ライフサイエンスコーパス: HPA axis

1 HPA axis activation is an important component of the com

2 HPA axis activity and other modifiers that accompany T2D

3 HPA axis activity was assessed by examination of circadi

4 HPA axis dysregulation was associated with behavioral an

5 HPA axis genetic variation and activity were important p

6 HPA axis hyperresponsiveness to a visceral stressor is r

7 amic inactivation by muscimol disrupts acute HPA axis response specifically to loud noise.

8 cated that context preexposures reduce acute HPA axis responses to loud noise.

9 roids programme the sensitivity of the adult HPA axis to gonadal steroids in adulthood.

10 e, particularly the sensitivity of the adult HPA axis to testosterone.

11 522), a functional genetic variant affecting HPA axis function, influenced threat-related amygdala re

12 At each age, HPA axis function was tested by hypoglycaemic challenge

13 asma levels, but did not significantly alter HPA-axis activity of non-stressed control rats.

14 indings are the first to demonstrate altered HPA axis reactivity in depressed preschoolers.

15 These findings suggest that altered HPA axis functioning occurs after repeated low-level For

16 postnatal growth are associated with altered HPA axis function in later life.

17 status are features associated with altered HPA axis reactivity.

18 The altered HPA-axis stress response observed in participants expose

19 results demonstrate that juvenile HFD alters HPA axis reactivity leading to an enhancement of amygdal

20 rn can affect body temperature, behavior and HPA axis activation.

21 on to the mothers on open field behavior and HPA axis function of the offspring.

22 ces alterations in despair-like behavior and HPA axis function, reminiscent of MDD.

23 te the effects of 8-OHDPAT on behavioral and HPA axis function in response to an innate fear-inducing

24 eA would increase anxiety-like behaviors and HPA axis reactivity to stress, and further, that an ERbe

25 rm gender dependent effects on behaviour and HPA axis status.

26 ce that the amygdala stimulates both CRF and HPA axis systems in the adult, our data suggest an oppos

27 contribute importantly to Fos expression and HPA axis activation after YO treatment.

28 mice null for urocortin 2 were generated and HPA axis activity, ingestive, and stress-related behavio

29 o the liver, secondary to hypoleptinemia and HPA axis activity, in promoting higher hepatic gluconeog

30 ths-old, CSF levels of CRF were measured and HPA axis activity was characterized by examining diurnal

31 care exhibited significantly blunted SNS and HPA axis responses to psychosocial stress compared with

32 the tonic inhibition of steroidogenesis and HPA axis activity and have important implications for th

33 The autonomic nervous system and HPA axis are key components of the neuroendocrine respon

34 elopment of the autonomic nervous system and HPA axis in children exposed to early-life deprivation a

35 lic dysregulation in atypical depression and HPA-axis hyperactivity in melancholic depression.

36 Although reduced adrenal inflammation and HPA-axis activation mediated by LPS were found in Mx1(Cr

37 ocortical MyD88 for adrenal inflammation and HPA-axis activation mediated by LPS.

38 both a biological perspective, by assessing HPA axis function with a weight-adjusted very-low-dose d

39 scher rats showed a significantly attenuated HPA axis response to chronic 'binge' pattern cocaine adm

40 ts and controls, who did not differ in basal HPA axis activity or response to pentagastrin.

41 psychotic features is also important because HPA axis abnormalities may be especially pronounced in p

42 e phenotypic and genetic correlation between HPA axis activity and the psychological variables percei

43 aluated verucerfont for its ability to block HPA axis activation and reduce stress-induced alcohol cr

44 Blunted HPA axis activity may increase risk for suicide attempt

45 cent MAM-treated animals displayed a blunted HPA axis corticosterone response to acute footshock that

46 elationship between genotype at 16 candidate HPA axis single-nucleotide polymorphisms (SNPs) and trea

47 in skin, which in turn activates the central HPA axis, with the requirement of a functional pituitary

48 The present study compared HPA axis responsiveness and regulation in 3- to 5-month-

49 and glucose homeostasis due to compensatory HPA axis activation but are hypertensive due to activati

50 Glucocorticoids control HPA axis activity through negative feedback to the pitui

51 Conversely, HPA axis responses to YO were significantly blunted in D

52 immunophilins are modulators of the cortisol-HPA axis response to stress and related chronic brain di

53 anxiety and activations of the amygdala, CRH/HPA axis, the sympathomedullary system and their sequell

54 orning when arousal systems, such as the CRH/HPA axis and the noradrenergic systems, are at their max

55 ygdala, the noradrenergic system and the CRH/HPA axis participate in multiple reinforcing positive fe

56 d UVB stimulated expression of the cutaneous HPA axis differs as a function of genotype: D2 responds

57 ic stressor that can activate this cutaneous HPA axis.

58 netics may have increased efficacy to dampen HPA axis responses.

59 Neuroendocrine studies have demonstrated HPA axis overactivity in major depression, a relationshi

60 in patients with major depressive disorder, HPA-axis hyperactivity, as reflected in DST results, may

61 tress and frequently exhibits a dysregulated HPA axis.

62 t, for females, the effects of ELS and early HPA-axis function may be detected much later in the intr

63 Vasopressin had no effects on either HPA axis responses or neuronal activation in response to

64 s (interneurons) is consistent with enhanced HPA axis inhibition, whereas reduced amygdalar expressio

65 stressed (PNS) offspring display exaggerated HPA axis responses to a physical stressor (systemic inte

66 Here we investigate whether exaggerated HPA axis responses associated with chronic variable stre

67 ed estimation equations were used to examine HPA axis activity (plasma ACTH and cortisol), immune act

68 rry control towels in small cages to examine HPA axis responses as determined by plasma corticosteron

69 a part of the effect of oestradiol on fetal HPA axis function is mediated by an interaction between

70 pigenetic state of genes that regulate fetal HPA axis reactivity as well as the epigenomic status of

71 have found that oestradiol stimulates fetal HPA axis activity.

72 aternal adrenal to the activity of the fetal HPA axis, and related these findings to fetal lung devel

73 s show that reduced 5-HT clearance following HPA axis activation is likely mediated, at least in part

74 en aged 3 through 5.6 years were studied for HPA axis reactivity in response to experimental psychoso

75 he central CRF system and independently from HPA axis activation.

76 e exposures failed to restore the habituated HPA axis response.

77 All subjects had HPA axis studies.

78 However, HPA axis reactivity has a moderating effect on IBS sympt

79 fic study of how such factors moderate human HPA axis activity has been limited.

80 in the NTS, and this normalized hyperactive HPA axis responses to IL-1beta.

81 NS rats overrides programming of hyperactive HPA axis responses to immune challenge in a sex-dependen

82 Specifically, we asked if HPA axis activation is required for diabetic hyperglycem

83 ocampal and prefrontal volumes, and impaired HPA axis feedback control.

84 ed immunodeficiency, we found alterations in HPA axis function, manifested as an increase in circulat

85 privation have suggested that alterations in HPA axis reactivity are evident in early "depressive-lik

86 in the aBST may contribute to alterations in HPA axis responses to emotional stress in sensitization

87 ts may trigger different adaptive changes in HPA axis regulation during alcohol withdrawal with conco

88 esting an important role for SK4 channels in HPA axis function.

89 ecting neurons in limbic sites implicated in HPA axis inhibition tended to show diminished activation

90 the anteroventral BST nuclei are involved in HPA axis excitation.

91 ther investigation of mechanisms involved in HPA axis regulation and response to stress in MS pathoge

92 essment of alleles for six genes involved in HPA axis regulation.

93 l natriuretic peptide all may participate in HPA axis activation, resulting in elevated plasma cortis

94 ets, and inflammation-associated pathways in HPA axis regulation and behavior, and highlight areas fo

95 dversity and functional genetic variation in HPA axis responsiveness to stress may mediate risk for p

96 characterize vHF function, because increased HPA axis activity is implicated in neuropsychiatric dist

97 To determine if increased HPA axis activation occurs during a specific circadian p

98 gical range effectively normalizes increased HPA axis activity in rats with uDM, this effect is neith

99 did not suggest that wheel running increases HPA-axis negative feedback through GR-mediated mechanism

100 ing levels of these neurosteroids may induce HPA axis dysfunction, thereby increasing sensitivity to

101 ficiency on IL-6 expression and IL-6-induced HPA axis activation during turpentine-induced inflammati

102 at 5-HT(2C)Rs are necessary for 5-HT-induced HPA axis activation.

103 ssociated with alterations in stress-induced HPA axis activation and, importantly, are not attenuated

104 ary for development of a full stress-induced HPA axis activation.

105 m by which exposure to UVB activates a local HPA axis in skin, which in turn activates the central HP

106 This is the first evidence of the local HPA axis in skin contributing to the central neuroendocr

107 and used salivary cortisol levels to measure HPA axis stress response.

108 model, constitutively formed NO may modulate HPA axis activity in the absence of changes in its synth

109 onal manipulation can substantially modulate HPA axis responses to pharmacological activation in huma

110 indicate that the actions of T in modulating HPA axis activity involve 5alpha-reductase within the ce

111 We used pregnant mice with a normal HPA axis carrying fetuses with CRH deficiency to charact

112 Disruption of normal HPA axis activity is a major risk factor of neuropsychia

113 However, 3beta-diol normalized HPA axis responses to IL-1beta in PNS males.

114 This blunting of HPA axis activity in response to cocaine is associated w

115 provide evidence for possible continuity of HPA axis alterations in depressive disorders across the

116 tus (uDM) to investigate the contribution of HPA axis suppression to leptin-mediated glucose lowering

117 models for depression and for disruption of HPA axis function can allow for the testing of potential

118 Chronic stress-induced enhancement of HPA axis excitability predicts increased excitatory and/

119 epinephrine in chronic stress enhancement of HPA axis excitability.

120 hway activation, we quantified expression of HPA axis components at the gene and protein levels in sk

121 As indexes of HPA axis activation following T and DHT replacement, ser

122 ate forebrain GABA circuits in inhibition of HPA axis activity during the SHRP.

123 on: (1) fast-feedback mediated inhibition of HPA axis activity is critically dependent upon stressor

124 to our knowledge, the first investigation of HPA axis reactivity in very young children with a clinic

125 waking provides a simple, dynamic measure of HPA axis activity.

126 lanation for the longstanding observation of HPA axis stimulation in response to 5-HT and thereby giv

127 , and coping may help clarify the origins of HPA axis disturbance in psychiatric disorders and the me

128 and NPMD patients have distinct profiles of HPA axis dysregulation.

129 se is whether its effect on the reduction of HPA axis activation in response to stress is due to the

130 onal PrP(c)-dependent hormonal regulation of HPA axis may contribute to the sleep homeostasis.

131 ivity in major depression, a relationship of HPA axis activity to cognitive performance and a potenti

132 cell transplantation and the restoration of HPA axis function would be a feasible and useful therape

133 ognitive performance and a potential role of HPA axis genetic variation in cognition.

134 Studies of HPA axis activation and the role of relative adrenal ins

135 discussed in the context of prior studies of HPA axis reactivity in clinically depressed children and

136 (that did not increase physical activity) on HPA axis habituation to repeated stress and modulation o

137 pring's behavioral response to stress and on HPA axis functions.

138 study to differentiate them biologically on HPA axis indices.

139 ed the effect of natural variations in BW on HPA axis function in juvenile and adult pigs.

140 t emotional memory and whether it depends on HPA axis deregulation.

141 dicate that the inhibitory effects of DHT on HPA axis activity may be in part mediated via its conver

142 protein 5, that exerts negative feedback on HPA axis function.

143 esions of the amygdala have little impact on HPA axis responsiveness and regulation in contrast to le

144 The effects of stress on HPA axis activation and CRF mRNA and content in the PVN

145 tion and/or immediately following weaning on HPA axis and sympathoadrenal function, 2- to 3-year-old

146 ic properties, in blocking stress effects on HPA-axis activity and memory retrieval.

147 on did not alter the adrenal inflammation or HPA-axis activity under systemic inflammatory response s

148 g how local production of cortisol and other HPA axis molecules in skin influence overall systemic le

149 opregnanolone induces opioid inhibition over HPA axis responses to immune challenge.

150 atic granulomas showed the opposite pattern: HPA axis hormone levels were maintained at, or exceeded,

151 In late pregnancy, HPA axis responses to stressors, including IL-1beta, are

152 lters the typical development of the primate HPA axis resulting in increased rather than decreased ac

153 s.Despite facilitating the pace of recovery, HPA axis modulation and corticosteroids have failed to d

154 Neurosteroids can reduce HPA axis responses, so allopregnanolone and 3beta-andros

155 ased behavioural indices of fear and reduced HPA axis reactivity mediated via increased GR gene expre

156 the hypothesis that contextual cues regulate HPA axis response habituation.

157 ubregions of the BST differentially regulate HPA axis responses to acute stress.

158 uring locomotor sensitization down-regulated HPA axis activation and Sgk1 induction by acute ethanol.

159 dependent on the dorsal hippocampus require HPA-axis activation in order to be learned.

160 nthesizing enzyme) with finasteride restored HPA axis responses (rapidly increased pPVN CRH mRNA expr

161 Naloxone, an opioid antagonist, restores HPA axis responses to IL-1beta in pregnancy but had no a

162 symptoms, who typically have the most robust HPA-axis dysregulation.

163 nt study investigated the simultaneous roles HPA axis activity, clinical symptomatology and HPA genet

164 Significant HPA axis dysregulation, marked by higher basal corticotr

165 ic-pituitary-adrenal (HPA) axis and the skin HPA axis analog, in the current issue Skobowiat and Slom

166 hin the physiological range after stressors, HPA axis responses were suppressed in response to the ai

167 -adrenal responses to CRF challenge, suggest HPA axis hyperactivity caused by increased CRF hypothala

168 tentially negative effects of more sustained HPA-axis activation.

169 corticoid signaling within mPFC to terminate HPA axis activity is mediated by a local recruitment of

170 surviving a rabies virus infection and that HPA axis activity may influence this process.

171 current study, it was first established that HPA axis response habituation to repeated loud noise las

172 These results suggest that HPA axis and glucocorticoid receptor signaling mediate a

173 These results suggest that HPA axis hormones may play a role in regulating the esta

174 The HPA axis regulates corticosterone levels during periods

175 The HPA axis regulates the secretion of glucocorticoids (GCs

176 The HPA axis response to the acute administration of IFN-alp

177 Vasopressin can activate the HPA axis by stimulating vasopressin 1b (V1b) receptors l

178 eated swim, a stimulus known to activate the HPA axis.

179 route by which ip IL-1beta can activate the HPA axis.

180 esponsive thalamic nuclei might activate the HPA axis.

181 ively, following stress, THDOC activates the HPA axis due to dephosphorylation of KCC2 residue Ser940

182 increases body temperature and activates the HPA axis.

183 concentrations of IL-6 while activating the HPA axis in a dose-dependent manner.

184 We sought to determine if EALs affect the HPA axis response to a visceral stressor in irritable bo

185 , revealing a link between PPARalpha and the HPA axis in controlling energy homeostasis and immune re

186 nteraction between the immune system and the HPA axis in the pathophysiology of inflammatory diseases

187 d actions of sympathetic innervation and the HPA axis, which modulate spleen shrinkage and cellular i

188 esearch is potentially important because the HPA axis has prominent circadian and ultradian periodici

189 exacerfont, verucerfont potently blocked the HPA axis response to the dexamethasone-CRF test, but lef

190 involved in many activities modulated by the HPA axis.

191 rincipal hypophysiotropic factor driving the HPA axis, it is a potent inhibitor of the GnRH pulse gen

192 abnormality of cortisol feedback during the HPA axis quiescent period.

193 amic-pituitary-adrenal (HPA) axis during the HPA axis quiescent period.

194 jor depressive disorder should emphasize the HPA axis and its interplay with the serotonin system.

195 In response to stressful events, the HPA axis is activated triggering the successive release

196 ation of AT(1) receptors is required for the HPA axis response to isolation.

197 During habituation, the HPA axis likely requires input from cortical and limbic

198 nsiveness of the CRH neurones, and hence the HPA axis, following IL-1beta in late pregnancy is explai

199 itization to ethanol (EtOH), implicating the HPA axis in this process.

200 eA is an important structure involved in the HPA axis responses to predator odors, in support of prev

201 due to strong negative feedback loops in the HPA axis.

202 h arousal and metabolic states influence the HPA axis are poorly understood.

203 esponsive systems are known to influence the HPA axis, such as the vasopressin-vasopressin receptor s

204 A CRF/CRF1-mediated mechanism involving the HPA axis is proposed for acquisition, whereas an extrahy

205 178-199 is involved in the regulation of the HPA axis and behavior.

206 er these studies identify suppression of the HPA axis and ensuing reductions in hepatic acetyl CoA co

207 ical for hippocampal negative control of the HPA axis and support a direct role for adult neurogenesi

208 euroendocrine and molecular responses of the HPA axis and that the dorsal hippocampus, LSV, and PVN c

209 nt to block stress-induced activation of the HPA axis and the consequent impairment of retrieval of d

210 at least in part, the hyper-activity of the HPA axis and the hyper-emotional behavioral characterist

211 might be related to the hyperactivity of the HPA axis and to development of stress-related psychopath

212 he LPS- and IL-1-induced stimulations of the HPA axis and to the indoleaminergic responses to LPS, bu

213 impaired negative feedback regulation of the HPA axis and, increased depression-like behavior.

214 , 4 degrees C) potentiated activation of the HPA axis by acute immobilization stress, assessed by mea

215 to the PAmp, might mediate activation of the HPA axis by audiogenic stress.

216 from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part,

217 s result in alterations in regulation of the HPA axis by gamma-aminobutyric acid (GABA).

218 sues because of the prior suppression of the HPA axis by glucocorticoid negative feedback.

219 ic neurons involved in the regulation of the HPA axis display distinct neurochemical patterns that ma

220 of sex differences in the regulation of the HPA axis does not involve the amygdala or hippocampus.

221 ammation in MS, whereas hyperactivity of the HPA axis has been linked to neurodegeneration and increa

222 Disturbances of the HPA axis have been associated with memory impairments an

223 gically at-risk subjects, dysfunction of the HPA axis helps to distinguish those who will and will no

224 l pathways involved in the regulation of the HPA axis in mice.

225 The dysregulation of the HPA axis is complex, involving multidirectional crosstal

226 The principle regulator of the HPA axis is corticotrophin-releasing hormone (CRH), whic

227 heres ensures that the overall output of the HPA axis matches the severity of the threat.

228 early seen even though other elements of the HPA axis may have limited responses.

229 in mediating fast-feedback regulation of the HPA axis requires evaluation of the interactions between

230 is involved, we assessed the function of the HPA axis response to restraint stress following hormone

231 homeostasis by UVB through activation of the HPA axis that originate in the skin and require the pitu

232 esults in age-dependent dysregulation of the HPA axis through a mechanism affecting primarily the adr

233 life, mediated via fetal programming of the HPA axis through decreased glucocorticoid receptor (GR)

234 ated the effects of lead on responses of the HPA axis to a psychosocial laboratory stressor administe

235 f OT results in a heightened response of the HPA axis to certain stressors and that OT can attenuate

236 ponse, indicating enhanced reactivity of the HPA axis to subsequent Form.

237 al-related activation of the hormones of the HPA axis was no longer found on the 10th day of withdraw

238 alth through daily 'micro-management' of the HPA axis, a finding with potential medical implications

239 -1 in inflammation-induced activation of the HPA axis, although histochemical evidence to support rel

240 novel and critical cellular component of the HPA axis, and demonstrates the requirement of TrkB for t

241 ributes to termination and adaptation of the HPA axis, as well as potentially contributing to changes

242 aneous withdrawal produced activation of the HPA axis, as well as suppression of food intake and weig

243 er in humans, including hyperactivity of the HPA axis, impaired negative feedback regulation of the H

244 ers associated with hyperexcitability of the HPA axis, including Cushing's syndrome, epilepsy, and ma

245 bnormalities, including dysregulation of the HPA axis, manifested in abnormal cerebrospinal fluid cor

246 this marked effect on the development of the HPA axis, neonatal endotoxin exposure had long-lasting e

247 or inflammation-associated activation of the HPA axis, result in aberrant responses to subsequent str

248 and some of these include components of the HPA axis, such as CRF and CRF receptors, along with POMC

249 orepinephrine (NE) is a key regulator of the HPA axis, we hypothesized that leptin could suppress HPA

250 BST nuclei are involved in inhibition of the HPA axis, whereas the anteroventral BST nuclei are invol

251 amic levels of BDNF and disinhibition of the HPA axis.

252 may be reduced via the downregulation of the HPA axis.

253 ear EXT and dexamethasone suppression of the HPA axis.

254 CRH neurons, decreasing the activity of the HPA axis.

255 entiation, resulting in dysregulation of the HPA axis.

256 the hypothalamus is a major regulator of the HPA axis.

257 ich is known to result in suppression of the HPA axis.

258 -mediated negative feed-back response of the HPA axis.

259 corticoid-mediated negative feed-back of the HPA axis.

260 campus are involved in the regulation of the HPA axis.

261 yperphagia, polydypsia and activation of the HPA axis.

262 brain, leading to chronic activation of the HPA axis.

263 beta preceding LPS-induced activation of the HPA axis.

264 quisite for recovery from suppression of the HPA axis.

265 ibed to brain CRF, but not activation of the HPA axis.

266 that glutamate was a major activator of the HPA axis.

267 depression by means of dysregulation of the HPA axis.

268 ocation of the dysregulated component of the HPA axis.

269 avior through a mechanism independent of the HPA axis.

270 s to how exercise alters the function of the HPA axis.

271 site, inhibitory role of the amygdala on the HPA axis during early development, which fits with emerg

272 atory studies of GABAergic influences on the HPA axis under a variety of conditions.

273 Verucerfont effects on the HPA axis were evaluated using the dexamethasone-CRF test

274 eir relationship with ethanol actions on the HPA axis.

275 bility to impart inhibitory control over the HPA axis after chronic stress exposure.

276 Hypersensitivity reactions may prime the HPA axis to respond aberrantly to stressors, resulting i

277 Variation in genes regulating the HPA axis - particularly the glucocorticoid receptor - ma

278 IL-6 has been suggested to stimulate the HPA axis during immune activation independent of the inp

279 nxiety after acute stress by stimulating the HPA axis at the level of the anterior pituitary.

280 Finally, we confirm that the HPA axis response is defective in Crh(-/-)/IL-6(-/-) mic

281 Thus, the HPA axis responses to immune signals are suppressed in p

282 rovide both prostanoid-mediated drive to the HPA axis and an anti-inflammatory action that constrains

283 malian species in general is undoubtedly the HPA axis.

284 Finally, the HPA-axis response to peripheral or intracerebroventricul

285 nic stress and examined for changes in their HPA axis during pregnancy and postpartum, including asse

286 267 (57.7%) consented to assessment of their HPA axis function.

287 BNST of rat strains known to differ in their HPA-axis function.

288 Their relevance to HPA axis disturbances in psychiatric patients is largely

289 ateral septum is ideally situated to trigger HPA axis activation by stimuli that are potentially thre

290 aging-like profile is sufficient to trigger HPA-axis dysfunction, namely loss of plasmatic corticost

291 steroid production in the brain may underlie HPA axis hyper-responsiveness in prenatally programmed o

292 over, corticosterone, which is released upon HPA axis activation, blocks 5-HT uptake by OCT3.

293 One way could be via HPA axis-dependent impairment of serotonin transporter (

294 required for diabetic hyperglycemia, whether HPA axis normalization can be achieved using a dose of l

295 However, it is unclear whether HPA axis abnormalities are present in fully recovered pa

296 se distinctions may work in conjunction with HPA axis dysregulation to influence the etiology and the

297 mming of the hypothalamic transcriptome with HPA axis dysfunction, noting a marked decreased in the e

298 ssessed telomere length or its relation with HPA-axis activity in individuals at risk for depression,

299 uthors investigated whether variation within HPA axis genes predicts antidepressant outcomes within t

300 At 2.5 years, HPA axis and sympathoadrenal (catecholamine) responses t