コーパス検索結果 (left1)
通し番号をクリックするとPubMedの該当ページを表示します
1 CRH (corticotropin-releasing hormone), a peptide release
2 CRH actions in NAc may vary by the individual's stress h
3 CRH functions in the contexts of acute and chronic stres
4 CRH(+) fibers are found in nucleus accumbens (NAc), wher
5 CRH(+) NAc afferents were selectively enriched in NAc-pr
6 CRH, at nanomolar, presumed-stress levels, rapidly aboli
7 CRH-mediated spine loss required network activity and th
9 e role of a specific isoform of CREB1/CRH-1, CRH-1e, in Caenorhabditis elegans memory formation and c
10 show that a specific isoform of CREB1/CRH-1, CRH-1e, is primarily responsible for memory related func
12 current and activity-induced expression of a CRH-1/CREB transcriptional target (gem-4 Copine), which
13 Chemogenetic stimulation of AmPir activated CRH neurons and induced an increase in blood stress horm
16 alin inflammatory pain test, we administered CRH or the CRH receptor antagonist alpha-helical CRH(9-4
20 more, we report striking synchronicity among CRH neurons even across hemispheres, which suggests tigh
22 ned anxiety and activations of the amygdala, CRH/HPA axis, the sympathomedullary system and their seq
23 e findings show that activation of amygdalar CRH+ neurons induces resilience, and suppresses the gain
24 deactivating calcineurin decrease CRTC-1 and CRH-1 activity and induce transcriptional responses simi
25 he synergistic actions of corticosterone and CRH at hippocampal synapses underlie memory impairments
26 el synergistic actions of corticosterone and CRH on hippocampal synaptic plasticity and spine structu
27 on of the stress hormones corticosterone and CRH recapitulated the physiological and structural defec
29 e, synergistic actions of corticosterone and CRH underlie enduring memory impairments after concurren
32 ces include a substantial increase of MT and CRH immunoreactivity in the dorsal lateral septum (LS) a
35 32% and 74% of nonneuroendocrine TH, TRH and CRH neurons were responsive to GH in the PVH of Fluoro-G
36 %, 49% and 75% of neuroendocrine TH, TRH and CRH neurons, and 67%, 32% and 74% of nonneuroendocrine T
37 h we name CRH2, to CRH1 (previously known as CRH) and urocortin1/urotensin1 (UCN1/UTS1) in primitive
41 ng data and future experiments targeting Bar(CRH) neurons and their synaptic afferents to study mictu
42 signaling uncovered a specific link between CRH-activated CRHR1, sAC, and endosome-based signaling.
47 regulated kinase 1/2 activation triggered by CRH-stimulated CRHR1, but only sAC activity is essential
48 uropeptides found in the mammalian PVN (CCK, CRH, ENK, NTS, SS, VIP, OXT, AVP), we provide the first
50 sible for the LTM related functions of CREB1/CRH-1 while being dispensable for its innate chemotaxis
51 ates the role of a specific isoform of CREB1/CRH-1, CRH-1e, in Caenorhabditis elegans memory formatio
52 We show that a specific isoform of CREB1/CRH-1, CRH-1e, is primarily responsible for memory relat
53 mation in the animal and expression of CREB1/CRH-1e in a single pair of neurons is sufficient to resc
54 dies of the impact of the OXT/OXTR and CRHBP/CRH pathways in males and females will be important in d
56 potential roles for the molecularly-defined, CRH-dependent circuit in modulation of reward and motiva
57 dentifies secretagogin neurons as a distinct CRH-releasing neuron population reliant on secretagogin'
61 CRH expression from over-use and exhaustion, CRH is also enhanced by glucocorticoids at both the leve
62 cortisol secretion in response to exogenous CRH stimulation, inferring rapid feedback inhibition at
64 idual's stress history, suggesting roles for CRH in neuroplasticity and adaptation of the reward circ
68 or the CRH receptor antagonist alpha-helical CRH(9-41) (ahCRH) intracerebroventricularly to male and
69 pal CRH expression, and blocking hippocampal CRH receptor type-1 (CRHR1) immediately following early-
70 ggest that persistently elevated hippocampal CRH-CRF(1) interaction contributes importantly to the st
71 Early-life adversity increases hippocampal CRH expression, and blocking hippocampal CRH receptor ty
72 establishing the contribution of hippocampal CRH-CRFR(1) signaling to these processes highlights the
77 rations of corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) cause a depolarizati
78 etagogues, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) to control the relea
79 etagogues, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) to control the relea
82 s including corticotropin-releasing hormone (CRH) and neurotensin (NT), secreted in response to the m
84 europeptide Corticotropin Releasing Hormone (CRH) based on the immobilization of half-antibody fragme
85 t level of corticotrophin-releasing hormone (CRH) can activate a dynamic pituitary-adrenal peripheral
86 pression of corticotropin-releasing hormone (CRH) can at least partially account for the various effe
87 lly labeled corticotropin-releasing hormone (CRH) cells, which represent a major regulator of the str
90 europeptide corticotropin-releasing hormone (CRH) from hippocampal interneurons, activating receptors
91 release of corticotropin-releasing hormone (CRH) from the paraventricular nucleus (PVN) of the hypot
92 ypothalamic corticotropin-releasing hormone (CRH) gene expression and potently enhances GR-dependent
93 eurohormone corticotropin-releasing hormone (CRH) in hypothalamic neurons has been implicated as a ke
94 or intra-LC corticotropin releasing hormone (CRH) infusion supported aversion learning with intra-LC
101 strate that corticotropin-releasing hormone (CRH) neurons are modulated by the stress-derived neurost
102 e (TRH) and corticotropin-releasing hormone (CRH) neurons expressed GH-induced pSTAT5, respectively.
104 y inputs to corticotropin-releasing hormone (CRH) neurons in the hypothalamic paraventricular nucleus
105 napses onto corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypot
108 ngth in PVN corticotropin-releasing hormone (CRH) neurons, with GLP-1R activation promoting a protein
109 sterone and corticotropin-releasing hormone (CRH) on synaptic physiology and dendritic spine structur
112 hippocampal corticotropin-releasing hormone (CRH) permeate memory-forming hippocampal synapses, yet i
113 ypothalamic corticotropin-releasing hormone (CRH) regulates neuroendocrine functions such as adrenal
117 tion of the corticotropin-releasing hormone (CRH) system within the extended amygdala appears to medi
118 nges to the corticotropin-releasing hormone (CRH) system; and structural, functional, and epigenetic
119 ticoids and corticotropin releasing hormone (CRH) underlie the physiology of change and adaptation.
121 europeptide corticotropin-releasing hormone (CRH) within the hippocampus during stress influences neu
122 f amygdalar corticotropin-releasing hormone (CRH)+ neurons abolished the increase in DRv TPH2+ neuron
123 the role of corticotropin-releasing hormone (CRH), a hypothalamic hormone also released during stress
124 a implicate corticotropin-releasing hormone (CRH), acting through its CRH1 receptor, in stress- and d
125 Although corticotropin-releasing hormone (CRH), produced by parvocellular neurons of the hypothala
127 to measure corticotropin-releasing hormone (CRH), urocortin (Ucn), beta-endorphin (beta-END), ACTH,
128 pression of corticotropin-releasing hormone (CRH), urocortin, proopiomelanocortin (POMC), and POMC-de
129 tocin (MT), corticotropin-releasing hormone (CRH), vasoactive intestinal polypeptide, tyrosine hydrox
130 e mammalian corticotropin-releasing hormone (CRH), were specifically activated by nutritive sugars.
131 europeptide corticotropin-releasing hormone (CRH), which influence the integrity of dendritic spines
132 PA axis is corticotrophin-releasing hormone (CRH), which is made in the parventricular nucleus and is
133 effects of corticotropin-releasing hormone (CRH), which is released from inflamed tissues by cellula
134 raced local corticotropin-releasing hormone (CRH)-expressing inhibitory interneurons with extensive p
135 to both the corticotropin-releasing hormone (CRH)-immunoreactive cell bodies and dendrites within the
138 ting genes, corticotropin releasing hormone (CRH; P=0.05) and glucocorticoid receptor (NR3C1; P=0.002
139 dogenous corticotropin-releasing hormone(+) (CRH(+)) LC inputs from the amygdala increase tonic LC ac
143 third intracellular loop (IC3) of the human CRH-R1alpha important for cAMP and ERK1/2 pathways activ
144 orticoid release, whereas extra-hypothalamic CRH has a key role in stressor-triggered behaviors.
145 oids at both the level of extra-hypothalamic CRH sites and at the level of the placenta and fetal pro
146 ith intracellular mechanisms in hypothalamic CRH neuroendocrine neurons that initiate the adrenocorti
147 sted whether the innervation of hypothalamic CRH neurons of rat pups that received augmented maternal
148 pathway in rat paraventricular hypothalamic CRH (corticotropin-releasing hormone) neuroendocrine neu
152 hese mice, resulting in a modest increase in CRH expression in the paraventricular nucleus, hypoplast
156 aused the recruitment of previously inactive CRH neurons in an intensity-dependent manner, thus incre
157 ectopic expression of BDNF in vivo increased CRH, whereas reduced expression of BDNF, or its receptor
158 atter function of glucocorticoids increasing CRH gene expression underlies the physiology of change t
161 ndent increase in the activity of individual CRH cells, and by an increase in the pool of responsive
164 on supported aversion learning with intra-LC CRH infusion associated with increased olfactory bulb NE
165 tial specificity of the effect of early-life CRH exposure on adult behavior, the tetracycline-off sys
166 undamental physiological feature of limiting CRH expression from over-use and exhaustion, CRH is also
168 e AAV1-directed axonal tracing to verify NAc CRH(+) fiber projections and established the identity of
171 ctions of the stress-activated neuropeptide, CRH, contribute to the deleterious effects of early-life
172 usion, these data demonstrate the ability of CRH to affect the behavioral responses to an inflammator
173 urther show that two specific amino acids of CRH-1 are required for the process of memory formation i
174 es are to uncover how the dynamic actions of CRH integrate with the well-established roles of adrenal
175 arval zebrafish, we recorded the activity of CRH cells, while the larvae were exposed to stressors of
177 though previous, nonselective attenuation of CRH production or action, genetically in mice and pharma
180 cesses of the half-antibody and detection of CRH, using cyclic voltammetry and electrochemical impeda
181 r was obtained for the specific detection of CRH, within a range of 10.0-80.0 mug mL(-1), with a limi
183 1 and CRH2 likely evolved via duplication of CRH during a whole-genome duplication early in the verte
186 icular nucleus resulted in an enhancement of CRH expression and an up-regulation of hypothalamic leve
189 lacks agonistic effects on the expression of CRH in the central amygdala and antagonizes GR-mediated
193 hereas the reduced excitatory innervation of CRH-expressing neurons dissipated by adulthood, increase
195 ndicated the capacity of differing levels of CRH activity in different brain areas to produce behavio
200 Here we demonstrate a novel mechanism of CRH-induced anxiety that relies on modulation of endocan
201 cord blood leukocyte promoter methylation of CRH (P=0.05) and NR3C1 (P=0.04); and 33% lower (P=0.07)
202 s, the stressor strength-dependent output of CRH neurons emerges by a dual mechanism that involves bo
203 which the level, rather than the pattern, of CRH determines the dynamics of glucocorticoid hormone se
205 sal GC levels by enhancing the production of CRH through an increase in the biosynthesis of PC2, whic
208 ood, increased NRSF levels and repression of CRH expression persisted, suggesting that augmented earl
209 hat stressor strength-dependent responses of CRH neurons emerge via an intensity-dependent increase i
211 nscription factor in C. elegans Silencing of CRH-1e-expressing neurons during training for LTM format
213 els, and had no effect on UVB stimulation of CRH and Ucn levels in the plasma, demonstrating the requ
214 as a cellular entry point into the study of CRH-mediated, anxiety-like behaviors and their therapeut
215 manner that might promote the suppression of CRH expression and studied the cellular mechanisms under
218 does not affect the overall transcription of CRH, the mineralocorticoid receptor (MR), the serotonin
219 area (AmPir), contained neurons upstream of CRH neurons that were activated by volatile predator odo
222 otentiates the inhibitory effects of GABA on CRH neurons, decreasing the activity of the HPA axis.
223 hibitory synaptic contacts were increased on CRH neurons; however, the excitatory/inhibitory input ra
225 miniature excitatory synaptic currents onto CRH neurons were reduced in "care-augmented" rats compar
226 that positive feedback of neurosteroids onto CRH neurons is required to mount the physiological respo
231 d receptor (NR3C1; P=0.002); lower placental CRH transcript abundance (P=0.04); lower cord blood leuk
232 d HPA axis responses (rapidly increased pPVN CRH mRNA expression, ACTH, and corticosterone secretion)
233 ndent on the processing of its precursor pro-CRH by the action of two members of the family of prohor
238 1 corticotropin-releasing hormone receptor (CRH-R1) influences biological responses important for ad
244 se studies suggest that forebrain-restricted CRH signaling during development can permanently alter s
245 k against an existing algorithm, which shows CRH delivers very similar or slightly improved results a
246 s, we induced transient, forebrain-specific, CRH overexpression during early-life (pre-puberty, CRHOE
248 ntegrator of stress responses, and, as such, CRH gene variation may contribute to individual differen
249 d CRHR2 in patients with IC/BPS, and suggest CRH signaling may be associated with IC/BPS symptoms.
255 amination of the cAMP response revealed that CRH-activated CRHR1 generates cAMP after endocytosis.
257 d anxiety responses, these data suggest that CRH signaling coordinates a disruption of tonic AEA acti
258 es modulates intestinal inflammation and the CRH receptor 2 (CRHR2) suppresses postnatal angiogenesis
259 e amygdala, the noradrenergic system and the CRH/HPA axis participate in multiple reinforcing positiv
260 he morning when arousal systems, such as the CRH/HPA axis and the noradrenergic systems, are at their
261 onally, the association constant between the CRH and the immobilized half-antibody was calculated at
262 lving multidirectional crosstalk between the CRH/ACTH pathways, autonomic nervous system, vasopressin
264 ropin-releasing factor (CRF), encoded by the CRH gene, is a key integrator of stress responses, and,
267 le nucleotide polymorphism (rs110402) in the CRH receptor 1 (CRHR1) gene show behavioral and neuroend
268 ildhood trauma and sequence variation in the CRH receptor 1 gene (CRHR1) that increase risk for affec
269 during the formalin interphase period in the CRH-treated group compared to saline control groups; how
272 we found that CRH, through activation of the CRH receptor type 1 (CRHR1), evokes a rapid induction of
274 o functionally dissect the complexity of the CRH/CRHR1 system is to unravel the identity of CRHR1-exp
277 matory pain test, we administered CRH or the CRH receptor antagonist alpha-helical CRH(9-41) (ahCRH)
280 t vertebrate genomes possess, in addition to CRH, another gene that resembles CRH in sequence and syn
283 d stresscopin-related peptide, paralogous to CRH, were also identified based on the conserved signali
285 reased subjective and heart rate response to CRH and a relationship between stress and craving in coc
286 and increase in excitability in response to CRH and AVP the patterns of electrical excitability and
291 enatal cocaine enhanced the CORT response to CRH/saline injections up to 60 min in males but not in f
292 d the relationship of this second vertebrate CRH gene, which we name CRH2, to CRH1 (previously known
295 athematical modelling to investigate whether CRH and AVP promote distinct patterns of electrical exci
296 mathematical modeling to investigate whether CRH and AVP promote distinct patterns of electrical exci
298 ver, repeated stimulation of mast cells with CRH (1 muM) leads to downregulation of CRHR-1 and upregu