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1                                              CRH (corticotropin-releasing hormone), a peptide release
2                                              CRH functions in the contexts of acute and chronic stres
3                                              CRH, at nanomolar, presumed-stress levels, rapidly aboli
4                                              CRH-mediated spine loss required network activity and th
5 et, and interacts with the CREB homologue-1 (CRH-1) transcription factor in vivo.
6 t of corticotropin-releasing hormone type 1 (CRH(1)) receptors, in the treatment of recurrent major d
7  include endocrine neurons producing DH44, a CRH-like peptide, and insulin-like peptides.
8 current and activity-induced expression of a CRH-1/CREB transcriptional target (gem-4 Copine), which
9  Chemogenetic stimulation of AmPir activated CRH neurons and induced an increase in blood stress horm
10 h in turn increased the production of active CRH and GC.
11                             Levels of active CRH peptide are dependent on the processing of its precu
12  by using GR activation in the CeA for acute CRH induction and long-lasting behavioral modulation.
13 alin inflammatory pain test, we administered CRH or the CRH receptor antagonist alpha-helical CRH(9-4
14 sing hormone/hypothalamic-pituitary-adrenal (CRH/HPA) axis and the sympathomedullary system.
15                  The CRHR1 preferred agonist CRH stimulated tube formation, proliferation, and migrat
16                            CVS did not alter CRH median eminence immunoreactivity, indicating that CV
17 more, we report striking synchronicity among CRH neurons even across hemispheres, which suggests tigh
18  activity appeared highly synchronized among CRH neurons, and also across hemispheres.
19 ned anxiety and activations of the amygdala, CRH/HPA axis, the sympathomedullary system and their seq
20 deactivating calcineurin decrease CRTC-1 and CRH-1 activity and induce transcriptional responses simi
21 he synergistic actions of corticosterone and CRH at hippocampal synapses underlie memory impairments
22 el synergistic actions of corticosterone and CRH on hippocampal synaptic plasticity and spine structu
23 on of the stress hormones corticosterone and CRH recapitulated the physiological and structural defec
24          Mechanistically, corticosterone and CRH synergized at the spine-actin regulator RhoA, promot
25 e, synergistic actions of corticosterone and CRH underlie enduring memory impairments after concurren
26          Mechanistically, corticosterone and CRH, via their cognate receptors, acted synergistically
27 fter microinjections of CRH (0.2 microg) and CRH (0.4 microg), and NREM and total sleep were decrease
28 ces include a substantial increase of MT and CRH immunoreactivity in the dorsal lateral septum (LS) a
29  of Pa and its innervation by 5-HT, ORX, and CRH suggest that it may relay stress signals between the
30  circuits to coordinate responses to OXT and CRH.
31 measurement of orexins, orexin receptors and CRH in multiple brain regions.
32 h we name CRH2, to CRH1 (previously known as CRH) and urocortin1/urotensin1 (UCN1/UTS1) in primitive
33  the hypothalamus, amygdala, and midbrain as CRH neurons, although no double labeling was found.
34                                          Bar(CRH) neurons have unexpectedly long dendrites, which may
35                               Axons from Bar(CRH) neurons project to the lumbosacral spinal cord and
36 er for corticotrophin-releasing hormone (Bar(CRH) ).
37 ng data and future experiments targeting Bar(CRH) neurons and their synaptic afferents to study mictu
38  signaling uncovered a specific link between CRH-activated CRHR1, sAC, and endosome-based signaling.
39 ced a downregulation of CRH mRNA and blunted CRH and corticosterone release after 5-HT compound admin
40 ponses, recorded for 60min, were affected by CRH but not by ahCRH treatment.
41 aptic structure and function, are engaged by CRH and contribute to spine destabilization.
42 el granular exo-endocytic pathway induced by CRH on peritoneal MC.
43 ative membrane trafficking route mediated by CRH.
44 regulated kinase 1/2 activation triggered by CRH-stimulated CRHR1, but only sAC activity is essential
45 uropeptides found in the mammalian PVN (CCK, CRH, ENK, NTS, SS, VIP, OXT, AVP), we provide the first
46  pathway an ideal candidate for coordinating CRH synthesis and release.
47 dies of the impact of the OXT/OXTR and CRHBP/CRH pathways in males and females will be important in d
48 ion of BDNF, or its receptor TrkB, decreased CRH expression and normal HPA functions.
49 dentifies secretagogin neurons as a distinct CRH-releasing neuron population reliant on secretagogin'
50 resents a novel mechanism of endocannabinoid-CRH interactions in regulating amygdala output.
51 tivity, indicating that CVS does not enhance CRH storage within the median eminence.
52 in corticotroph excitability and exaggerated CRH/AVP-stimulated ACTH secretion in vitro.
53 CRH expression from over-use and exhaustion, CRH is also enhanced by glucocorticoids at both the leve
54  cortisol secretion in response to exogenous CRH stimulation, inferring rapid feedback inhibition at
55 anges in the expression of extrahypothalamic CRH.
56 ted higher stress (P < .001) and craving for CRH compared with controls.
57 hese findings support a mechanistic role for CRH-CRFR(1) signaling in stress-evoked spine loss and de
58       These findings indicate that forebrain CRH hyper-signaling in early-life is sufficient to incre
59       By using immunohistochemistry we found CRH-ir neurons surrounded by PTH2R-ir fibers and TIP39-i
60 or the CRH receptor antagonist alpha-helical CRH(9-41) (ahCRH) intracerebroventricularly to male and
61 ggest that persistently elevated hippocampal CRH-CRF(1) interaction contributes importantly to the st
62 establishing the contribution of hippocampal CRH-CRFR(1) signaling to these processes highlights the
63            In conclusion, the stress hormone CRH co-opts mechanisms that contribute to the plasticity
64 (CRHBP), an antagonist of the stress hormone CRH, is specifically expressed in OxtrINs.
65 ss hormones corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone.
66 rations of corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) cause a depolarizati
67 etagogues, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) to control the relea
68 etagogues, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) to control the relea
69         The corticotropin-releasing hormone (CRH) and its type 1 receptor (CRHR1) play a central role
70 s including corticotropin-releasing hormone (CRH) and neurotensin (NT), secreted in response to the m
71 levated PVN corticotropin-releasing hormone (CRH) and parvocellular arginine vasopressin (AVP) mRNA e
72 pothalamic corticotrophin-releasing hormone (CRH) and then stimulation of the adrenal by ACTH.
73 t level of corticotrophin-releasing hormone (CRH) can activate a dynamic pituitary-adrenal peripheral
74 pression of corticotropin-releasing hormone (CRH) can at least partially account for the various effe
75 lly labeled corticotropin-releasing hormone (CRH) cells, which represent a major regulator of the str
76 ction with corticotrophin releasing hormone (CRH) drive.
77 in cFos and corticotropin-releasing hormone (CRH) expression.
78        The corticotrophin-releasing hormone (CRH) family of peptides modulates intestinal inflammatio
79 europeptide corticotropin-releasing hormone (CRH) from hippocampal interneurons, activating receptors
80  release of corticotropin-releasing hormone (CRH) from the paraventricular nucleus (PVN) of the hypot
81 ypothalamic corticotropin-releasing hormone (CRH) gene expression and potently enhances GR-dependent
82 eurohormone corticotropin-releasing hormone (CRH) in hypothalamic neurons has been implicated as a ke
83 or intra-LC corticotropin releasing hormone (CRH) infusion supported aversion learning with intra-LC
84             Corticotropin-releasing hormone (CRH) is a central integrator in the brain of endocrine a
85             Corticotropin-releasing hormone (CRH) is a major regulator of the hypothalamic-pituitary-
86             Corticotropin releasing hormone (CRH) is disrupted in individuals with PTSD and early-lif
87             Corticotropin-releasing hormone (CRH) is secreted under stress and regulates the hypothal
88             Corticotropin-releasing hormone (CRH) is suggested to be involved in the regulation of pa
89 lamic (PVH) corticotropin-releasing hormone (CRH) neuroendocrine neurons mount neurosecretory and tra
90 strate that corticotropin-releasing hormone (CRH) neurons are modulated by the stress-derived neurost
91 y inputs to corticotropin-releasing hormone (CRH) neurons in the hypothalamic paraventricular nucleus
92             Corticotropin-releasing hormone (CRH) neurons in the parvocellular paraventricular nucleu
93 ypothalamic corticotropin-releasing hormone (CRH) neurons show extensive coexpression with neurotensi
94 ypothalamic corticotropin-releasing hormone (CRH) neurons, which control stress hormone levels.
95 ngth in PVN corticotropin-releasing hormone (CRH) neurons, with GLP-1R activation promoting a protein
96 sterone and corticotropin-releasing hormone (CRH) on synaptic physiology and dendritic spine structur
97 ived either corticotropin releasing hormone (CRH) or saline intravenously.
98 asopressin, corticotropin-releasing hormone (CRH) or thyrotropin-releasing hormone.
99 hippocampal corticotropin-releasing hormone (CRH) permeate memory-forming hippocampal synapses, yet i
100             Corticotropin releasing hormone (CRH) plays a major role in central nervous system respon
101 ypothalamic corticotropin-releasing hormone (CRH) regulates neuroendocrine functions such as adrenal
102             Corticotropin-releasing hormone (CRH) released from the paraventricular nucleus of the hy
103         The corticotropin-releasing hormone (CRH) system coordinates neuroendocrine and behavioral re
104 ferences in corticotropin-releasing hormone (CRH) system function.
105        The corticotrophin-releasing hormone (CRH) system integrates the stress response and is associ
106         The corticotropin-releasing hormone (CRH) system is implicated in the pathogenesis of several
107 tion of the corticotropin-releasing hormone (CRH) system within the extended amygdala appears to medi
108 nges to the corticotropin-releasing hormone (CRH) system; and structural, functional, and epigenetic
109 ticoids and corticotropin releasing hormone (CRH) underlie the physiology of change and adaptation.
110 europeptide corticotropin-releasing hormone (CRH) within the hippocampus during stress influences neu
111 CRFR(1)) of corticotropin-releasing hormone (CRH), a hippocampal neuropeptide released during stress.
112 the role of corticotropin-releasing hormone (CRH), a hypothalamic hormone also released during stress
113 a implicate corticotropin-releasing hormone (CRH), acting through its CRH1 receptor, in stress- and d
114    Although corticotropin-releasing hormone (CRH), produced by parvocellular neurons of the hypothala
115             Corticotropin-releasing hormone (CRH), through the hypothalamic pituitary adrenal axis an
116  to measure corticotropin-releasing hormone (CRH), urocortin (Ucn), beta-endorphin (beta-END), ACTH,
117 pression of corticotropin-releasing hormone (CRH), urocortin, proopiomelanocortin (POMC), and POMC-de
118 tocin (MT), corticotropin-releasing hormone (CRH), vasoactive intestinal polypeptide, tyrosine hydrox
119 e mammalian corticotropin-releasing hormone (CRH), were specifically activated by nutritive sugars.
120 europeptide corticotropin-releasing hormone (CRH), which influence the integrity of dendritic spines
121 PA axis is corticotrophin-releasing hormone (CRH), which is made in the parventricular nucleus and is
122  effects of corticotropin-releasing hormone (CRH), which is released from inflamed tissues by cellula
123 erestingly, corticotropin-releasing hormone (CRH)-1 receptors, which integrate neuroendocrine, behavi
124 raced local corticotropin-releasing hormone (CRH)-expressing inhibitory interneurons with extensive p
125 to both the corticotropin-releasing hormone (CRH)-immunoreactive cell bodies and dendrites within the
126 eactive for corticotropin-releasing hormone (CRH).
127 express the corticotropin-releasing hormone (CRH).
128  resembling corticotropin-releasing hormone (CRH).
129 ting genes, corticotropin releasing hormone (CRH; P=0.05) and glucocorticoid receptor (NR3C1; P=0.002
130 dogenous corticotropin-releasing hormone(+) (CRH(+)) LC inputs from the amygdala increase tonic LC ac
131                                 However, how CRH-producing neurons in an intact animal respond to dif
132                   Thus, our work reveals how CRH neurons respond to different levels of acute stress
133                                     However, CRH is also secreted outside the brain where it exerts p
134  third intracellular loop (IC3) of the human CRH-R1alpha important for cAMP and ERK1/2 pathways activ
135 orticoid release, whereas extra-hypothalamic CRH has a key role in stressor-triggered behaviors.
136 oids at both the level of extra-hypothalamic CRH sites and at the level of the placenta and fetal pro
137 ith intracellular mechanisms in hypothalamic CRH neuroendocrine neurons that initiate the adrenocorti
138 sted whether the innervation of hypothalamic CRH neurons of rat pups that received augmented maternal
139  pathway in rat paraventricular hypothalamic CRH (corticotropin-releasing hormone) neuroendocrine neu
140  release but were associated with changes in CRH receptor type 1 expression.
141         To investigate the role of the GR in CRH neurons, we have targeted the deletion of the GR, sp
142 hese mice, resulting in a modest increase in CRH expression in the paraventricular nucleus, hypoplast
143 arly life or adulthood causes an increase in CRH release in a variety of neural sites.
144           In vitro, the T allele resulted in CRH promoter activity that was higher following both sti
145   Supporting the importance of 5-HT(2C)Rs in CRH neuronal activity, genetic inactivation of 5-HT(2C)R
146 aused the recruitment of previously inactive CRH neurons in an intensity-dependent manner, thus incre
147            Previous work has shown increased CRH immunoreactivity in extrahypothalamic sites after ka
148 ectopic expression of BDNF in vivo increased CRH, whereas reduced expression of BDNF, or its receptor
149 atter function of glucocorticoids increasing CRH gene expression underlies the physiology of change t
150 amplitude of Ca(2+) transients in individual CRH neurons in response to such stressors.
151         The response magnitude of individual CRH cells covaried with stressor intensity.
152 ndent increase in the activity of individual CRH cells, and by an increase in the pool of responsive
153                                  Intravenous CRH elevated heart rates in all groups; however, cocaine
154 on supported aversion learning with intra-LC CRH infusion associated with increased olfactory bulb NE
155 tial specificity of the effect of early-life CRH exposure on adult behavior, the tetracycline-off sys
156 undamental physiological feature of limiting CRH expression from over-use and exhaustion, CRH is also
157                                        Local CRH signaling onto adult-born neurons promotes and/or st
158                             In BALB/cJ mice, CRH (0.4 microg) increased wakefulness and decreased NRE
159         In cultured rat hippocampal neurons, CRH application reduced dendritic spine density in a tim
160 usion, these data demonstrate the ability of CRH to affect the behavioral responses to an inflammator
161 es are to uncover how the dynamic actions of CRH integrate with the well-established roles of adrenal
162 cient to account for hindbrain activation of CRH neuroendocrine neurons during glycemic challenge.
163 arval zebrafish, we recorded the activity of CRH cells, while the larvae were exposed to stressors of
164                                  Addition of CRH (1 muM) to LAD2 cells, which are "primed" with SP fo
165 though previous, nonselective attenuation of CRH production or action, genetically in mice and pharma
166 l microdomains of IC3 in the coordination of CRH-R1 signaling activity.
167 oreover, intracerebroventricular delivery of CRH rescued the conditioned fear deficit in CeAGRKO mice
168 s fixed for immunohistochemical detection of CRH.
169 n of 5-HT(2C)Rs produced a downregulation of CRH mRNA and blunted CRH and corticosterone release afte
170 1 and CRH2 likely evolved via duplication of CRH during a whole-genome duplication early in the verte
171  as evidenced by the fact that the effect of CRH is mimicked by forskolin and 8-bromo-cAMP.
172                 After transient elevation of CRH during development only, behavioral testing in adult
173 icular nucleus resulted in an enhancement of CRH expression and an up-regulation of hypothalamic leve
174 results in a decrease in the excitability of CRH neurons.
175  latency (FSL) and decreased excitability of CRH neurons.
176 lacks agonistic effects on the expression of CRH in the central amygdala and antagonizes GR-mediated
177  glucocorticoids to direct the expression of CRH.
178 forebrain-restricted inducible expression of CRH.
179  We also found that intra-mPFC injections of CRH (20 ng) significantly increased anxiety-related beha
180 hereas the reduced excitatory innervation of CRH-expressing neurons dissipated by adulthood, increase
181             Subjects received 1 microg/kg of CRH intravenously.
182 ndicated the capacity of differing levels of CRH activity in different brain areas to produce behavio
183 d blood samples were obtained, and levels of CRH and corticotropin (ACTH) were measured by radioimmun
184 iers of the G allele had lower CSF levels of CRH but higher levels of ACTH.
185  the effects of this allele on CSF levels of CRH, plasma levels of ACTH, behavior, and ethanol consum
186              UVB stimulated plasma levels of CRH, Ucn, beta-END, ACTH, and CORT and increased skin ex
187 t and becomes disrupted for higher levels of CRH.
188 PC2, which is essential in the maturation of CRH from its prohormone, pro-CRH.
189     Here we demonstrate a novel mechanism of CRH-induced anxiety that relies on modulation of endocan
190 cord blood leukocyte promoter methylation of CRH (P=0.05) and NR3C1 (P=0.04); and 33% lower (P=0.07)
191 ituation to handling, ICV microinjections of CRH (0.04, 0.2, and 0.4 microg), AST (0.1, 0.4, and 1.0
192 ificantly decreased after microinjections of CRH (0.2 microg) and CRH (0.4 microg), and NREM and tota
193 leep were decreased after microinjections of CRH (0.4 microg).
194 s, the stressor strength-dependent output of CRH neurons emerges by a dual mechanism that involves bo
195 which the level, rather than the pattern, of CRH determines the dynamics of glucocorticoid hormone se
196 irtuin 1 (Sirt1) regulates the production of CRH post-translationally by affecting PC2.
197 sal GC levels by enhancing the production of CRH through an increase in the biosynthesis of PC2, whic
198 dendrites and decrease at the soma region of CRH neurons.
199       We find the differential regulation of CRH relies upon the cAMP response-element binding protei
200 ood, increased NRSF levels and repression of CRH expression persisted, suggesting that augmented earl
201 hat stressor strength-dependent responses of CRH neurons emerge via an intensity-dependent increase i
202                           While restraint of CRH by glucocorticoids is a fundamental physiological fe
203 els, and had no effect on UVB stimulation of CRH and Ucn levels in the plasma, demonstrating the requ
204  as a cellular entry point into the study of CRH-mediated, anxiety-like behaviors and their therapeut
205 manner that might promote the suppression of CRH expression and studied the cellular mechanisms under
206                         The synchronicity of CRH neurons within and across hemispheres ensures that t
207 ranscriptional responses similar to those of CRH-1 null worms.
208 does not affect the overall transcription of CRH, the mineralocorticoid receptor (MR), the serotonin
209  area (AmPir), contained neurons upstream of CRH neurons that were activated by volatile predator odo
210 th restraining and enhancing capabilities on CRH gene expression.
211 remodeling of synaptic contacts was found on CRH neurons in response to chronic stress.
212 otentiates the inhibitory effects of GABA on CRH neurons, decreasing the activity of the HPA axis.
213 with the known effects of glucocorticoids on CRH expression in the brain, carriers of the G allele ha
214 hibitory synaptic contacts were increased on CRH neurons; however, the excitatory/inhibitory input ra
215                      The effects of THDOC on CRH neurons are mediated by actions on GABA(A)R delta su
216  miniature excitatory synaptic currents onto CRH neurons were reduced in "care-augmented" rats compar
217 that positive feedback of neurosteroids onto CRH neurons is required to mount the physiological respo
218                               In particular, CRH and NT have synergistic effects on mast cell secreti
219 e, the molecular mechanism regulating phasic CRH release remains poorly understood.
220                                    Placental CRH concentrations were quantified in maternal blood col
221 d receptor (NR3C1; P=0.002); lower placental CRH transcript abundance (P=0.04); lower cord blood leuk
222 d HPA axis responses (rapidly increased pPVN CRH mRNA expression, ACTH, and corticosterone secretion)
223 ta in virgin and in late pregnant rats, pPVN CRH neurones are activated only in virgin rats.
224 ndent on the processing of its precursor pro-CRH by the action of two members of the family of prohor
225 e maturation of CRH from its prohormone, pro-CRH.
226  revealed that approximately one-half of PVH CRH-containing neurons coexpressed 5-HT(2C)R mRNA.
227              We examined neuroendocrine, PVN CRH neurons and report that social isolation alters the
228 sical stress has sex-specific effects on PVN CRH neurons.
229 nd the selective urocortin 3 (UCN3) receptor CRH-R2, but not UCN3 itself.
230  1 corticotropin-releasing hormone receptor (CRH-R1) influences biological responses important for ad
231 ever, the molecular mechanisms that regulate CRH are not fully understood.
232 addition to CRH, another gene that resembles CRH in sequence and syntenic environment.
233 and by an increase in the pool of responsive CRH cells at the population level.
234 nner, thus increasing the pool of responsive CRH cells.
235 ization of nonhypothalamic stress-responsive CRH systems.
236 se studies suggest that forebrain-restricted CRH signaling during development can permanently alter s
237 r data may suggest that functionally similar CRH variants could influence risk for externalizing diso
238 s, we induced transient, forebrain-specific, CRH overexpression during early-life (pre-puberty, CRHOE
239                               UVB stimulated CRH gene and protein expression in the brain that was lo
240 ntegrator of stress responses, and, as such, CRH gene variation may contribute to individual differen
241                                     As such, CRH gene variation may influence risk for alcohol use an
242 tivity and anxiety-related behavior and that CRH release in the mPFC may differentially regulate HPA
243                           Here we found that CRH expression is augmented in hippocampus of middle-age
244                  Functionally, we found that CRH signaling in the amygdala promotes an anxious phenot
245                                We found that CRH triggers substantial exocytosis, which is even stron
246                  Specifically, we found that CRH, through activation of the CRH receptor type 1 (CRHR
247                         We hypothesized that CRH hyper-signaling in the forebrain during early develo
248                         We hypothesized that CRH receptor activity in the mPFC contributes to stress-
249       Live, time-lapse imaging revealed that CRH reduced spine density by altering dendritic spine dy
250 amination of the cAMP response revealed that CRH-activated CRHR1 generates cAMP after endocytosis.
251                        Our data suggest that CRH promoter variation that confers increased stress rea
252 d anxiety responses, these data suggest that CRH signaling coordinates a disruption of tonic AEA acti
253 es modulates intestinal inflammation and the CRH receptor 2 (CRHR2) suppresses postnatal angiogenesis
254 e amygdala, the noradrenergic system and the CRH/HPA axis participate in multiple reinforcing positiv
255 he morning when arousal systems, such as the CRH/HPA axis and the noradrenergic systems, are at their
256 lving multidirectional crosstalk between the CRH/ACTH pathways, autonomic nervous system, vasopressin
257               Production of CRHBP blocks the CRH-induced potentiation of postsynaptic layer 2/3 pyram
258 ropin-releasing factor (CRF), encoded by the CRH gene, is a key integrator of stress responses, and,
259                       To better evaluate the CRH-mediated behavioral alterations in the formalin infl
260       Single nucleotide polymorphisms in the CRH receptor 1 (CRHR1) gene interact with ELS experience
261 le nucleotide polymorphism (rs110402) in the CRH receptor 1 (CRHR1) gene show behavioral and neuroend
262 ildhood trauma and sequence variation in the CRH receptor 1 gene (CRHR1) that increase risk for affec
263 during the formalin interphase period in the CRH-treated group compared to saline control groups; how
264 r understanding the diverse functions of the CRH family of peptides across vertebrates.
265 ons and confers decreased sensitivity of the CRH promoter to glucocorticoids in vitro.
266              Moreover, administration of the CRH receptor type 1 (CRFR(1)) blocker NBI 30775 directly
267 we found that CRH, through activation of the CRH receptor type 1 (CRHR1), evokes a rapid induction of
268 s suggest a time-dependent activation of the CRH system following activation of kainate receptors, wh
269 o functionally dissect the complexity of the CRH/CRHR1 system is to unravel the identity of CRHR1-exp
270 he cell contour, both being dependent on the CRH genes.
271 dent manner, and this action depended on the CRH receptor type 1.
272 GABA)-containing, inhibitory synapses on the CRH synthesizing neurons.
273 matory pain test, we administered CRH or the CRH receptor antagonist alpha-helical CRH(9-41) (ahCRH)
274 otide polymorphism (SNP) is found within the CRH promoter (-248C--> T).
275 imicking infection, robustly activates these CRH neurons via a noradrenergic input arising from the n
276                                         This CRH-stimulated mechanism is mediated through activation
277 t vertebrate genomes possess, in addition to CRH, another gene that resembles CRH in sequence and syn
278 alpain recruitment contributed critically to CRH-induced spine loss.
279                                  Exposure to CRH provoked spine loss and dendritic regression in hipp
280 response of cocaine-dependent individuals to CRH administration.
281 ontaining dendritic spines were resistant to CRH.
282 reased subjective and heart rate response to CRH and a relationship between stress and craving in coc
283  and increase in excitability in response to CRH and AVP the patterns of electrical excitability and
284  and increase in excitability in response to CRH and AVP the patterns of electrical excitability and
285 d the subjective and physiologic response to CRH in cocaine-dependent individuals and controls.
286                 This oscillatory response to CRH is dose dependent and becomes disrupted for higher l
287                The corticotropin response to CRH was independent of sex and cocaine dependence.
288 or the transition to bursting in response to CRH.
289 or the transition to bursting in response to CRH.
290 enatal cocaine enhanced the CORT response to CRH/saline injections up to 60 min in males but not in f
291       Women had higher cortisol responses to CRH (P = .03).
292 d the relationship of this second vertebrate CRH gene, which we name CRH2, to CRH1 (previously known
293 ase expression of functional CRHR-1, whereas CRH induces NK-1 gene expression.
294 mathematical modeling to investigate whether CRH and AVP promote distinct patterns of electrical exci
295 athematical modelling to investigate whether CRH and AVP promote distinct patterns of electrical exci
296                 Treatment of LAD2 cells with CRH (1 muM) for 6 hours induces gene expression of NK-1
297 ver, repeated stimulation of mast cells with CRH (1 muM) leads to downregulation of CRHR-1 and upregu
298                          Co-stimulation with CRH and AVP results in complex patterns of excitability
299                          Co-stimulation with CRH and AVP results in complex patterns of excitability
300                 The structural motifs within CRH-R1 that mediate G protein activation and signaling s

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