Involvement of cAMP‐Response Element Binding Protein in Corticotropin‐Releasing Factor (CRF)‐Induced Down‐Regulation of CRF Receptor 1 Gene Expression in Rat Anterior Pituitary Cells

Kasagi, Yoko; Horiba, Nobuo; Sakai, Ken; Fukuda, Yoshiko; Suda, Toshio

doi:10.1046/j.1365-2826.2002.00816.x

Cited by 27 publications

(14 citation statements)

References 42 publications

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“…During chronic opiate exposure, an increase in cellular adenosine 3′,5′-monophosphate (cAMP) activities is a celluar measure to counter the inhibition of cAMP by opiates [50]. Therefore, the downregulation of CRF-R1 mRNA expression during morphine withdrawal is also a postulated homeostatic adaptation to counteract the overactivation of cAMP [51]. In addition, we also showed here that mitragynine significantly lowered the mRNA levels of both CRF-R1 and CRF-R2 in morphine-withdrawn fish, a trend that correlates with the attenuation of both anxiety behavior and whole cortisol production.…”

Section: Discussionmentioning

confidence: 99%

Mitragynine Attenuates Withdrawal Syndrome in Morphine-Withdrawn Zebrafish

et al. 2011

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A major obstacle in treating drug addiction is the severity of opiate withdrawal syndrome, which can lead to unwanted relapse. Mitragynine is the major alkaloid compound found in leaves of Mitragyna speciosa, a plant widely used by opiate addicts to mitigate the harshness of drug withdrawal. A series of experiments was conducted to investigate the effect of mitragynine on anxiety behavior, cortisol level and expression of stress pathway related genes in zebrafish undergoing morphine withdrawal phase. Adult zebrafish were subjected to two weeks chronic morphine exposure at 1.5 mg/L, followed by withdrawal for 24 hours prior to tests. Using the novel tank diving tests, we first showed that morphine-withdrawn zebrafish display anxiety-related swimming behaviors such as decreased exploratory behavior and increased erratic movement. Morphine withdrawal also elevated whole-body cortisol levels, which confirms the phenotypic stress-like behaviors. Exposing morphine-withdrawn fish to mitragynine however attenuates majority of the stress-related swimming behaviors and concomitantly lower whole-body cortisol level. Using real-time PCR gene expression analysis, we also showed that mitragynine reduces the mRNA expression of corticotropin releasing factor receptors and prodynorphin in zebrafish brain during morphine withdrawal phase, revealing for the first time a possible link between mitragynine's ability to attenuate anxiety during opiate withdrawal with the stress-related corticotropin pathway.

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Section: Discussionmentioning

confidence: 99%

Mitragynine Attenuates Withdrawal Syndrome in Morphine-Withdrawn Zebrafish

et al. 2011

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“…The CRF R1 is coupled to the stimulatory G protein Gα s and can thus activate PKA and subsequently CREB (Kasagi et al , 2002). We found that treatment with a CRF R1 antagonist before stress exposure blocked the ability of FS to lead to increased levels of pCREB within a discrete set of brain regions.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, CRF receptor type 1 (CRF R1 ) mediates neuroendocrine and behavioral responses to stress as well as to drugs of abuse. The activation of CRF R1 stimulates the G protein G αs , leading to the activation of Protein Kinase A, and the transcription factor CREB (Kasagi, et al , 2002; Mcevoy, et al , 2002). As chronic stress has been shown to increase pCREB expression (Kwon, et al , 2006), examining the role of CRF R1 activation in the ability of FS to induce phosphorylation of CREB could help delineate the signaling pathways underlying stress-induced augmentation of cocaine reward.…”

Section: Introductionmentioning

confidence: 99%

Stress-Induced Potentiation of Cocaine Reward: A Role for CRFR1 and CREB

Kreibich

Briand

Cleck

et al. 2009

Neuropsychopharmacol

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Both clinical and preclinical research have shown that stress can potentiate drug use, however the underlying mechanisms of this interaction are unknown. Previously, we have shown that a single exposure to forced swim (FS) reinstates extinguished conditioned place preference (CPP) to cocaine and that cAMP response element binding protein (CREB) is necessary for this response. CREB can be activated by corticotropin releasing factor (CRF) receptor type 1 (CRFR1) binding, which mediates neuroendocrine and behavioral responses to stress as well as to drugs of abuse. The present experiments investigate whether changes in cocaine reward elicited by previous exposure to stress are mediated by CREB and/or CRFR1. Chronic exposure to FS in advance of conditioning enhances the acquisition of cocaine CPP in wildtype mice but this is blocked in CREB deficient mice. In addition, pretreatment with the CRFR1 antagonist, antalarmin, prior to FS exposure blocks the enhancement of stress induced acquisition of cocaine CPP. Furthermore, FS induced increase in phosphorylated CREB (pCREB), specifically in the nucleus accumbens (NAc) and the lateral septum (LS) is also blocked by antalarmin. Taken together, these studies suggest that both CREB and CRFR1 activation are necessary for stress-induced potentiation of drug reward.

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“…The perisynaptic and subsynaptic distributions of CRFr labeling at excitatory synapses suggests that the activation of the CRF receptors affects excitatory postsynaptic currents. This modulation may reflect, in part, the activation of cAMP response element-binding protein (CREB; Kasagi et al, 2002). In other limbic brain regions, CREB is actively involved in the regulation of the expression of AMPA GluR1 subunits that are essential for AMPA receptor-mediated glutamatergic transmission (Olson et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Electron microscopic localization of corticotropin‐releasing factor (CRF) and CRF receptor in rat and mouse central nucleus of the amygdala

Treweek

Jaferi

Colago

et al. 2008

J of Comparative Neurology

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Corticotrophin-releasing factor (CRF) is expressed in the central nucleus of the amygdala (CeA), where the CRF receptor (CRFr) plays an important role in anxiety-and stress-related behaviors. To determine the subcellular sites of CRFr activation in this region, we examined the electron microscopic immunolabeling of antisera recognizing CRF or CRFr. The ultrastructural analysis was principally conducted in the lateral subdivision of the rat CeA, with comparisons being made in mice so as to optimally utilize mutant mice in control experiments. The CRFr labeling was seen in many small dendrites and dendritic spines as well as in a few somata, large dendrites, axons, and axon terminals or more rarely in glial processes. Approximately 35% of the CRFr-labeled dendrites contained CRF immunoreactivity, which was distributed diffusely throughout the cytoplasm, or specifically affiliated with either endomembranes or large dense-core vesicles. The CRFimmunoreactive vesicles also were present in somata and axon terminals with or without CRFr labeling. The CRF immunoreactivity was usually absent from both terminals and dendrites joined by asymmetric, excitatory-type synapses, where a postsynaptic location of the CRFr was commonly observed. Numerous terminals containing both CRF and CRFr were seen, however, within the neuropil and sometimes apposing the excitatory synapses. These results provide ultrastructural evidence for a primary involvement of CRF receptors in modulation of the postsynaptic excitability of CeA neurons, an effect that may be limited by the availability of CRF. The findings have important implications for understanding CRF mediation of rapid responses to stress. Indexing termsautoregulation; stress; autonomic; limbic; drug addictionThe central nucleus of the amygdala (CeA) and bed nucleus of the stria terminalis (BNST) are critical components of the glucocorticoid-sensitive extrahypothalamic circuit involved in fear and anxiety as well as stress and addictive disorders (Gray and Bingaman, 1996;Aston-Jones et al., 1999;Curtis et al., 2002;Cook, 2004;Santibanez et al., 2005). Both regions contain neurons that express CRF (Swanson et al., 1983;Bale and Vale, 2004;Asan et al., 2005), and have extensive bidirectional connections with each other (Erb et al., 2001). The CRFcontaining neurons are mainly located in the CeA lateral subdivision (CeL) that 1) receives substantial input from midline thalamic nuclei implicated in arousal and attention (Li and Kirouac, 2008), and 2) projects extensively to hypothalamic and brainstem regions involved in neuroendocrine and autonomic responses (Veening et al., 1984;Moga and Gray, 1985 Sakanaka et al., 1986;Van Bockstaele et al., 1998;Wu et al., 1999;Curtis et al., 2002). The involvement of these neurons in drug addiction is strongly supported by the marked elevation of CRF peptide and mRNA in the CeA of rats receiving chronic morphine or cocaine administration (Maj et al., 2003;Erb et al., 2005;Wang et al., 2006). In addition, there is accumulating evidence for CRF-...

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Involvement of cAMP‐Response Element Binding Protein in Corticotropin‐Releasing Factor (CRF)‐Induced Down‐Regulation of CRF Receptor 1 Gene Expression in Rat Anterior Pituitary Cells

Cited by 27 publications

References 42 publications

Mitragynine Attenuates Withdrawal Syndrome in Morphine-Withdrawn Zebrafish

Mitragynine Attenuates Withdrawal Syndrome in Morphine-Withdrawn Zebrafish

Stress-Induced Potentiation of Cocaine Reward: A Role for CRFR1 and CREB

Electron microscopic localization of corticotropin‐releasing factor (CRF) and CRF receptor in rat and mouse central nucleus of the amygdala

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