ライフサイエンスコーパス: neuronal excitation

1 ation of ASICs in the medulla also triggered neuronal excitation.

2 anging from epithelial HCO3 (-) secretion to neuronal excitation.

3 s and extrasynaptic receptors in controlling neuronal excitation.

4 t unconjugated CGRP8-37, prevented sustained neuronal excitation.

5 conversion of light mechanical stimuli into neuronal excitation.

6 )) from internal stores and elicit prolonged neuronal excitation.

7 le in the brain by controlling the extent of neuronal excitation.

8 dynamin, ERK, and PKC suppressed persistent neuronal excitation.

9 athways and contributes to the regulation of neuronal excitation.

10 hibits the Kir3.1/3.2 channels, resulting in neuronal excitation.

11 as mediated by the alpha7 nAChR and required neuronal excitation.

12 s inhibit Kir3 (GIRK) channels, resulting in neuronal excitation.

13 of these hormonal actions would increase VMN neuronal excitation.

14 e stability will have major consequences for neuronal excitation.

15 t transcriptional changes observed following neuronal excitation.

16 ement as the sole basis for the drug-induced neuronal excitation.

17 BA may exert depolarizing actions leading to neuronal excitation.

18 uch as 175 microm, depending on the level of neuronal excitation.

19 lated responding, moreover, was dominated by neuronal excitations.

20 on, which correlated positively with delayed neuronal excitations.

21 sitive feedback loop, whereby sleep loss and neuronal excitation accelerate the accumulation of Abeta

22 We report that neuronal excitation acts with ER Ca(2+) stores to induce

23 Neuronal excitation and cardiorespiratory effects follow

24 A model to link neuronal excitation and CSAD activation by a Ca2+-depend

25 emerging data point to an imbalance between neuronal excitation and inhibition in at least a subgrou

26 These data suggest that neuronal excitation and inhibition, depending on the ana

27 ns in many genes affecting the ratio between neuronal excitation and inhibition.

28 tory brainstem is based on an interaction of neuronal excitation and inhibition.

29 Thus, calexcitin is implicated in neuronal excitation and plasticity.

30 ammatory pain hypersensitivity by increasing neuronal excitation and reducing inhibition.

31 the BAD-K(ATP) axis in metabolic control of neuronal excitation and seizure responses.

32 ed calcium channels (VGCCs) are essential to neuronal excitation and signal transduction.

33 NS implies that they serve distinct roles in neuronal excitation and signaling within the bowel.

34 hosphate (InsP(6)) levels rise and fall with neuronal excitation and silence, respectively, in the hi

35 xidant sensor in sensory neurons, initiating neuronal excitation and subsequent physiological respons

36 action in cryptochrome that alters levels of neuronal excitation, and represent a vital step forward

37 red spontaneously active cells, and enhanced neuronal excitations associated with movement.

38 ced elevation of extracellular glutamate and neuronal excitation augmented chemoreflex-mediated press

39 al neuron excitability, facilitating greater neuronal excitation by a subsequent stimulus.

40 Here, we induced neuronal excitation by anodal transcranial direct curren

41 To examine the inhibition of neuronal excitation by GIRKs, we overexpressed GIRKs in

42 smitter, GABA provides the dominant mode for neuronal excitation by inducing membrane depolarization

43 hat acidosis may inhibit low [Ca2+]o-induced neuronal excitation by inhibiting the activity of the cs

44 Neuronal excitation can be substantially modulated by al

45 Neuronal excitation can induce new mRNA transcription, a

46 ole treatment, which decreases glutamatergic neuronal excitation, decreases the synthesis and levels

47 By contrast, increasing neuronal excitation during the same period in wild-type

48 X formation in the adult rat brain following neuronal excitation evoked by seizure activity in vivo.

49 rring irritant compounds because the initial neuronal excitation evoked is followed by a long-lasting

50 Patterns of neuronal excitation in complex populations can be mapped

51 n the cerebellar cortex limits the extent of neuronal excitation in part through activation of metabo

52 iated inhibition is critical for restraining neuronal excitation in the brain, and therefore potentia

53 sistent with pyrethroids producing increased neuronal excitation in the cortex following a low-dose i

54 smitter, GABA, serves as the major source of neuronal excitation in the developing brain.

55 Therefore, we tested the hypothesis that neuronal excitation in the RP mediates tachycardia seen

56 ct stimulation of superior colliculus evoked neuronal excitation in ZIv and caused inhibition of spon

57 nal fluid, and Fra-like activity (indicating neuronal excitation) in paraventricular nucleus.

58 Zn(2+) release occurs with neuronal excitation, including seizure events, and exert

59 y, but was less effective in attenuating the neuronal excitations induced by GLU or associated with m

60 yers, or indeed whether modulation reflected neuronal excitation, inhibition, or both.

61 ced ANK3 exon 1b isoform expression disrupts neuronal excitation-inhibition balance.

62 Both auditory and visual stimuli produced neuronal excitation, involving a greater than 5-fold inc

63 Neuronal excitation is generally associated with an incr

64 Neuronal excitation is required for normal brain functio

65 Neuronal excitation is unexpected in the presence of thi

66 associated with fluctuations in spontaneous neuronal excitation, less is known about state-dependent

67 However, recent data demonstrate that neuronal excitation modulates both the pial and meningea

68 In both subgroups, neuronal excitations occurred with short latencies (4-8

69 on of the ARC or vlPAG respectively leads to neuronal excitation of the both nuclei during EA.

70 xogenous Plk2 expression or chronic elevated neuronal excitation, produces exaggerated homeostatic re

71 an attenuation of alpha activity induced by neuronal excitation related to stimulus onset.

72 rotein-synthesis-dependent implementation of neuronal excitation-repression equilibria.

73 naptic Ca2+ channels are crucial elements in neuronal excitation-secretion coupling.

74 Ischemia and seizure cause excessive neuronal excitation that is associated with brain acidos

75 TRPA1 channels are required for neuronal excitation, the release of inflammatory neurope

76 The device serves to regulate neuronal excitation through G-protein-coupled, metabotro

77 cal excitation is overwhelmed by spontaneous neuronal excitation through the modulation of alpha osci

78 S by demonstrating their inhibition produced neuronal excitation to alter basal cardiorespiratory fun

79 ochondria as a novel regulatory mechanism in neuronal excitation-transcription coupling.

80 The excessive neuronal excitation underlying several clinically import

81 In separate experiments, neuronal excitation was found to be suppressed by anesth

82 both calcium-signaling genes responsible for neuronal excitation, were deleted in 16 cases and duplic

83 bradycardia through TRPV1 sensitization and neuronal excitation, which may contribute to the pathoge