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1 ORs that colocalize with the stress hormone, corticotropin releasing factor.
2 e diuretic hormone 44 (DH44), an ortholog of corticotropin-releasing factor.
3 he transmembrane domains of the glucagon and corticotropin releasing factor 1 (CRF1) receptors to dev
6 ist (eticlopride), D2R agonist (quinpirole), corticotropin-releasing factor 1 (CRF1) antagonist (anta
7 urthermore, pharmacologic inhibition (with a corticotropin-releasing factor 1 receptor antagonist) of
8 derivatives was synthesized and evaluated as corticotropin releasing factor-1 (CRF(1)) receptor antag
9 s was identified as potent and orally active corticotropin-releasing factor-1 (CRF(1)) receptor antag
10 ctive withdrawal-like state characterized by corticotropin-releasing factor-1 (CRF(1)) receptor antag
12 ation of 8, an earlier lead pyrazinone-based corticotropin-releasing factor-1 (CRF(1)) receptor antag
13 rmittent access to palatable food results in corticotropin-releasing factor-1 (CRF1) receptor antagon
18 t of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neu
19 alcohol drinking by increased expression of corticotropin-releasing factor and its feedback regulati
20 ween the N/OFQ and Hcrt systems in which the corticotropin-releasing factor and N/OFQ systems coordin
22 by a variety of central (eg, neuropeptide Y, corticotropin-releasing factor, and neuromedin U) and pe
23 oactive intestinal polypeptide, substance P, corticotropin-releasing factor, and neuropeptide Y), ena
24 cial behavior (especially neuropeptide Y and corticotropin-releasing factor) are modulated by alcohol
27 88-induced c-Fos activation were observed in corticotropin releasing factor-containing neurons of the
28 eus of the hypothalamus and primarily in non-corticotropin releasing factor-containing neurons of the
29 gh an interaction between the stress hormone corticotropin releasing factor (CRF) and glutamate relea
33 blocked by intravenous pretreatment with the corticotropin releasing factor (CRF) antagonist, astress
39 of this study was to examine the ability of corticotropin releasing factor (CRF) or antibody to insu
42 icotine withdrawal was mediated by increased corticotropin releasing factor (CRF) receptor-1 expressi
43 e agonists and developed antagonists for the corticotropin releasing factor (CRF) receptors are new t
45 lar nucleus (PVN) have been shown to inhibit corticotropin releasing factor (CRF) synthesis via GABA(
50 ontains a large number of neurons expressing corticotropin releasing factor (CRF), a neuropeptide tha
51 intracerebroventricular (icv) injections of corticotropin releasing factor (CRF), a putative anxioge
52 hanism underlying this response, we measured corticotropin releasing factor (CRF), an upstream modula
53 analyzed brain regional, CCK-8, substance P, corticotropin releasing factor (CRF), and neuropeptide Y
54 for 15 days and measured mRNA expression of corticotropin releasing factor (CRF), neuropeptide Y (NP
61 were measured at baseline and in response to corticotropin-releasing factor (CRF) (0.5 microg kg(1))
62 c raphe nucleus, including a coordination of corticotropin-releasing factor (CRF) actions at both of
64 f chronic nicotine SA on the coexpression of corticotropin-releasing factor (CRF) and arginine vasopr
66 ocus of the present review is on the role of corticotropin-releasing factor (CRF) and CRF-related pep
68 mRNA was found to partially colocalize with corticotropin-releasing factor (CRF) and growth hormone-
69 ajor site of extrahypothalamic expression of corticotropin-releasing factor (CRF) and its G-protein-c
72 laced on the neuropharmacological actions of corticotropin-releasing factor (CRF) and norepinephrine
80 ng the endocrine arm of the stress response, corticotropin-releasing factor (CRF) can act in the brai
81 s-induced release of neuromodulators such as corticotropin-releasing factor (CRF) can drive drug-depe
83 ses and how the stress-related neuropeptide, corticotropin-releasing factor (CRF) directs this by a b
84 regulation of the central extrahypothalamic corticotropin-releasing factor (CRF) expression is assoc
92 hypersecretion of the stress neuromediator, corticotropin-releasing factor (CRF) has been implicated
93 rofiling of relevant PI cells identified the corticotropin-releasing factor (CRF) homolog, DH44, as a
94 ike ShA cocaine self-administration, reduced corticotropin-releasing factor (CRF) immunodensity in th
96 gates the regulation of cytosolic calcium by corticotropin-releasing factor (CRF) in midbrain dopamin
97 ed body of work indicates a crucial role for corticotropin-releasing factor (CRF) in neurobiological
98 vioral studies support a modulatory role for corticotropin-releasing factor (CRF) in regulating the d
99 termined the role of the stress neurohormone corticotropin-releasing factor (CRF) in stress-induced b
100 was used to study immunoreactivity (IR) for corticotropin-releasing factor (CRF) in the guinea pig e
101 ed on previous work hypothesizing a role for corticotropin-releasing factor (CRF) in the IC during cr
102 lores the relationship between dynorphin and corticotropin-releasing factor (CRF) in the induction of
104 bout the distribution of the stress hormone, corticotropin-releasing factor (CRF) in the mouse brain.
106 dies have found that the stress neurohormone corticotropin-releasing factor (CRF) inhibits 5-HT neuro
107 literature suggests that catecholamines and corticotropin-releasing factor (CRF) interact in a seria
108 Stress induces the release of the peptide corticotropin-releasing factor (CRF) into the ventral te
115 ntial findings suggest that the neuropeptide corticotropin-releasing factor (CRF) is instrumental in
119 The present experiments examined whether corticotropin-releasing factor (CRF) modulates memory co
120 rning of day 15, we measured AT(1) receptors corticotropin-releasing factor (CRF) mRNA and immunoreac
122 rsal mPFC enhanced restraint-induced Fos and corticotropin-releasing factor (CRF) mRNA expression in
123 re to elicit reliable increases in Fos-ir or corticotropin-releasing factor (CRF) mRNA in the PVH.
125 and anxiety and activates a subpopulation of corticotropin-releasing factor (CRF) neurons in the bed
126 cohol intake specifically recruited GABA and corticotropin-releasing factor (CRF) neurons in the mPFC
128 the relationship between corticosterone and corticotropin-releasing factor (CRF) on both beta-amyloi
129 ed the effect of an intravenous injection of corticotropin-releasing factor (CRF) on fructose malabso
130 nced fear memory but did not increase either corticotropin-releasing factor (CRF) or corticosterone.
138 duction and Abeta elevation are dependent on corticotropin-releasing factor (CRF) receptor 1 signalin
146 ife social isolation increases the levels of corticotropin-releasing factor (CRF) receptors in the se
149 induced relapse through alterations in brain corticotropin-releasing factor (CRF) regulation of neuro
154 o negative reinforcement is a recruitment of corticotropin-releasing factor (CRF) signaling within th
155 Previous studies have implicated the brain corticotropin-releasing factor (CRF) stress systems in m
156 likely resulting from dysregulation of brain corticotropin-releasing factor (CRF) stress systems.
157 ment of the extrahypothalamic stress peptide corticotropin-releasing factor (CRF) system and activati
160 ess systems, including the extrahypothalamic corticotropin-releasing factor (CRF) system, following l
162 f neonatal amygdala (Neo-A) lesions on brain corticotropin-releasing factor (CRF) systems and hypotha
165 authors investigated the effect of blocking corticotropin-releasing factor (CRF) Type I and Type II
170 -regulated by a major stress neuromodulator, corticotropin-releasing factor (CRF), acting on CRF type
172 nsistent with this, the CEA highly expresses corticotropin-releasing factor (CRF), an important modul
173 ceruleus (LC)-norepinephrine (NE) neurons to corticotropin-releasing factor (CRF), an integral mediat
174 ays a role in the relationship among stress, corticotropin-releasing factor (CRF), and alcohol abuse.
175 he LC include excitatory amino acids (EAAs), corticotropin-releasing factor (CRF), and endogenous opi
176 (Dh44), a neuropeptide related to vertebrate corticotropin-releasing factor (CRF), and its receptor,
177 vitro and their modulation by dopamine (DA), corticotropin-releasing factor (CRF), and their combinat
179 to the BNSTDL, is thought to communicate via corticotropin-releasing factor (CRF), but studies have y
182 -protein-coupled receptor B1 family includes corticotropin-releasing factor (CRF), growth hormone-rel
183 -adrenal (HPA) axis-activating neuropeptide, corticotropin-releasing factor (CRF), may be the keyston
184 ological studies indicate the involvement of corticotropin-releasing factor (CRF), noradrenaline, dop
189 Stress may impact on this system through corticotropin-releasing factor (CRF), which densely inne
190 ral amygdala noradrenergic substrates [via a corticotropin-releasing factor (CRF)-dependent mechanism
191 lacement regimens were tested for changes in corticotropin-releasing factor (CRF)-enhanced startle (i
192 allenge has been shown previously to cause a corticotropin-releasing factor (CRF)-mediated increase i
208 two endogenous CRF-related peptide ligands, corticotropin-releasing factor [CRF rat/human (r/h)] and
209 known as maternal aggression) is impaired by corticotropin-releasing factor-(CRF) related peptides, b
210 ed neural cell density, stress neuropeptide (corticotropin releasing factor--CRF) levels, and plasma
211 This study tested the hypothesis that the corticotropin-releasing factor (CRF1) antagonist GSK5616
212 ers of the corticoliberin family include the corticotropin releasing factors (CRFs), sauvagine, the u
214 ed with brain region-specific alterations of corticotropin-releasing factor expression and promoter m
216 oupled receptors, which bind peptides of the corticotropin releasing factor family and are key mediat
218 ortin 2, a recently identified member of the corticotropin-releasing factor family, is expressed in d
219 ivery of Urocortin I (UcnI), a member of the corticotropin-releasing factor family, suppresses feedin
220 ylglycines (NPPGs) as a novel class of human corticotropin releasing factor (h-CRF(1)) antagonists.
222 ephalin, thyrothropin-releasing hormone, and corticotropin-releasing factor immunoreactive cells in t
223 CRFR1) mediates the physiological actions of corticotropin-releasing factor in the anterior pituitary
224 doxical observations of increased release of corticotropin-releasing factor in the face of low cortis
225 tuitary-adrenal axis, including signaling by corticotropin-releasing factor, in the pathophysiology o
230 ated increments in restraint-induced Fos and corticotropin-releasing factor mRNA expression in the ne
231 w stress interacts with the neuromodulators, corticotropin-releasing factor, norepinephrine, dopamine
232 w explores the role of brain stress systems (corticotropin-releasing factor, norepinephrine, orexin [
233 s in the anterior hypothalamus that may gate corticotropin-releasing factor output from the amygdala
234 s an activation of the brain stress system's corticotropin-releasing factor outside of the hypothalam
235 in stress and appetite regulation, including corticotropin releasing factor, pro-opiomelanocortin B,
237 The CRF system consists of two receptors, corticotropin releasing factor receptor 1 (CRF1R) and co
239 opin releasing factor receptor 1 (CRF1R) and corticotropin releasing factor receptor 2 (CRF2R), a non
240 analysis showed significant upregulation of corticotropin releasing factor receptor 2 (CrfR2) in the
242 nvestigated here the interaction between the corticotropin releasing factor receptor type 1 (CRF1R) a
243 tuted pyridyl)pyrazolo[1,5-a]-1,3,5-triazine corticotropin releasing factor receptor-1 (CRF(1)) recep
244 methoxyphenyl)pyrazolo[1,5-a]-1,3,5-triazine corticotropin releasing factor receptor-1 (CRF(1)) recep
245 cyclic imidazo[4,5-b]pyridin-2-ones as human corticotropin-releasing factor receptor (CRF(1)) antagon
246 ss, the physiological consequence of central corticotropin-releasing factor receptor (CRF-R) activati
247 viously reported differential involvement of corticotropin-releasing factor receptor (CRFR) 1 and 2 i
250 In addition, we examined the role of the corticotropin-releasing factor receptor 1 (CRF(1)) in th
251 We aimed to characterize the effects of the corticotropin-releasing factor receptor 1 (CRF-R1) antag
252 noradrenergic (NE) receptors (alpha1) via a corticotropin-releasing factor receptor 1 (CRF-R1)-depen
253 rial evaluating the efficacy of GSK561679, a corticotropin-releasing factor receptor 1 (CRF1 receptor
257 Similarly to what has been observed for the corticotropin-releasing factor receptor 1 (CRFR1), SAP97
258 me proliferator-activated receptor gamma and corticotropin-releasing factor receptor 1 were notable e
259 ecifically activated by either neurokinin I, corticotropin-releasing factor receptor 1, or dopamine D
261 mutants with constitutive activation of the corticotropin-releasing factor receptor family homologue
262 d, we took the CRF(2(a))R and the homologous corticotropin-releasing factor receptor type 1 (CRF(1)R)
263 esent study investigated whether blockade of corticotropin-releasing factor receptor type 1 (CRF-R1)
264 n reflect reductions in anandamide driven by corticotropin-releasing factor receptor type 1 (CRF1) po
265 we investigated interactions of the class B corticotropin-releasing factor receptor type 1 (CRF1R) w
267 ular membrane compartments, we show that the corticotropin-releasing factor receptor type 1 has a spe
268 ure of the transmembrane domain of the human corticotropin-releasing factor receptor type 1 in comple
272 vation of the central stress response, while corticotropin-releasing factor receptor type 2 (CRFR2) h
273 eviously, we observed abnormal expression of corticotropin-releasing factor receptor type 2 (CRFR2) t
275 ing affinity of 4-anilinopyrimidines against corticotropin-releasing factor receptor-1 (CRF(1)) (e.g.
277 n in the BNST is unaffected by alpha1-AR and corticotropin-releasing factor receptor-1 (CRFR(1)) anta
278 Effects on attention were attenuated by the corticotropin-releasing factor receptor-1 antagonist ant
283 ry-adrenal axis), (4) the (gastrointestinal) corticotropin-releasing factor system, and (5) the intes
286 ess effect by counteracting the functions of corticotropin-releasing factor, the primary stress-media
287 peptides (ghrelin, nesfatin-1, somatostatin, corticotropin-releasing factor, thyrotropin-releasing ho
289 This hypothesis was investigated for the corticotropin-releasing factor type 1 (CRF(1)) receptor
290 A, alpha(1b) adrenergic (alpha(1b) ADR), and corticotropin-releasing factor type 1 (CRF-R1) and 2 (CR
291 hich oxytocin (OTR), vasopressin (V1aR), and corticotropin-releasing factor type 1 (CRF1) or type 2 r
293 icated that repeated social stress decreased corticotropin-releasing factor type 1 receptor and incre
295 disrupts this LTCC-based mechanism; instead, corticotropin-releasing factor type 1 receptors (CRF1s)
296 disrupts this LTCC-based mechanism; instead, corticotropin-releasing factor type 1 receptors (CRF1s)
297 re sensitive to central anorectic effects of corticotropin-releasing factor type 2 (CRF(2)) receptor
299 demonstrated that the mechanism involved the corticotropin-releasing factor type 2 receptor, cAMP ele
300 n the amygdala, which required activation of corticotropin-releasing factor type-1 (CRF-R1) receptors
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