ライフサイエンスコーパス: plasma corticosterone

1 There was no difference in plasma corticosterone.

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

3 and vasopressin neurons along with decreased 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 ghrelin-KO mice during the clamps, increased plasma corticosterone and growth hormone.

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

21 rols, defeated B6 females exhibited elevated plasma corticosterone and increased c-Fos activation in

22 he WS-induced burying response and increased plasma corticosterone and interleukin-1beta (IL-1beta).

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

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

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

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

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

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

29 Stress elevated plasma corticosterone and upregulated the expression of

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

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

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

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

34 lase (Th)], glucocorticoid receptor (GR) and plasma corticosterone, as well as brain-derived neurotro

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

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

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

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

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

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

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

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

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

44 We compared circulating plasma corticosterone concentrations and body condition

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

46 ees C, and measured cloacal temperatures and plasma corticosterone concentrations at baseline and aft

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

48 st body temperature can significantly affect plasma corticosterone concentrations in reptiles, which

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

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

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

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

53 Adrenalectomy reduced plasma corticosterone concentrations to below detectable

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

55 Plasma corticosterone concentrations were higher in male

56 Plasma corticosterone concentrations were higher in OT-/

57 Significantly increased plasma corticosterone concentrations were observed in ve

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

59 Plasma corticosterone concentrations were similar betwee

60 to 29 degrees C showed a robust increase in plasma corticosterone concentrations with restraint stre

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

62 eleterious consequences of high postischemic plasma corticosterone concentrations.

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

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

65 While sex differences in stressor-induced plasma corticosterone (CORT) elevations and defensive be

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

67 take and increases anxiety-like behavior and plasma corticosterone (cort) levels in rats, whereas cen

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

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

70 ubordinate mice had higher concentrations of plasma corticosterone (CORT) than alpha males.

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

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

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

74 Restoring plasma corticosterone did not reverse the anxiolytic phe

75 149+/-2 mmoles/L), with a marked increase in plasma corticosterone (e.g. male offspring; 11.9 [9.3-14

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

77 eurons, and plasma analyses showed increased plasma corticosterone following NTS A2 stimulation.

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

79 KLF15 works primarily through CBG to control plasma corticosterone homeostasis.

80 lation between body temperature and baseline plasma corticosterone in field-caught lizards.

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

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

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

84 Moreover, MIA males had delayed recovery of plasma corticosterone in response to a novel social enco

85 ted in the adrenal cortex of obese mice, and plasma corticosterone is increased, which can be counter

86 tory stage (ELHS), assessed by high baseline plasma corticosterone, is a potential mechanism to elici

87 nt stress, illustrated by a decrease of both plasma corticosterone level and c-fos expression in the

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

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

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

91 Plasma corticosterone levels after bacterial lipopolysac

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

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

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

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

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

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

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

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

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

101 also had smaller spleens and lower baseline plasma corticosterone levels compared to controls.

102 nt decrease in plasma leptin and increase in plasma corticosterone levels compared to controls.

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

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

105 d female mice displayed similar increases in plasma corticosterone levels following CNSDS exposure re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 Plasma corticosterone levels were equally reduced in bot

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

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

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

124 Plasma corticosterone levels were increased by LPS at a

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

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

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

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

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

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

131 glucocorticoid system function peripherally (plasma corticosterone levels).

132 reased startle hyperreactivity and decreased plasma corticosterone levels, similar to phenotypes exhi

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

134 hese changes were positively correlated with plasma corticosterone levels.

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

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

137 ress evoked repeated transient elevations of plasma corticosterone levels.

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

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

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

141 Plasma corticosterone, measured after 4 trials, varied s

142 Plasma corticosterone, microbiota composition, and cecal

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

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

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

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

147 s to test the effects of body temperature on plasma corticosterone (predominant glucocorticoid in rep

148 Finally, chronic MAP4343 countered the plasma corticosterone reduction induced by CIE.

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

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

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

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

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

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

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

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

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

158 taneous implants to chronically elevate free plasma corticosterone (the rodent homolog of cortisol; '

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

160 We also measured plasma corticosterone to assess the actions of FKBP5 inh

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

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

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

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

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

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

167 Basal plasma corticosterone was slightly decreased in TIP39 kn

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

169 80% and elevated both tail-flick latency and plasma corticosterone when compared to saline-treated an