ライフサイエンスコーパス: ERN

1 ERN activity was largest under conditions of high respon

2 ERN amplitude correlated with fMRI activation in both th

3 onflict-detection theory claims that ACC and ERN activity represent the detection of response conflic

4 negative (ERN) expression, rates for ERP and ERN diverged; that is, rates for ERP increased with adva

5 ied by ER expression, rates for both ERP and ERN flattened after 50 years of age.

6 f adaptive behavior differs between TRNs and ERNs.

7 inding was due to a significantly attenuated ERN amplitude in lesion patients compared with both sibl

8 moderator such that a more enhanced baseline ERN was associated with greater reduction in anxiety sym

9 Results indicated that baseline ERN was a significant treatment moderator such that a mo

10 ppears that the dynamics of coupling between ERN and post-error slowing between men and women is comp

11 A blunted ERN was associated with more severe negative symptoms an

12 e unaffected by pharmacogenetic factors, but ERN was decoupled from behavioral adaptation by SSRI adm

13 specially among individuals with an enhanced ERN.

14 determine the neural source of the enhanced ERN.

15 Here, we show that monkeys exhibit ERN and Pe components when they commit errors during a s

16 reased with advancing age, whereas rates for ERN flattened after 50 years.

17 In controls, error trials generated greater ERN activity than correct trials.

18 However, ERN and error positivity were unaffected by pharmacogene

19 ents with OCD showed significantly increased ERN amplitudes.

20 pants who avoided negative events had larger ERNs than those who were biased to learn more from posit

21 ct of conflict, positive learners had larger ERNs when having to choose among two good options (win/w

22 utational model further predicts that larger ERNs should be associated with better learning to avoid

23 on errors, the error-related negativity (Ne/ERN), in a task in which two types of errors could occur

24 etection are responsible for the observed Ne/ERN amplitude reductions.

25 Our data revealed a pattern of Ne/ERN amplitudes that closely mirrored the amount of monet

26 ndent change in posterror slowing and the Ne/ERN amplitude, questioning a direct link between the amp

27 slowing and whether the amplitude of the Ne/ERN predicts posterror slowing in the current task setti

28 s, we found an amplitude reduction in the Ne/ERN, contradicting the existence of a direct relationshi

29 ant correlations between the single-trial Ne/ERN amplitude and error-related reaction times.

30 The single-trial Ne/ERN distribution showed a reduced variance for middle-ag

31 rogen receptor-positive (ERP) and -negative (ERN) expression, rates for ERP and ERN diverged; that is

32 upling between the error-related negativity (ERN) and consecutive behavioural slowing.

33 ave focused on the error-related negativity (ERN) and error positivity (Pe) on error trials, as well

34 The error-related negativity (ERN) and error-related functional MRI (fMRI) activation

35 The error-related negativity (ERN) and positivity (Pe) are components of event-related

36 processing, namely error-related negativity (ERN) and positivity.

37 ration of both the error-related negativity (ERN) and the novelty-related frontocentral N2.

38 as measured by the error-related negativity (ERN) in the event-related potential, is a reliable findi

39 The error-related negativity (ERN) is an electrophysiological marker thought to reflec

40 e amplitude of the error-related negativity (ERN), a negative deflection in the electroencephalogram

41 We recorded the error-related negativity (ERN), an event-related brain potential proposed to refle

42 ies found that the error-related negativity (ERN), an event-related potential (ERP) originating in th

43 ted with a blunted error-related negativity (ERN), indicating a deficit in error monitoring.

44 as measured by the error-related negativity (ERN), is a transdiagnostic neurobiological marker of anx

45 c of an error, the error-related negativity (ERN).

46 The error-related negativity (ERN, or N(E)), an event-related brain potential, reflect

47 2, response-locked error-related negativity (ERN/Ne), and response-locked error positivity (Pe), meas

48 erroneous trials (error-related negativity--ERN) was diminished in patients with unilateral and bila

49 simvastatin, plus extended-release niacin ([ERN], 1,500 to 2,000 mg/day), with ezetimibe added as ne

50 ription factor, ERF Required for Nodulation (ERN), which contains a highly conserved AP2 DNA binding

51 o tested for effects of response conflict on ERN magnitude.

52 e and beyond other measures (i.e., N2, P300, ERN/Ne, age, sex, IQ, impulsivity, depression, anxiety,

53 : 1.21 [p = 0.017]) and the simvastatin plus ERN group (baseline HR: 1.25 [p = 0.001] and on-study HR

54 adaptive networks with enzymatic regulation (ERNs) have been investigated in detail.

55 Moreover, uncertain responses showed similar ERN activity as aware errors, in comparison with decreas

56 P2; error-monitoring, as indexed by smaller ERN/Ne; and adjusting response strategy posterror, as in

57 ough reduced compared with control subjects, ERN amplitude was greater in patients with higher neurot

58 However, there was no evidence that ERN reduced CV risk, despite favorable lipoprotein chang

59 ogether, these novel findings highlight that ERN may help guide treatment decisions regarding engagem

60 This theory predicts that ERN and ACC activity should increase directly with the d

61 We propose that ERN is a component of the Nod factor signal transduction

62 We show that ERN is necessary for Nod factor-induced gene expression

63 The ERN and the error positivity (Pe) were recorded from 33

64 The ERN modestly increased 1-year apoA-1 (7%), decreased apo

65 The ERN occurs only when subjects are aware of making an err

66 The ERN was profoundly blunted in the patient group, regardl

67 The ERN, hemodynamic responses following errors, and intrain

68 ver the error-detection theory, although the ERN was not associated with posterror slowing, as predic

69 A flanker task was used to elicit the ERN at baseline and 12 weeks later, following either CBT

70 bility and score agreement were high for the ERN, CRN, and Pe.

71 findings suggest that the PCC generates the ERN and communicates with the dACC to subserve error pro

72 acity to alter individual differences in the ERN, providing evidence that the ERN is not entirely sta

73 confidence responses that might increase the ERN amplitude.

74 nd magnetoencephalography data localized the ERN to the posterior cingulate cortex (PCC).

75 Moreover, the ERN has been assessed in relation to a number of persona

76 Increased intraindividual correlation of the ERN and activity of the presupplementary motor area was

77 to be at odds with prominent theories of the ERN and aMCC.

78 rors, and intraindividual correlation of the ERN and blood oxygen level-dependent activity were compa

79 s demonstration of macaque homologues of the ERN and Pe forms a keystone in the bridge linking human

80 Additionally, increased correlation of the ERN and presupplementary motor area may indicate stronge

81 ar, the reinforcement learning theory of the ERN may need to be modified because it may not suffice a

82 cifically, the error-detection theory of the ERN states that the ERN reflects ACC processing that is

83 ow a linear increase in the amplitude of the ERN with increasingly late responses.

84 to date has assessed the reliability of the ERN, Pe, and CRN.

85 cortex (aMCC), the neuronal generator of the ERN.

86 he dACC as the hemodynamic reflection of the ERN.

87 s of response similarity and conflict on the ERN, using a task that involved hand and foot movements.

88 es about the neural system that produces the ERN - one based on principles of reinforcement learning

89 uals with schizophrenia, indicating that the ERN and Pe are differentially related to psychotic illne

90 However, recent studies demonstrate that the ERN decreases after unaware errors.

91 Results also revealed that the ERN increased pre- to post-treatment among patients rand

92 Together these findings suggest that the ERN is activated by aware motor errors as well as sensor

93 We hypothesized that the ERN is dependent upon awareness, and predicted that prev

94 nces in the ERN, providing evidence that the ERN is not entirely static in patients with anxiety diso

95 Furthermore, we found that the ERN predicted consecutive behavioural slowing within sub

96 These results demonstrate that the ERN predicts the degree to which participants are biased

97 -detection theory of the ERN states that the ERN reflects ACC processing that is directly related to

98 We conclude that the ERN reflects medial frontal activity involved in the det

99 Thus, the ERN motif and residue Asp-142 in the loop 2 are of criti

100 To date, little is known about whether the ERN can inform the choice between first-line anxiety dis

101 anxiety disorder treatments and whether the ERN changes following treatment completion.

102 he study was to therefore assess whether the ERN is a treatment moderator and index of symptom change

103 al prefrontal damage, however, correct-trial ERN activity was equal to error-trial ERN activity.

104 -trial ERN activity was equal to error-trial ERN activity.