ライフサイエンスコーパス: corticosterone

1 nd the glucocorticoid receptor (activated by corticosterone).

2 ibitor, metyrapone and mimicked by exogenous corticosterone.

3 and can be elicited by the administration of corticosterone.

4 levating plasma angiotensin II, potassium or corticosterone.

5 e abrogated by an intra-arterial infusion of corticosterone.

6 sive precursors are selectively modulated by corticosterone.

7 in, and molybdenum levels, and males, higher corticosterone.

8 counted for by the subgroup bearing elevated corticosterone.

9 ed result in elevated plasma vasopressin and corticosterone.

10 ther corticotropin-releasing factor (CRF) or corticosterone.

11 he behavioral effects of stress and systemic corticosterone.

12 opressin neurons along with decreased plasma corticosterone.

13 nd restores prefrontal BDNF expression after corticosterone.

14 ap water, fetal weight was always reduced by corticosterone.

15 ceptor sensitivity in mice administered with corticosterone.

16 in muscle glycogen storage in mice receiving corticosterone.

17 res with the stress hormones epinephrine and corticosterone.

18 ice exhibited a threefold increase in plasma corticosterone.

19 hese effects were abrogated by coinfusion of corticosterone.

20 Systemic administration of corticosterone (0.3-3 mg/kg) to male Sprague-Dawley rats

21 S GLP-1-expressing neurons, we microinjected corticosterone (0.5 mug) directly into the hindbrain fou

22 The OCT3 inhibitor corticosterone (10 mg kg(-1) ) had no effect.

23 ldren (reductions of 17-hydroxyprogesterone, corticosterone, 11-deoxycortisol and testosterone).

24 ition, MSI quantified changes in subregional corticosterone/11-dehydrocorticosterone ratio, distribut

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 elation of place maps across sessions, while corticosterone administration did not.

31 CMS-induced increase in the serum levels of corticosterone, adrenocorticotropic hormone, interleukin

32 her early-life changes in the stress hormone corticosterone affect gut microbiota by experimentally i

33 BMI associated with lower maternal cortisol, corticosterone and 11-dehydrocorticosterone.

34 resulted in a significant decrease in plasma corticosterone and a consequent increase in ACTH, as exp

35 uced and phase advanced the peak of both the corticosterone and ACTH rhythms.

36 we demonstrate novel synergistic actions of corticosterone and corticotropin-releasing hormone (CRH)

37 We show that corticosterone and cortisol and their less active precur

38 Therefore, the synergistic actions of corticosterone and CRH at hippocampal synapses underlie

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

41 Mechanistically, corticosterone and CRH synergized at the spine-actin reg

42 Therefore, synergistic actions of corticosterone and CRH underlie enduring memory impairme

43 Mechanistically, corticosterone and CRH, via their cognate receptors, act

44 70 nm) causes behavioural arousal, elevating corticosterone and delaying sleep onset.

45 During stress, adrenal corticosterone and hippocampal corticotropin-releasing h

46 Although C1 stimulation elevated plasma corticosterone and increased both vagal and sympathetic

47 ) mice showed elevated levels of circulating corticosterone and increased hippocampal Bdnf expression

48 However, corticosterone and normetanephrine failed to potentiate

49 these effects, we examined the abilities of corticosterone and normetanephrine to potentiate cocaine

50 Thus, despite similar effects on plasma corticosterone and on hypothalamic stress-sensitive cell

51 days of CUS decreased basal plasma levels of corticosterone and produced a shorter latency to immobil

52 reduced chronic stress-induced elevations in corticosterone and proinflammatory cytokine levels and d

53 ed plus maze or sacrificed for basal diurnal corticosterone and quantification of neuronal glucocorti

54 d behavioral emotionality, high basal plasma corticosterone and reduced gene expression of Bdnf, Cort

55 ss-predictive cues exhibited increased serum corticosterone and significantly greater reinstatement o

56 Withdrawal elevated corticosterone and somatic signs and blunted circadian v

57 s extrinsic to the host, such as exposure to corticosterone and to a lesser extent reduced food avail

58 mimicked by infusing rats with Intralipid or corticosterone and were corrected by leptin replacement.

59 Glucocorticoids (cortisol and corticosterone) and their inactive versions (cortisone a

60 eight gain, an abnormal circadian pattern of corticosterone, and an attenuated increase of corticoste

61 Plasma adrenocorticotropic hormone, corticosterone, and cytokine concentrations were measure

62 sed rats presented high levels of C-peptide, corticosterone, and glucose (P <0.05).

63 Corticosterone application attenuated inhibitory synapti

64 ginine vasopressin within the SCN and plasma corticosterone are both markedly phase advanced in Bdr m

65 costerone rhythms, but the overall levels of corticosterone are increased.

66 that MC3-R(-/-) mice exhibit elevated nadir corticosterone as well as a blunted fasting-induced acti

67 they displayed higher levels of blood serum corticosterone, as well as decreased body weight.

68 s not impacted by systemic administration of corticosterone at a dose that maintained elevated plasma

69 in nonstressed animals by administration of corticosterone at a dose that reproduced stress-induced

70 assay to measure endogenous acyl-ghrelin and corticosterone at time points surrounding auditory fear

71 Intraventricular corticosterone attenuated cocaine self-administration an

72 esulted in lower stress-driven production of corticosterone, augmented mouse proinflammatory immune r

73 pacity of sustained increases in circulating corticosterone (B) alone to alter dendritic spine morpho

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

75 ditionally, we found that a systemic dose of corticosterone blocked the depressive-like phenotype eli

76 one 2-fold in human trophoblast cells and of corticosterone by 90% in rat adrenocortical cells when c

77 termine the long term integrated response to corticosterone by impacting on the transcriptional machi

78 ic-pituitary-adrenal (HPA) axis feedback and corticosterone circadian levels.

79 A-axis dysfunction, namely loss of plasmatic corticosterone circadian oscillation, and promotes reduc

80 e displayed significant elevations in plasma corticosterone compared to CTL (p<0.002).

81 ed BNST CRF expression did not affect plasma corticosterone concentration but did decrease CRFR1 rece

82 n contrast, after 60 min of restraint plasma corticosterone concentration was significantly lower in

83 g for stronger positive correlations between corticosterone concentrations and colony nest abundance

84 accounting for positive correlations between corticosterone concentrations and number of fledgling ch

85 tress condition had better memory and higher corticosterone concentrations than rats trained at the l

86 tomidate, and vehicle groups, whereas plasma corticosterone concentrations were briefly (60-120 mins)

87 sed food intake, reduced plasma glucagon and corticosterone concentrations, and decreased ectopic lip

88 nt on body condition, immune metrics, plasma corticosterone concentrations, total antioxidant capacit

89 ch results from decreases in plasma ACTH and corticosterone concentrations.

90 riod, highest whole-body thyroid hormone and corticosterone content, and highest SMR, and these trait

91 mice and resulted in a shorter time to peak corticosterone (CORT) and a more rapid decay of CORT fol

92 that exposure to the primary glucocorticoid corticosterone (CORT) in adolescent mice recapitulates m

93 We examined the role of corticosterone (CORT) in SEFL.

94 Corticosterone (CORT) is known to negatively correlate w

95 e behavior and amygdala dysfunction, reduces corticosterone (CORT) levels, and exerts repair-related

96 e PFC were found to be correlated with blood corticosterone (CORT) levels.

97 el, learned helplessness (LH), and a chronic corticosterone (CORT) model in mice, we tested if ketami

98 (Ucn), beta-endorphin (beta-END), ACTH, and corticosterone (CORT) or the brain was fixed for immunoh

99 bjected to (1) a forced swim test (FST), (2) corticosterone (Cort) or vehicle injections, (3) CRS for

100 The rodent adrenal hormone corticosterone (CORT) reaches the brain in hourly ultrad

101 s the adrenocorticotropic hormone (ACTH) and corticosterone (CORT) response to stressors, and androge

102 eactivity, including basal and stress-evoked corticosterone (CORT) responses.

103 d behaviors in mice treated chronically with corticosterone (CORT), a mouse model of stress.

104 servation in which even a modest increase in corticosterone (CORT), caused by a single vehicle inject

105 ited elevated and prolonged levels of plasma corticosterone (CORT), interleukin (IL)-6 and IL-10 (but

106 hol following exposure to the stress hormone corticosterone (CORT).

107 Three weeks after corticosterone delivery, there was reduced sensitivity t

108 st traumatic experience a suppression of the corticosterone-dependent response protects against the d

109 dent model of depression, exhibited elevated corticosterone, depressive-like behavior, memory deficit

110 Restoring plasma corticosterone did not reverse the anxiolytic phenotype

111 mmoles/L), with a marked increase in plasma corticosterone (e.g. male offspring; 11.9 [9.3-14.8] vs.

112 eceptor antagonist RU38486 did not block the corticosterone effect.

113 raction of corticosterone with OCT3 mediates corticosterone effects on drug-seeking behavior and esta

114 Corticosterone effects on reinstatement were attenuated

115 (2)-mediated dopamine clearance may underlie corticosterone effects.

116 signalling in these tissues in mice drinking corticosterone either from day (D) 11 to D16 or D14 to D

117 In animal models, corticosterone elevations are associated with hippocampa

118 Do stress hormones, such as corticosterone, enhance bird susceptibility to mosquitoe

119 ch produce antidepressant effects in chronic corticosterone-exposed animals through GABAergic synapti

120 pressant effects on acute stress- or chronic corticosterone-exposed mice, respectively, through GABAe

121 pressant effects in acute stress- or chronic corticosterone-exposed mice, respectively.

122 LTD), without significant effects on chronic corticosterone-exposed mice.

123 Acute corticosterone exposure accelerated metamorphosis increa

124 and delayed metamorphosis, although chronic corticosterone exposure accelerated rate of metamorphosi

125 reductions in either host immunity (through corticosterone exposure) or antiparasite behaviours (thr

126 Using a mouse model of excess corticosterone exposure, we found that the ability of gl

127 ing ChIP-exo in mouse liver under endogenous corticosterone exposure, we report here that monomeric G

128 on in hippocampal neurogenesis after chronic corticosterone exposure.

129 We also show that the reported corticosterone extraproduction during the RF active phas

130 Corticosterone failed to re-establish extinguished prefe

131 Delivery of corticosterone for 7 d (without stressors) or RU486 (bef

132 y, or given daily subcutaneous injections of corticosterone, for 10 consecutive days.

133 oA-I-KO mice had less LPS clearance, reduced corticosterone generation, and impaired leukocyte recrui

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

135 c activity in skeletal muscle of mice in the corticosterone group relative to vehicle control.

136 to the vehicle control group, mice receiving corticosterone had a significant enhancement in pancreat

137 Corticosterone-implanted chicks and their siblings were

138 erfluorotetradecanoate to decreased baseline corticosterone in both sexes; and perfluorododecanoate w

139 cotropic hormone replacement elevated plasma corticosterone in ghr-/-, compared with WT mice, indicat

140 g of a single natural (cortisol in human and corticosterone in mice) and synthetic [e.g., dexamethaso

141 The aberrant increase of plasma corticosterone in neonates increased the plasma concentr

142 ntravitreous injection of the glucocorticoid corticosterone in rat eyes induced choroidal enlargement

143 ven Tspo cKO mice lost their ability to form corticosterone in response to adrenocorticotropic hormon

144 orticosterone, and an attenuated increase of corticosterone in response to stress.

145 or receptor for the stress hormone cortisol (corticosterone in rodents) and is widely expressed in ex

146 perarousal, generalization, and dysregulated corticosterone in stress-susceptible male mice.

147 ogenic effects of the glucocorticoid hormone corticosterone in the open-field, elevated plus maze, an

148 ally modifying the level of stress hormones (corticosterone) in brood mates, we demonstrate that the

149 levels of the glucocorticoid stress hormone, corticosterone, in broiler chickens produced a pessimist

150 atins acutely inhibited aldosterone, but not corticosterone, in response to different secretagogues.

151 ear response, anxiety-related behaviors, and corticosterone increase of the stressed cagemate, sugges

152 ing, or blockade of pups' alarm odor-induced corticosterone increase prevented transfer of fear.

153 ng, aberrant basal circadian fluctuations of corticosterone, increased amygdalar glucocorticoid recep

154 rtical Abeta and pTau levels and circulating corticosterone indicate a potential role for GCs in medi

155 Stress and the major stress hormone corticosterone induce profound influences in the brain.

156 transmission, because an elevation of pups' corticosterone induced by the odor of the frightened mot

157 t stimulated ERK42/44 corrected long-lasting corticosterone-induced behavioral abnormalities.

158 nd that this potentiation appears to involve corticosterone-induced blockade of dopamine clearance vi

159 Corticosterone-induced hyperglycemia, insulin resistance

160 fed to control intake, aiming to prevent the corticosterone-induced increase in food consumption, (3)

161 dipose triglyceride lipase inhibitor blocked corticosterone-induced increases in plasma glucose conce

162 surface NMDA receptor expression, reflecting corticosterone-induced inhibition of NMDA receptor endoc

163 l blockade of NAc dopamine receptors blocked corticosterone-induced potentiation of reinstatement.

164 demonstrated that AKG effectively attenuated corticosterone-induced protein degradation and rescued t

165 Treating leptin- and corticosterone-infused rats with an adipose triglyceride

166 ketogenesis; these effects were reversed by corticosterone infusion.

167 Systemic corticosterone injection immediately after the traumatic

168 terozygous (Sst(HZ)) mice show that elevated corticosterone is not sufficient to reproduce the behavi

169 that the daily rhythm of the glucocorticoid, corticosterone, is regulated by both light responsive an

170 nce correlates with an inverted U profile of corticosterone level in the circulation and of brain-der

171 mone, which was only partly reflected in the corticosterone level.

172 an increase in startle amplitude and plasma corticosterone levels 30 min following intra-BNST PACAP

173 kinase (ERK), P70S6K), as well as increased corticosterone levels and activation of the innate immun

174 able to demonstrate increased intra-adrenal corticosterone levels and an increase in steroidogenic a

175 ne taking is associated with elevated plasma corticosterone levels and that systemic infusion of coca

176 In these mice, plasma corticosterone levels are elevated, suggesting that olfa

177 displayed a two-fold increase in circulating corticosterone levels compared to CTL.

178 ped normally but at the age of 1 year, their corticosterone levels decreased; this was associated wit

179 al polypeptide (VIP) had no effect on plasma corticosterone levels even in previously stressed male r

180 [d-Ala(2)]GIP increased murine corticosterone levels in a GIPR-dependent manner.

181 We conclude that changes in corticosterone levels in chickens are sufficient to caus

182 on resulted in significantly enhanced plasma corticosterone levels in Gipr(-/-) mice.

183 TR4 knockdown decreases circulating ACTH and corticosterone levels in mice harboring ACTH-secreting t

184 ase from the pituitary and lowers peripheral corticosterone levels in response to acute stress.

185 However, this was transient, as corticosterone levels normalized later, followed by the

186 were not explained by differences in plasma corticosterone levels or numbers of Fos-labeled neurons

187 lasma adrenocorticotropic hormone (ACTH) and corticosterone levels were determined.

188 drawal symptoms or alterations in the plasma corticosterone levels were observed after 7 days of abst

189 Conversely, basal corticosterone levels were reduced, whereas food depriva

190 stress (increased fecal deposition and blood corticosterone levels), and alleviated by antalarmin (co

191 ponded to LPS by a 5-fold increase of plasma corticosterone levels, which were only moderately lower

192 for hormonal response to stress or in blood corticosterone levels.

193 hippocampal damage leads to high circulating corticosterone levels.

194 e was assessed through measurement of plasma corticosterone levels.

195 sessment, as well as accompanying attenuated corticosterone levels.

196 deficits are associated with elevated serum corticosterone levels; however, in the F2 and F3 generat

197 ctivation of NTS GLP-1-expressing neurons by corticosterone may represent a homeostatic response to c

198 ollected for adrenocorticotropic hormone and corticosterone measurement.

199 microbial endotoxin exposure through direct corticosterone-mediated effects on NKp46-expressing inna

200 ined the relationship between baseline fecal corticosterone metabolite concentrations and mercury con

201 Baseline fecal corticosterone metabolite concentrations were negatively

202 In recently hatched chicks, baseline fecal corticosterone metabolite concentrations were weakly neg

203 Faecal corticosterone metabolites (FCM) levels, offspring repro

204 Plasma corticosterone, microbiota composition, and cecal short-

205 amined stress physiology (plasma glucose and corticosterone), mitochondrial performance and the muscl

206 Using the mouse corticosterone model of anxiety/depression, we assessed

207 Corticosterone modified dendritic spine density in these

208 We found that chronic corticosterone not only induces marked deficits in olfac

209 te and product (11-dehydrocorticosterone and corticosterone) of the glucocorticoid-amplifying enzyme

210 We examined the effects of stress and corticosterone on behavioral and neurochemical responses

211 Endocannabinoid-dependent effects of corticosterone on inhibitory synaptic transmission in th

212 te numerous descriptions of rapid effects of corticosterone on neuronal function, the intracellular m

213 ing in the PL to the effects of stress-level corticosterone on PL neurotransmission and cocaine seeki

214 -natal day 10 caused an aberrant increase of corticosterone on post-natal day 15 and induced GHS in a

215 ays of non-invasive administration of either corticosterone or vehicle control, we tested the birds'

216 Increased levels of serum corticosterone, part of the stress response, accompanied

217 alar activity, but not the elevated level of corticosterone per se, reduces the stability of spatial

218 ndently dampened stress-induced increases in corticosterone plasma levels, but did not significantly

219 Corticosterone potentiated cocaine-induced increases in

220 in mice to directly test the hypothesis that corticosterone potentiates cocaine-primed reinstatement

221 reviously reported that stress, via elevated corticosterone, potentiates cocaine-primed reinstatement

222 an enhancement of 5-HT outflow in the DR of corticosterone-pretreated mice in response to fluoxetine

223 such desensitization was more pronounced in corticosterone-pretreated mice.

224 rough promoting LPS clearance and modulating corticosterone production and leukocyte recruitment.

225 ly of genotype, a dose-dependent increase in corticosterone production in the skin, mainly after 24h

226 ph tumor growth as well as enhances ACTH and corticosterone production, whereas TR4 knockdown decreas

227 ngs suggest that stress-induced increases in corticosterone promote cocaine seeking by mobilizing 2-a

228 Physiological levels of corticosterone promote HSC migration via the GC receptor

229 persisted after subdiaphragmatic vagotomy or corticosterone receptor blockade.

230 and links HF feeding to increased levels of corticosterone, reduced glucocorticoid levels do not sig

231 no effect on PACAP-induced increased plasma corticosterone, reduction of food intake, and body weigh

232 the lateral hypothalamic area (LHA) regulate corticosterone release and a variety of behaviours and p

233 HPA activity, based upon averaged values of corticosterone release from each animal obtained from re

234 In addition to significantly reduced corticosterone release in response to these two distinct

235 e FOS+GOS combination reduced stress-induced corticosterone release.

236 LA), which correlates with protracted plasma corticosterone release.

237 fear memory without blunting stress-induced corticosterone release.

238 The adrenal stress hormones epinephrine and corticosterone released by emotional arousal regulate th

239 Intra-accumbens administration of corticosterone reproduced the behavioral effects of stre

240 Lastly, corticosterone rescued the anxiety-like phenotype and me

241 Corticosterone response deteriorated in the placebo-trea

242 ce resulted in a significant blunting of the corticosterone response during pregnancy.

243 treated animals displayed a blunted HPA axis corticosterone response to acute footshock that did not

244 ial pressure response, but help maintain the corticosterone response to restraint stress.

245 rrent hypoglycemia improves the glucagon and corticosterone responses and largely ameliorates insulin

246 eptor type 2 (SSTR2) normalizes glucagon and corticosterone responses to hypoglycemic clamp in diabet

247 s oxytocin injections reduced behavioral and corticosterone responses to immobilization, whereas inje

248 trasonic vocalizations (USVs), freezing, and corticosterone responses were quantified.

249 t both the vlSCN and dmSCN contribute to the corticosterone rhythm by both reducing plasma ACTH and d

250 m phase misalignment, the peak of the plasma corticosterone rhythm is shifted and the amplitude reduc

251 d, the phase is dissociated from that of the corticosterone rhythm.

252 ACTH-independent pathway contributes to the corticosterone rhythm.

253 d to the aberrant light cycle maintain daily corticosterone rhythms, but the overall levels of cortic

254 asal, diurnal and stressor-stimulated plasma corticosterone secretion and basal plasma adrenocorticot

255 enhanced low-glucose-stimulated glucagon and corticosterone secretion to normal levels in diabetic ra

256 ess level triggers similar stress responses (corticosterone secretion) in brood bystanders.

257 Stimulation of GCG neurons had no effect on corticosterone secretion, body weight, or conditioned ta

258 the stress-related hormones epinephrine and corticosterone selectively modulate acute HSV-1 and HSV-

259 xpression of organic cation transporter 3, a corticosterone-sensitive uptake(2) transporter, was dete

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.

262 In contrast, corticosterone significantly decreased the levels of HSV

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.

265 Ank3+/- mice also exhibited elevated serum corticosterone, suggesting that reduced Ank3 expression

266 gut microbiota by experimentally inhibiting corticosterone synthesis with metyrapone.

267 urons are more responsive to epinephrine and corticosterone than are sensory neurons, demonstrating t

268 ose housed with vasectomised males had lower corticosterone than those with castrated males.

269 a pattern of adrenocorticotropic hormone and corticosterone that was similar to patients undergoing c

270 explore the relationships between PFASs and corticosterone (the major glucocorticoid in birds), and

271 t was recapitulated by intra-PL injection of corticosterone, the CB1R agonist WIN 55,212-2, or the mo

272 nvestigate how chronic and acute exposure to corticosterone, the dominant amphibian glucocorticoid ho

273 ma ACTH and differentially regulating plasma corticosterone through an ACTH- and sympathetic nervous

274 either SCN subregion independently regulates corticosterone through the sympathetic nervous system, w

275 l of anxiety/depression based on addition of corticosterone to drinking water.

276 posure markedly increased serum cortisol and corticosterone together with increases in monoacylglycer

277 However, when corticosterone-treated animals were pair-fed to control

278 decision making, dubbed 'pessimism', whereby corticosterone-treated birds showed an increased expecta

279 Corticosterone-treated birds were more likely than contr

280 yl-d-glucose clearance was reduced by 33% in corticosterone-treated dams (P < 0.05).

281 On the final day of administration, corticosterone-treated mice were hyperinsulinaemic (P <

282 sed Slc2a2 glucose transporter expression in corticosterone-treated mice, on D16 only (P < 0.05).

283 ng isolated NPCs with conditioned media from corticosterone-treated primary astrocytes.

284 Corticosterone treatment 1 h after PSS-exposure prevente

285 Corticosterone treatment acutely decreased NAc dopamine

286 ressor (electric footshock) nor stress-level corticosterone treatment alone reinstates cocaine seekin

287 metamorphosis and survival depended on both corticosterone treatment and infection status.

288 Depending upon gestational age, corticosterone treatment increased phosphorylation of th

289 ChIP sequencing of GR showed that corticosterone treatment induced a dose-dependent associ

290 The ability of systemic stress-level corticosterone treatment to potentiate cocaine-primed re

291 plication rate increased only in the chronic corticosterone treatment.

292 Corticosterone treatments affected immune function, as b

293 In the control and chronic corticosterone treatments, ranavirus infection decreased

294 Corticosterone upregulated the stress-inducible mechanis

295 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

297 Although elevated plasma levels of corticosterone were normalized by i.v. leptin infusion a

298 Cortisol and corticosterone were significantly higher in maternal tha

299 irst direct evidence that the interaction of corticosterone with OCT3 mediates corticosterone effects

300 ion) and resilience (spine proliferation) to corticosterone within the orbital cortex.