan

63 s occur in both the simple spike and complex spike firing of Purkinje cells.

64 id not yield increases in either CS-elicited spike firing or freezing to the tone CS.

65 urons in model networks may exhibit periodic spike firing or synchronized membrane potentials that gi

66 voked, as well as the depolarization-induced spike firing pattern of ganglion cells.

67 lates On and Off EPSPs, and the light-evoked spike firing pattern of On-Off ganglion cells.

68 ble of supporting a diversity of multineuron spike firing patterns from overlapping sets of neurons.

69 constant-velocity motion produces irregular spike firing patterns, and spike counts typically have a

70 gating to regulate membrane excitability and spike firing patterns.

71 ns were not simply movement-related in their spike-firing patterns but instead were selectively modul

72 tex, and they also had similar accommodating spike-firing patterns.

73 and a larger DAP amplitude, and enhanced the spike-firing precision and reliability of the calyx term

74 lectrodes, cell resting potential (V(m)) and spike firing properties were unaffected over 10-15 min r

75 hways; 2) complex-spike responses and simple-spike firing rate are correlated across the Purkinje cel

76 the Purkinje cell population; and 3) simple-spike firing rate at the time of an instruction for lear

77 epetitions of a learning instruction, simple-spike firing rate becomes progressively depressed in Pur

78 e found to increase or decrease their simple spike firing rate during microsaccades.

79 onse to a learning instruction causes simple-spike firing rate of Purkinje cells in the floccular com

80 nesthetized adult rats demonstrated that the spike firing rate was increased by the GluN2C/D potentia

81 on, resulting in a nonlinear increase in the spike firing rate, particularly at temperatures above ap

82 ciated with a subsequent reduction in simple spike firing rate.

83 nce always reflected a significant change in spike firing rate.

84 hich information is contained in the average spike firing rate.

85 lation of Purkinje cell membrane current and spike-firing rate.

86 s of spikelets are preceded by higher simple spike firing rates but, following the complex spike, sim

87 greater pressure-dependent increases in ACC spike firing rates in EA rats compared with controls.

88 se including sound evoked potentials and the spike firing rates of AC neurons were recorded right aft

89 position of the cursor was controlled by the spike firing rates recorded from the same site.

90 in primary visual cortex, V1, increase their spike firing rates to signal image segmentation and atte

91 ed increases in contrast by decreasing their spike firing rates, two types of inhibitory neurons in t

92 oth K+ channel blockers increased average CS spike-firing rates.

93 report that modulation targets properties of spike firing rather than action potential shape, involve

94 In a majority of Purkinje cells, simple spike firing recorded before and during adaptation demon

95 ynaptic mechanisms that enable this accurate spike firing remain poorly understood.

96 Analysis of Purkinje cell complex spike firing revealed that feedback in the cerebellar nu

97 The dose-response relation for spike firing rose at lower odour concentrations than the

98 ty of LA neurons exhibited context-dependent spike firing; short-latency spike firing was greater to

99 aneously recorded neurons synchronized their spike firing similarly during both the high-gamma-band a

100 GDP-beta-S, DA induced a further decrease in spike firing, suggesting the involvement of a non-GIRK c

101 ptors mediate stress-induced changes in mPFC spike firing that contribute to extinction impairments.

102 sistently decreased ( approximately 22%) and spike firing threshold (V(th)) was raised ( approximatel

103 EPSPs and bringing the neuron closer to the spike-firing threshold than the callosal pathway.

104 )-mediated Ca(2+) signals strongly inhibited spike firing through activation of K(+) membrane conduct

105 til, at the highest pre-pulse concentrations spike firing was abolished despite the continued presenc

106 ontext-dependent spike firing; short-latency spike firing was greater to both CSs when they were pres

107 In this regard, dopaminergic enhancement of spike firing was prevented by inhibitors of protein kina

108 EtOH inhibition of spike firing was prevented by the GABAA antagonist picro

109 Thus, the structure of spike firing was reorganized during learning in relation

110 r, conditioning-related changes in CS-evoked spike firing were solely determined by the associative h

111 eptors (D1R and D2R), and that MCH increases spike firing when both D1R and D2R are activated.

112 responses, as well as in action potential ("spike") firing, wherein all mitral cells affiliated with