ライフサイエンスコーパス: plasma corticosterone

1 There was no difference in plasma corticosterone.

2 and vasopressin neurons along with decreased plasma corticosterone.

3 vated-mice exhibited a threefold increase in plasma corticosterone.

4 essor without altering the diurnal rhythm in plasma corticosterone.

5 7:00 and 19:00 h to assess diurnal rhythm of plasma corticosterone.

6 +/- 5 beats min(-1), saline versus Dex) and plasma corticosterone (5 +/- 2 versus 24 +/- 4 microg dl

7 icotropin releasing factor--CRF) levels, and plasma corticosterone activation in El and ddY mice in a

8 Plasma corticosterone also was evaluated both before and

9 glands resulted in a significant decrease in plasma corticosterone and a consequent increase in ACTH,

10 on (100 ng, i.p.) induced large increases in plasma corticosterone and a substantial, but short-lived

11 ats, and the slope of the regression between plasma corticosterone and ACTH increased from am to pm a

12 oise exposures led to similar habituation of plasma corticosterone and ACTH responses, heart rate, an

13 Moreover, the plasma corticosterone and adrenal cAMP responses to cort

14 weighed and blood collected for analysis of plasma corticosterone and adrenocorticotropic hormone (A

15 Plasma corticosterone and adrenocorticotropic hormone we

16 examine HPA axis responses as determined by plasma corticosterone and adrenocorticotropin hormone (A

17 Plasma corticosterone and adrenocorticotropin hormone le

18 It also increased plasma corticosterone and decreased plasma prolactin.

19 Although C1 stimulation elevated plasma corticosterone and increased both vagal and sympa

20 Thus, despite similar effects on plasma corticosterone and on hypothalamic stress-sensiti

21 MORKO mice showed a significant elevation in plasma corticosterone and pituitary proopiomelanocortin

22 this dose produced a significant increase in plasma corticosterone and plasma glucose in both SHM and

23 g, i.v.) produced dose-related elevations in plasma corticosterone and prolactin; these hormonal resp

24 elevated behavioral emotionality, high basal plasma corticosterone and reduced gene expression of Bdn

25 ween electric footshock-induced increases in plasma corticosterone and the acquisition, or lack there

26 lline methiodide (BMI) resulted in increased plasma corticosterone and, in contrast to NE treatment,

27 uate nucleus neuropeptide Y mRNA expression, plasma corticosterone, and glucagon levels together with

28 ated swim produced a persistent elevation in plasma corticosterone, and, consistent with prolonged bl

29 s of arginine vasopressin within the SCN and plasma corticosterone are both markedly phase advanced i

30 wever, vagotomy did not alter stimulation of plasma corticosterone at 1 or 2 h after low-dose IL-1 be

31 arginine-vasopressin (AVP), plasma ACTH and plasma corticosterone (B) were measured in four and 24 m

32 There were no marked differences in plasma corticosterone between genotypes, suggesting that

33 Both increase plasma corticosterone, but they have opposing actions on

34 aternal separation would elevate anxiety and plasma corticosterone compared to a nonhandled group.

35 SR mice displayed significant elevations in plasma corticosterone compared to CTL (p<0.002).

36 Increased BNST CRF expression did not affect plasma corticosterone concentration but did decrease CRF

37 In contrast, after 60 min of restraint plasma corticosterone concentration was significantly lo

38 itioned fear, coincident with an increase in plasma corticosterone concentration.

39 wever, in the corticosterone implanted rats, plasma corticosterone concentrations at 45 and 90 min po

40 These mice have approximately 80% higher plasma corticosterone concentrations compared with wild-

41 s of overt toxicity, significantly increased plasma corticosterone concentrations in SHM rats up to 4

42 ed from crossing heterozygotes displayed low plasma corticosterone concentrations resulting from a ma

43 OT deficient (OT-/-) female mice had higher plasma corticosterone concentrations than wild type (OT+

44 enal (HPA) axis activity, with elevated mean plasma corticosterone concentrations that resulted from

45 Adrenalectomy reduced plasma corticosterone concentrations to below detectable

46 carboetomidate, and vehicle groups, whereas plasma corticosterone concentrations were briefly (60-12

47 Plasma corticosterone concentrations were higher in male

48 Plasma corticosterone concentrations were higher in OT-/

49 Significantly increased plasma corticosterone concentrations were observed in ve

50 In multiple anesthetic dose studies, plasma corticosterone concentrations were persistently l

51 Plasma corticosterone concentrations were similar betwee

52 treatment on body condition, immune metrics, plasma corticosterone concentrations, total antioxidant

53 atase inhibitor DARPP-32; and late-afternoon plasma corticosterone concentrations.

54 eleterious consequences of high postischemic plasma corticosterone concentrations.

55 ssion and post-traumatic stress disorder, on plasma corticosterone (CORT) and on c-fos mRNA and brain

56 f-administering rats displayed reduced basal plasma corticosterone (CORT) levels but showed an augmen

57 Measures of plasma corticosterone (CORT) levels were also obtained.

58 OF or ether fumes both produced increases in plasma corticosterone (CORT) levels; notably, peak level

59 blocked IS-induced increased CBT, increased plasma corticosterone (CORT), decreased CBG, aphagia and

60 e exhibited elevated and prolonged levels of plasma corticosterone (CORT), interleukin (IL)-6 and IL-

61 l dopamine (DA) systems in the regulation of plasma corticosterone (CORT).

62 Restoring plasma corticosterone did not reverse the anxiolytic phe

63 149+/-2 mmoles/L), with a marked increase in plasma corticosterone (e.g. male offspring; 11.9 [9.3-14

64 als on the EPM, and exhibited an increase in plasma corticosterone following EPM and restraint that w

65 Gipr(-/-) mice exhibited significantly lower plasma corticosterone, glucocorticoid-treated HF-fed Gip

66 nocorticotropic hormone replacement elevated plasma corticosterone in ghr-/-, compared with WT mice,

67 The aberrant increase of plasma corticosterone in neonates increased the plasma c

68 of corticosterone to the amygdala increases plasma corticosterone in response to a behavioral stress

69 There was a brief 3-fold increase in plasma corticosterone levels 10 min after isolation.

70 e found an increase in startle amplitude and plasma corticosterone levels 30 min following intra-BNST

71 El mice exhibited significantly elevated plasma corticosterone levels 60 min following exposure t

72 Plasma corticosterone levels after bacterial lipopolysac

73 ticosterone content and abnormally increased plasma corticosterone levels after restraint stress, whe

74 Central administration of GLP-1 increases plasma corticosterone levels and elicits c-fos expressio

75 administration of NE provoked an increase in plasma corticosterone levels and Fos induction in the bo

76 is may, in part, be a consequence of reduced plasma corticosterone levels and reduced anxiety.

77 t cocaine taking is associated with elevated plasma corticosterone levels and that systemic infusion

78 Pre-test plasma corticosterone levels and the response of plasma

79 In these mice, plasma corticosterone levels are elevated, suggesting th

80 -like growth factor (IGF)-I are reduced, and plasma corticosterone levels are increased concomitantly

81 gous for the IL-6 transgene had normal basal plasma corticosterone levels but, after restraint stress

82 These animals had a marked increase in plasma corticosterone levels during the course of coliti

83 ntestinal polypeptide (VIP) had no effect on plasma corticosterone levels even in previously stressed

84 This effect was accompanied by a rise in plasma corticosterone levels in a dose- and time-depende

85 havioral stress significantly increased peak plasma corticosterone levels in both groups to a similar

86 ales, but not males, also had elevated basal plasma corticosterone levels in comparison with controls

87 privation resulted in significantly enhanced plasma corticosterone levels in Gipr(-/-) mice.

88 Basal- and toxin A-stimulated plasma corticosterone levels in ob/ob and db/db mice wer

89 The increased plasma corticosterone levels in the IL-6 transgenic mice

90 nduction of repeated transient elevations in plasma corticosterone levels mimicked the effects of rep

91 memory were not explained by differences in plasma corticosterone levels or numbers of Fos-labeled n

92 te putamen), as well as significantly higher plasma corticosterone levels than Group Random.

93 tion (LHSS) to evaluate whether the elevated plasma corticosterone levels that accompany food restric

94 Aged wild-type mice developed elevated plasma corticosterone levels that correlated with learni

95 In contrast, despite elevated plasma corticosterone levels throughout life, this gluco

96 In accordance with these findings, plasma corticosterone levels were decreased.

97 Baseline, peak, and clearance plasma corticosterone levels were determined.

98 Plasma corticosterone levels were equally reduced in bot

99 s absence in adrenalectomized mice, in which plasma corticosterone levels were essentially undetectab

100 anxiety, depression and fear memory, and the plasma corticosterone levels were evaluated under both b

101 and a modest, but significant, elevation of plasma corticosterone levels were found at the nadir tim

102 Plasma corticosterone levels were increased by LPS at a

103 Hippocampal MR and GR mRNA expression and plasma corticosterone levels were not significantly alte

104 al withdrawal symptoms or alterations in the plasma corticosterone levels were observed after 7 days

105 Furthermore, evening plasma corticosterone levels were reduced (30% decrease;

106 Pre-test plasma corticosterone levels were similar between LCR an

107 otropin at 20 hrs after the onset of sepsis, plasma corticosterone levels were similar to those in sh

108 ormone-deficient mice (CRH-/-) with very low plasma corticosterone levels would alter surfactant pool

109 ins responded to LPS by a 5-fold increase of plasma corticosterone levels, which were only moderately

110 ion correlated with a significant decline in plasma corticosterone levels.

111 ress evoked repeated transient elevations of plasma corticosterone levels.

112 ke state was assessed through measurement of plasma corticosterone levels.

113 te normal body size, and have elevated basal plasma corticosterone levels.

114 All five stressors increased plasma corticosterone levels: tail pinch, 246%; cold str

115 xhibit high concentrations of stress-induced plasma corticosterone, linking this behavior to the stre

116 Plasma corticosterone, measured after 4 trials, varied s

117 Plasma corticosterone, microbiota composition, and cecal

118 ne arterial pressure selectively in BHR, and plasma corticosterone only in female BHR.

119 L administration without increases in either plasma corticosterone or aldosterone as normally seen in

120 s (anxiety-related behaviors), to changes in plasma corticosterone or glucose levels, or to altered a

121 ulenin did not prevent effects of fasting on plasma corticosterone or hypothalamic levels of neuropep

122 ist had no effect on PACAP-induced increased plasma corticosterone, reduction of food intake, and bod

123 ed by the reduction of corticotropin-induced plasma corticosterone release and adrenal contents of cA

124 utilized to examine corticotropin-stimulated plasma corticosterone release as well as adrenal levels

125 dala (BLA), which correlates with protracted plasma corticosterone release.

126 ontrast, anterior BST lesions attenuated the plasma corticosterone response and decreased c-fos mRNA

127 maximum phase misalignment, the peak of the plasma corticosterone rhythm is shifted and the amplitud

128 eased basal, diurnal and stressor-stimulated plasma corticosterone secretion and basal plasma adrenoc

129 n behavior, but there was a marked effect on plasma corticosterone secretion between the groups.

130 to food-restricted rats and the magnitude of plasma corticosterone suppression was determined at two

131 ng plasma ACTH and differentially regulating plasma corticosterone through an ACTH- and sympathetic n

132 ma corticosterone levels and the response of plasma corticosterone to exposure to the EPM and restrai

133 The response of plasma corticosterone to the final stressor on day 15 wa

134 Blood pressure, heart rate and plasma corticosterone values were measured at rest durin

135 or 6 weeks (late) after adjuvant injection, plasma corticosterone was assayed and food intake was re

136 MTII (0.5 nmol)-induced increase in plasma corticosterone was attenuated by the selective MC

137 Basal plasma corticosterone was lower in MS than in NH females

138 Basal plasma corticosterone was slightly decreased in TIP39 kn

139 Furthermore, levels of plasma corticosterone were significantly correlated (inv

140 80% and elevated both tail-flick latency and plasma corticosterone when compared to saline-treated an