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 genetic variation and activity were important p

5 HPA axis hyperresponsiveness to a visceral stressor is r

6 l programming of the PVN results in aberrant HPA axis responsiveness when exposed to the hormonal cha

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 systems involved in homeostatic adjustments (HPA axis, immuno-inflammatory activation, neuroendocrine

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

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

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

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

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

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

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 sequences on CD8 T cell immunity by altering HPA axis activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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 brain GR to ascertain its role in behaviour, HPA-axis regulation and adrenal structure.

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 function that corresponded with the blunted HPA axis reactivity.

47 ultiorgan transcriptomics demonstrates broad HPA axis target engagement through altering levels of kn

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

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

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

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

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

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

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

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

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

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

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

59 ic stressor that can activate this cutaneous HPA axis.

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

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

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

63 tress and frequently exhibits a dysregulated HPA axis.

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

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

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

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

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

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

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

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

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

73 have found that oestradiol stimulates fetal HPA axis activity.

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

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

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

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

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 f discussion of sex differences in the human HPA axis is also included.

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

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

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

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

85 l, we find limited support for alteration in HPA axis functioning as a general mechanism for the heal

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

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

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

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

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

91 h in GR, early altered in AD and involved in HPA axis control and cognitive functions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 ing evidence that activation of the maternal HPA axis can have intergenerational consequences via, fo

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

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

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

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

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

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

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

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

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

118 ABA) on neuronal and vascular development of HPA axis regions, such as the paraventricular nucleus (P

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

120 epinephrine in chronic stress enhancement of HPA axis excitability.

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

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

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

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

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

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

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

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

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

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

135 tonomic function, and biochemical markers of HPA-axis activity; inflammatory processes; and trophic f

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 nvolved in glucocorticoid signaling pathway (HPA axis) in the ventral hippocampus, whereas upregulati

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 g institutional care in infancy show reduced HPA axis responsivity, even years after they are placed

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

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

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

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

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

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

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

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

165 Significant HPA axis dysregulation, marked by higher basal corticotr

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

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 The HPA axis regulates corticosterone levels during periods

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

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

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

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

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

179 increases body temperature and activates the HPA axis.

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

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

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

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

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

185 involved in many activities modulated by the HPA axis.

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

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

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

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

190 ment reopens a window of opportunity for the HPA axis to recalibrate based on significant improvement

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

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

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

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

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

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

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

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

199 biota, tryptophan-kynurenine metabolism, the HPA axis, neurogenesis and BDNF, epigenetics, and obesit

200 Moreover, the HPA axis exhibits prominent circadian activity and synch

201 Deregulation of the HPA axis and a feed-forward effect on PFC GR sensitivity

202 idence that a greater diurnal decline of the HPA axis and a larger CAR are associated with improvemen

203 178-199 is involved in the regulation of the HPA axis and behavior.

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

205 potential of CTRND05 as a suppressor of the HPA axis and serve as an exemplar of a potentially broad

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

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

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

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

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

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

212 , 4 degrees C) potentiated activation of the HPA axis by acute immobilization stress, assessed by mea

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

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

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

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

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

218 rding sex differences in the activity of the HPA axis following chronic stress and the underlying con

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

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

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

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

223 eta-analysis to test if dysregulation of the HPA axis is associated with worse cognitive capability.

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

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

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

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

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

229 Hyper-stimulation of the HPA axis results in sustained elevated levels of glucoco

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

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

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

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

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

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

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

237 -1 in inflammation-induced activation of the HPA axis, although histochemical evidence to support rel

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

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

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

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

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

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

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

245 Allostatic habituation of the HPA axis, such that glucocorticoid levels retain homeost

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

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

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

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

250 esponsive and synchronizing functions of the HPA axis.

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

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

253 entiation, resulting in dysregulation of the HPA axis.

254 on or anxiety also have hyperactivity of the HPA axis.

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

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

257 esponsive and time-keeping properties of the HPA axis.

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

259 esponse and impair the entrainability of the HPA axis.

260 yperphagia, polydypsia and activation of the HPA axis.

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

262 henotypes consistent with suppression of the HPA axis.

263 ear EXT and dexamethasone suppression of the HPA axis.

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

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

266 ocation of the dysregulated component of the HPA axis.

267 avior through a mechanism independent of the HPA axis.

268 environment has a substantial impact on the HPA axis and, perhaps, other stress-mediating systems.

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

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

271 The review focuses on the HPA axis-based interventions of corticotropin-releasing

272 eir relationship with ethanol actions on the HPA axis.

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

274 s a window of opportunity to recalibrate the HPA axis toward more typical reactivity when children sh

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

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

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

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

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

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

281 malian species in general is undoubtedly the HPA axis.

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

283 y in female mice significantly altered their HPA axis function specifically during pregnancy, modelin

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

285 267 (57.7%) consented to assessment of their HPA axis function.

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

287 Thus, HPA axis regulation of AgRP neurons is a previously unde

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 recruits and requires this pathway by which HPA axis activity stimulates AgRP neurons.

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