Effect of corticotropin releasing factor receptor 1 antagonist on extracellular norepinephrine, dopamine and serotonin in hippocampus and prefrontal cortex of rats in vivo

Isogawa, Koichi; Akiyoshi, Jotaro; Hikichi, Takatoshi; Yamamoto, Yoshiyuki; Tsutsumi, Takashi; Nagayama, Haruo

doi:10.1054/npep.2000.0806

Cited by 37 publications

(27 citation statements)

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“…infusion of CRF, Ucn1 or Ucn2 14,22,48,69 is effective at increasing immediate-early gene expression within caudal regions of the DRN. In addition, several stress paradigms, CRF and its related peptides and the use of CRFR1 antagonists cause different changes in levels of 5-HT and 5-HIAA in the terminal regions, [70][71][72][73][74][75][76] underscoring the role of CRF and CRFrelated peptides in the regulation of extracellular 5-HT levels under basal and stress conditions.…”

Section: Discussionmentioning

confidence: 99%

Urocortin-1 and -2 double-deficient mice show robust anxiolytic phenotype and modified serotonergic activity in anxiety circuits

et al. 2009

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The urocortin (Ucn) family of neuropeptides is suggested to be involved in homeostatic coping mechanisms of the central stress response through the activation of corticotropin-releasing factor receptor type 2 (CRFR2). The neuropeptides, Ucn1 and Ucn2, serve as endogenous ligands for the CRFR2, which is highly expressed by the dorsal raphe serotonergic neurons and is suggested to be involved in regulating major component of the central stress response. Here, we describe genetically modified mice in which both Ucn1 and Ucn2 are developmentally deleted. The double knockout mice showed a robust anxiolytic phenotype and altered hypothalamic-pituitary-adrenal axis activity compared with wild-type mice. The significant reduction in anxiety-like behavior observed in these mice was further enhanced after exposure to acute stress, and was correlated with the levels of serotonin and 5-hydroxyindoleacetic acid measured in brain regions associated with anxiety circuits. Thus, we propose that the Ucn/ CRFR2 serotonergic system has an important role in regulating homeostatic equilibrium under challenge conditions.

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Section: Discussionmentioning

confidence: 99%

Urocortin-1 and -2 double-deficient mice show robust anxiolytic phenotype and modified serotonergic activity in anxiety circuits

et al. 2009

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“…The amount of serotonergic tone influences HPA axis activity (Isogawa et al 2000). Therefore, we also characterized hormonal responses in subjects expressing either the long or short form of a functional polymorphism within the serotonin transporter gene.…”

Section: Discussionmentioning

confidence: 99%

“…Because the Asn40Asp substitution alters receptor binding and signal transduction, it is plausible that this polymorphism alters processes under opioidergic regulation (LaForge et al 2000a,b). The CRF neuron is also modulated by serotonergic fibers (Contesse et al 2000;Isogawa et al 2000). As opposed to ␤ -endorphin, which inhibits CRF secretion, serotonin activates the CRF neuron and stimulates CRF release.…”

Section: An A118g Nucleotide Exchange In Exon 1 Of the Mu-opioid Recementioning

confidence: 99%

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The Mu-Opioid Receptor Gene Polymorphism (A118G) Alters HPA Axis Activation Induced by Opioid Receptor Blockade

Wand

2002

Neuropsychopharmacology

230

166

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An A118G nucleotide exchange in exon 1 of the mu-opioid receptor causes an Asn40Asp substitution polymorphism in the receptor's extracellular domain. In vitro studies show that the Asp40 variant of the mu-opioid receptor binds ␤ -endorphin three times more avidly than the more commonStress threatens homeostasis and is counteracted by a series of physiological and behavioral responses that improve the chances for survival. A successful response to stress plays an important role in maintaining health and well-being. Abnormalities in the stress response heighten an individual's vulnerability to endocrine, metabolic, psychiatric, and immunological disorders (Kreek and Koob 1998; Bjorntorp and Rosmond 2000a,b;Chrousos 2000). The unique characteristics of an individual's stress response are the product of genetic and environmental determinants (Francis et al. 1999;Wust et al. 2000).Corticotropin releasing factor (CRF) neurons within the paraventricular nucleus of the hypothalamus initiate activation of the hypothalamic-pituitary-adrenal (HPA) axis (Bell et al. 1998 (Wand et al. 1998). Recently, a common A118G nucleotide exchange in exon 1 of the muopioid receptor has been identified that causes an Asn40Asp substitution polymorphism in the extracellular N-terminal domain of the mu-opioid receptor (Bergen et al. 1997;Wendel and Hoehe 1998). In vitro studies show that the Asp40 variant of the mu-opioid receptor binds ␤ -endorphin three times more avidly than the common Asn40 variant and also induces a 3-fold increase in agonist-induced activation of G protein-coupled potassium channels (Bond et al. 1998). Because the Asn40Asp substitution alters receptor binding and signal transduction, it is plausible that this polymorphism alters processes under opioidergic regulation (LaForge et al. 2000a,b). The CRF neuron is also modulated by serotonergic fibers (Contesse et al. 2000;Isogawa et al. 2000). As opposed to ␤ -endorphin, which inhibits CRF secretion, serotonin activates the CRF neuron and stimulates CRF release. The serotonin transporter regulates the concentration of serotonin within the synaptic cleft and thereby modulates magnitude and duration of serotonin-induced postsynaptic mediated signals (Lesch and Mossner 1998). Recently a functional polymorphism has been described in the promoter region of the transporter, which modulates transcriptional activity of this gene as well as tissue expression of transporter activity (Hanna et al. 1998;Heils et al. 1997;Little et al. 1998). Like the A118G polymorphism in the mu-opioid receptor, it is plausible that this functional polymorphism within the serotonin transporter is associated with altered HPA axis dynamics.The present study was designed to test whether the Asn40Asp substitution polymorphism in the mu-opioid receptor or a functional mutation in the polymorphic region of serotonin transporter influences HPA axis activation induced by opioid receptor blockade. METHODS SubjectsHealthy men were recruited by newspaper from the Baltimore area. Respondents gave informed conse...

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“…Evocation of anxiety responses by CRF infusion is accompanied by concomitant changes in forebrain 5-HT (Kagamiishi et al 2003) and NE transmission. Moreover, stress-induced alterations in extracellular 5-HT and NE are blocked by pretreatment with CRF receptor antagonists (Isogawa et al 2000;Price et al 1998). Taken together, these findings suggest that CRF can play a critical role in affective and anxiety disorders through its actions on 5-HT and NE systems associated with anxiety and depression.…”

Section: Introductionmentioning

confidence: 99%

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

et al. 2008

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Rationale-Central administration of corticotropin-releasing factor (CRF) elicits a specific pattern of behavioral responses resembling a stress-like state, and is anxiogenic in rodent models of anxiety.Objectives-Specific behaviors evoked by the administration of CRF were measured. The roles of CRF receptor subtypes and that of serotonergic and noradrenergic systems in mediating these responses were studied.Methods-Burying, grooming and head shakes were quantified in rats following intracerebroventricular administration of CRF and urocortin II and after pretreatment with antagonists. The role of forebrain norepinephrine in the behavioral responses to CRF (0.3 μg) was examined following pretreatment with the neurotoxin DSP-4 and that of serotonin after depletion using systemic administration of para-chlorophenylalanine (p-CPA).Results-CRF at 0.3 and 3.0 μg caused robust increases in burying, grooming and head shakes, but urocortin II was ineffective. Pretreatment with either antalarmin or propranolol significantly attenuated the CRF-evoked behaviors. Destruction of forebrain NE pathways blocked spontaneous burying behavior elicited by CRF and conditioned burying directed towards an electrified shock probe. In contrast, depletion of 5-HT selectively attenuated CRF-evoked grooming.Conclusions-Overt behavioral responses produced by CRF, burying, grooming, and head shakes, appeared to be mediated through the CRF 1 receptor. Spontaneous burying behavior evoked by CRF or conditioned burying directed towards a shock probe were disrupted by lesion of the dorsal noradrenergic bundle and may represent anxiety-like behavior caused by CRF activation of the LC. In contrast, CRF-evoked increases in grooming were dependent on serotonin.

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Effect of corticotropin releasing factor receptor 1 antagonist on extracellular norepinephrine, dopamine and serotonin in hippocampus and prefrontal cortex of rats in vivo

Cited by 37 publications

References 27 publications

Urocortin-1 and -2 double-deficient mice show robust anxiolytic phenotype and modified serotonergic activity in anxiety circuits

Urocortin-1 and -2 double-deficient mice show robust anxiolytic phenotype and modified serotonergic activity in anxiety circuits

The Mu-Opioid Receptor Gene Polymorphism (A118G) Alters HPA Axis Activation Induced by Opioid Receptor Blockade

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

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