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1 nd the glucocorticoid receptor (activated by corticosterone).
2 ed result in elevated plasma vasopressin and corticosterone.
3 in muscle glycogen storage in mice receiving corticosterone.
4 res with the stress hormones epinephrine and corticosterone.
5 ice exhibited a threefold increase in plasma corticosterone.
6 hese effects were abrogated by coinfusion of corticosterone.
7 ibitor, metyrapone and mimicked by exogenous corticosterone.
8 ut not on FKBP5 and UTS2B nor on circulating corticosterone.
9 and can be elicited by the administration of corticosterone.
10 levating plasma angiotensin II, potassium or corticosterone.
11 to the glucocorticoid receptor (GR) ligand, corticosterone.
12 e abrogated by an intra-arterial infusion of corticosterone.
13 sive precursors are selectively modulated by corticosterone.
14 in, and molybdenum levels, and males, higher corticosterone.
15 counted for by the subgroup bearing elevated corticosterone.
16 ther corticotropin-releasing factor (CRF) or corticosterone.
17 he behavioral effects of stress and systemic corticosterone.
18 ure variation in the stress-related hormone, corticosterone.
19 anism that ends with the production of 18-OH corticosterone.
20 h a second surge of exogenously administered corticosterone.
21 S GLP-1-expressing neurons, we microinjected corticosterone (0.5 mug) directly into the hindbrain fou
23 dosterone, cortisol, 11-deoxycorticosterone, corticosterone, 11-deoxcortisol, progesterone, and 19-no
25 ary morphogen controlling metamorphosis) and corticosterone (a stress hormone acting synergistically
26 n that light exposure can result in elevated corticosterone, a response that is not compatible with s
27 ety-like behaviors and circulating levels of corticosterone, a stress hormone, in female prairie vole
28 ted in both acute kidney injury and in deoxy-corticosterone acetate and sodium chloride (deoxy-cortic
29 costerone acetate and sodium chloride (deoxy-corticosterone acetate salt)-induced chronic hypertensiv
30 CMS-induced increase in the serum levels of corticosterone, adrenocorticotropic hormone, interleukin
31 her early-life changes in the stress hormone corticosterone affect gut microbiota by experimentally i
33 resulted in a significant decrease in plasma corticosterone and a consequent increase in ACTH, as exp
34 s, these tumors produced increased levels of corticosterone and aldosterone and showed a high prolife
35 ion, nest scores, sucrose consumption, fecal corticosterone and blood for hematology were collected.
36 we demonstrate novel synergistic actions of corticosterone and corticotropin-releasing hormone (CRH)
39 we demonstrate novel synergistic actions of corticosterone and CRH on hippocampal synaptic plasticit
40 Combined application of the stress hormones corticosterone and CRH recapitulated the physiological a
49 efeated B6 females exhibited elevated plasma corticosterone and increased c-Fos activation in the med
50 ) mice showed elevated levels of circulating corticosterone and increased hippocampal Bdnf expression
51 ld potential) required combined chronic high corticosterone and maternal presence (not maternal behav
53 these effects, we examined the abilities of corticosterone and normetanephrine to potentiate cocaine
55 ative relationship observed between baseline corticosterone and plasma oxidative damage to proteins.
56 days of CUS decreased basal plasma levels of corticosterone and produced a shorter latency to immobil
57 reduced chronic stress-induced elevations in corticosterone and proinflammatory cytokine levels and d
58 ed plus maze or sacrificed for basal diurnal corticosterone and quantification of neuronal glucocorti
59 d behavioral emotionality, high basal plasma corticosterone and reduced gene expression of Bdnf, Cort
61 ss-predictive cues exhibited increased serum corticosterone and significantly greater reinstatement o
64 mimicked by infusing rats with Intralipid or corticosterone and were corrected by leptin replacement.
66 eight gain, an abnormal circadian pattern of corticosterone, and an attenuated increase of corticoste
70 h)], glucocorticoid receptor (GR) and plasma corticosterone, as well as brain-derived neurotrophic fa
72 s not impacted by systemic administration of corticosterone at a dose that maintained elevated plasma
73 assay to measure endogenous acyl-ghrelin and corticosterone at time points surrounding auditory fear
75 esulted in lower stress-driven production of corticosterone, augmented mouse proinflammatory immune r
76 pacity of sustained increases in circulating corticosterone (B) alone to alter dendritic spine morpho
77 There were no marked differences in plasma corticosterone between genotypes, suggesting that behavi
78 ditionally, we found that a systemic dose of corticosterone blocked the depressive-like phenotype eli
79 one 2-fold in human trophoblast cells and of corticosterone by 90% in rat adrenocortical cells when c
80 although the immobilization-induced surge in corticosterone by itself has delayed detrimental effects
83 A-axis dysfunction, namely loss of plasmatic corticosterone circadian oscillation, and promotes reduc
86 ed the adult stress response, as measured by corticosterone concentration, such that a history of chr
87 el was associated with lower plasma baseline corticosterone concentrations and enhanced corticosteron
88 and measured cloacal temperatures and plasma corticosterone concentrations at baseline and after expo
89 temperature can significantly affect plasma corticosterone concentrations in reptiles, which may be
90 a through increased plasma catecholamine and corticosterone concentrations secondary to volume deplet
91 tress condition had better memory and higher corticosterone concentrations than rats trained at the l
94 degrees C showed a robust increase in plasma corticosterone concentrations with restraint stress, but
95 sed food intake, reduced plasma glucagon and corticosterone concentrations, and decreased ectopic lip
96 nt on body condition, immune metrics, plasma corticosterone concentrations, total antioxidant capacit
99 riod, highest whole-body thyroid hormone and corticosterone content, and highest SMR, and these trait
100 ss in two mouse strains by utilizing chronic corticosterone (CORT) administration or contextual fear
101 mice and resulted in a shorter time to peak corticosterone (CORT) and a more rapid decay of CORT fol
102 e sex differences in stressor-induced plasma corticosterone (CORT) elevations and defensive behaviors
103 ment of C57Bl/6J male breeders with low-dose corticosterone (CORT) for 28 days prior to mating yielde
104 that exposure to the primary glucocorticoid corticosterone (CORT) in adolescent mice recapitulates m
107 d increases anxiety-like behavior and plasma corticosterone (cort) levels in rats, whereas central GL
108 e behavior and amygdala dysfunction, reduces corticosterone (CORT) levels, and exerts repair-related
110 el, learned helplessness (LH), and a chronic corticosterone (CORT) model in mice, we tested if ketami
111 (Ucn), beta-endorphin (beta-END), ACTH, and corticosterone (CORT) or the brain was fixed for immunoh
112 bjected to (1) a forced swim test (FST), (2) corticosterone (Cort) or vehicle injections, (3) CRS for
118 (-/-) mice were also resilient to developing corticosterone (CORT)-induced escape deficits and chroni
120 L, 0.43 ng/uL, 0.0076 ng/uL for aldosterone, corticosterone, cortisol, and beta-estrone, respectively
121 Together, these observations suggest that corticosterone, delivered through drinking water even 24
123 st traumatic experience a suppression of the corticosterone-dependent response protects against the d
124 dent model of depression, exhibited elevated corticosterone, depressive-like behavior, memory deficit
127 raction of corticosterone with OCT3 mediates corticosterone effects on drug-seeking behavior and esta
129 signalling in these tissues in mice drinking corticosterone either from day (D) 11 to D16 or D14 to D
133 ch produce antidepressant effects in chronic corticosterone-exposed animals through GABAergic synapti
134 pressant effects on acute stress- or chronic corticosterone-exposed mice, respectively, through GABAe
138 and delayed metamorphosis, although chronic corticosterone exposure accelerated rate of metamorphosi
139 reductions in either host immunity (through corticosterone exposure) or antiparasite behaviours (thr
141 ing ChIP-exo in mouse liver under endogenous corticosterone exposure, we report here that monomeric G
149 to the vehicle control group, mice receiving corticosterone had a significant enhancement in pancreat
152 erfluorotetradecanoate to decreased baseline corticosterone in both sexes; and perfluorododecanoate w
154 g of a single natural (cortisol in human and corticosterone in mice) and synthetic [e.g., dexamethaso
155 ven Tspo cKO mice lost their ability to form corticosterone in response to adrenocorticotropic hormon
157 or receptor for the stress hormone cortisol (corticosterone in rodents) and is widely expressed in ex
159 ever, when stress was followed 24 h later by corticosterone in the drinking water, the surge in corti
160 ally modifying the level of stress hormones (corticosterone) in brood mates, we demonstrate that the
161 levels of the glucocorticoid stress hormone, corticosterone, in broiler chickens produced a pessimist
162 atins acutely inhibited aldosterone, but not corticosterone, in response to different secretagogues.
163 ear response, anxiety-related behaviors, and corticosterone increase of the stressed cagemate, sugges
164 ing, or blockade of pups' alarm odor-induced corticosterone increase prevented transfer of fear.
165 ng, aberrant basal circadian fluctuations of corticosterone, increased amygdalar glucocorticoid recep
167 chronic DBS showed a decrease in hippocampal corticosterone, indicating that DBS may have a regulator
169 transmission, because an elevation of pups' corticosterone induced by the odor of the frightened mot
171 nd that this potentiation appears to involve corticosterone-induced blockade of dopamine clearance vi
173 fed to control intake, aiming to prevent the corticosterone-induced increase in food consumption, (3)
174 dipose triglyceride lipase inhibitor blocked corticosterone-induced increases in plasma glucose conce
175 demonstrated that AKG effectively attenuated corticosterone-induced protein degradation and rescued t
176 bserve that PNN expression is increased in a corticosterone-induced stress model of disease and reduc
180 terozygous (Sst(HZ)) mice show that elevated corticosterone is not sufficient to reproduce the behavi
181 nce correlates with an inverted U profile of corticosterone level in the circulation and of brain-der
183 an increase in startle amplitude and plasma corticosterone levels 30 min following intra-BNST PACAP
184 kinase (ERK), P70S6K), as well as increased corticosterone levels and activation of the innate immun
185 able to demonstrate increased intra-adrenal corticosterone levels and an increase in steroidogenic a
186 ne taking is associated with elevated plasma corticosterone levels and that systemic infusion of coca
188 ped normally but at the age of 1 year, their corticosterone levels decreased; this was associated wit
189 tic responsiveness, and chronically elevated corticosterone levels driven by hypothalamic hyperactiva
190 al polypeptide (VIP) had no effect on plasma corticosterone levels even in previously stressed male r
191 e mice displayed similar increases in plasma corticosterone levels following CNSDS exposure relative
196 were not explained by differences in plasma corticosterone levels or numbers of Fos-labeled neurons
201 drawal symptoms or alterations in the plasma corticosterone levels were observed after 7 days of abst
203 percentage DNA methylation levels and serum corticosterone levels, whereas F3 males showed Pb- and P
204 ponded to LPS by a 5-fold increase of plasma corticosterone levels, which were only moderately lower
210 ctivation of NTS GLP-1-expressing neurons by corticosterone may represent a homeostatic response to c
212 microbial endotoxin exposure through direct corticosterone-mediated effects on NKp46-expressing inna
215 amined stress physiology (plasma glucose and corticosterone), mitochondrial performance and the muscl
220 ing in the PL to the effects of stress-level corticosterone on PL neurotransmission and cocaine seeki
222 ays of non-invasive administration of either corticosterone or vehicle control, we tested the birds'
223 ndently dampened stress-induced increases in corticosterone plasma levels, but did not significantly
224 in mice to directly test the hypothesis that corticosterone potentiates cocaine-primed reinstatement
225 reviously reported that stress, via elevated corticosterone, potentiates cocaine-primed reinstatement
226 st the effects of body temperature on plasma corticosterone (predominant glucocorticoid in reptiles)
227 rough promoting LPS clearance and modulating corticosterone production and leukocyte recruitment.
228 ngs suggest that stress-induced increases in corticosterone promote cocaine seeking by mobilizing 2-a
234 vealed that rapid-eye-movement sleep (REMS), corticosterone regulation, and coat state were most resp
235 and theta activity shared many pathways with corticosterone regulation, in particular pathways implic
236 the lateral hypothalamic area (LHA) regulate corticosterone release and a variety of behaviours and p
237 HPA activity, based upon averaged values of corticosterone release from each animal obtained from re
239 verexpression in BLA dampened stress-induced corticosterone release, reduced anxiety-like behaviors,
247 treated animals displayed a blunted HPA axis corticosterone response to acute footshock that did not
249 avoidance of the predator scent, a prolonged corticosterone response, and higher anxiety long after e
250 emory enhancement as well as the potentiated corticosterone response, indicating the dependence of th
251 eptor type 2 (SSTR2) normalizes glucagon and corticosterone responses to hypoglycemic clamp in diabet
252 s oxytocin injections reduced behavioral and corticosterone responses to immobilization, whereas inje
253 cuit functional connectivity, behavioral and corticosterone responses to trauma exposure, and post-tr
254 asal, diurnal and stressor-stimulated plasma corticosterone secretion and basal plasma adrenocorticot
257 Stimulation of GCG neurons had no effect on corticosterone secretion, body weight, or conditioned ta
258 uitry in the daily control of heart rate and corticosterone secretion, collectively establishing SCN
259 the stress-related hormones epinephrine and corticosterone selectively modulate acute HSV-1 and HSV-
260 hypothesize that stress-induced increases in corticosterone "set the stage" for relapse by promoting
261 er and length, whereas aged animals with low corticosterone showed an upward shift in these indices.
263 te the metabolic phenotype caused by chronic corticosterone, suggesting a peripheral mechanism for th
264 paired with males also showed an increase in corticosterone, suggesting an increased stress response.
266 urons are more responsive to epinephrine and corticosterone than are sensory neurons, demonstrating t
268 a pattern of adrenocorticotropic hormone and corticosterone that was similar to patients undergoing c
269 explore the relationships between PFASs and corticosterone (the major glucocorticoid in birds), and
270 t was recapitulated by intra-PL injection of corticosterone, the CB1R agonist WIN 55,212-2, or the mo
271 nvestigate how chronic and acute exposure to corticosterone, the dominant amphibian glucocorticoid ho
273 he ability of the intermediate product 18-OH corticosterone to exist as a lactol form, with the equil
274 posure markedly increased serum cortisol and corticosterone together with increases in monoacylglycer
276 decision making, dubbed 'pessimism', whereby corticosterone-treated birds showed an increased expecta
279 th mice that receive concurrent venlafaxine, corticosterone-treated mice also display reduced ex vivo
281 sed Slc2a2 glucose transporter expression in corticosterone-treated mice, on D16 only (P < 0.05).
283 ressor (electric footshock) nor stress-level corticosterone treatment alone reinstates cocaine seekin
285 nhanced negative biases in response to acute corticosterone treatment but without effects on antidepr
294 rats, pretreatment of male C57/BL6 mice with corticosterone (using a dose that reproduced stress-leve
296 cal alterations associated with chronic oral corticosterone were investigated using male nonobese dia
299 irst direct evidence that the interaction of corticosterone with OCT3 mediates corticosterone effects