Increase in cortical and midbrain tryptophan hydroxylase activity by intracerebroventricular administration of corticotropin releasing factor: block by adrenalectomy, by RU 38486 and by bilateral lesions to the central nucleus of the amygdala

Singh, Virendra; Hao-Phan, Tam; Corley, Karl C.; Boadle-Biber, Margaret C.

doi:10.1016/0197-0186(92)90129-f

Cited by 36 publications

(18 citation statements)

References 58 publications

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“…We have found that acute intracerebroventricular administration of CRH profoundly increases hippocampal extracellular 5-HT and 5-HIAA levels (A. C. E. Linthorst and J. M. H. M. Reul, unpublished observations), presumably via receptors located on raphe neurons and /or on neurons projecting to the raphe-hippocampal system (Chalmers et al, 1995(Chalmers et al, , 1996. These effects are in line with reports showing changes in midbrain tryptophan hydroxylase activity after acute intracerebroventricular CRH administration (Singh et al, 1992). Given that the microdialysis experiments presented here were performed on day 7 of CRH treatment, the absence of a difference in baseline 5-HT and 5-HIAA strongly suggests pertinent regulatory changes in 5-HT metabolism as a result of the chronic CRH treatment.…”

Section: Discussionsupporting

confidence: 79%

Long-Term Intracerebroventricular Infusion of Corticotropin-Releasing Hormone Alters Neuroendocrine, Neurochemical, Autonomic, Behavioral, and Cytokine Responses to a Systemic Inflammatory Challenge

et al. 1997

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Corticotropin-releasing hormone (CRH) was infused intracerebroventricularly into rats for 7 d via a miniosmotic pump (1 g ⅐ l Ϫ1 ⅐ hr Ϫ1 ). Body temperature and locomotor activity were recorded during the treatment using biotelemetry, whereas hippocampal serotonergic neurotransmission and free corticosterone levels were monitored using in vivo microdialysis on day 7 of CRH treatment. During the microdialysis experiment, behavioral activity was scored by assessing the time during which rats were active (locomotion, grooming, eating, drinking). Continuous intracerebroventricular infusion of CRH produced a transient increase in body temperature and locomotion. Moreover, intracerebroventricularly CRH-treated rats showed elevated free corticosterone levels with no apparent diurnal rhythm.Intraperitoneal administration of bacterial endotoxin [lipopolysaccharide (LPS); 100 g/kg body weight] on day 7 of CRH/ vehicle treatment produced a marked fever response in control animals, which was significantly blunted in intracerebroventricularly CRH-treated rats. Although free corticosterone levels reached similar peak concentrations in both intracerebroventricularly vehicle-and CRH-infused groups after LPS, this response was delayed significantly by ϳ1 hr in the intracerebroventricularly CRH-treated animals. Microdialysis experiments showed no changes in basal extracellular levels of serotonin and 5-hydroxyindoleacetic acid in intracerebroventricularly CRHinfused animals. Injection of LPS in intracerebroventricularly CRHtreated rats produced a blunted 5-HT response and a delayed onset of behavioral inhibition and other signs of sickness behavior. Assessment of the endotoxin-induced cytokine responses showed significantly enhanced plasma interleukin-1 (IL-1) and IL-6 bioactivities in the intracerebroventricularly CRH-infused animals 3 hr after injection of LPS, whereas tumor necrosis factor bioactivity responses were not different.Our data demonstrate that chronically elevated brain CRH levels produce marked changes in basal (largely CRH regulated) physiological and behavioral processes accompanied by aberrant responses to an acute challenge. The present study provides evidence that chronic CRH hypersecretion is an important factor in the etiology of stress-related disorders.

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Section: Discussionsupporting

confidence: 79%

Long-Term Intracerebroventricular Infusion of Corticotropin-Releasing Hormone Alters Neuroendocrine, Neurochemical, Autonomic, Behavioral, and Cytokine Responses to a Systemic Inflammatory Challenge

et al. 1997

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“…Similarly, tissue levels of 5-HT or its catabolite 5-hydroxyindoleacetic acid (5-HIAA) were unaltered by CRF (Dunn and Berridge 1987). In contrast, CRF increased activity of tryptophan hydroxylase, the rate-limiting enzyme in the synthesis of 5-HT, in cortex and midbrain (Singh et al 1991), and 5-HIAA levels, measured by microdialysis, in hypothalamus and prefrontal cortex (Lavicky and Dunn 1993). Each of these studies used relatively indirect measures of 5-HT activity.…”

Section: The Serotonergic Dorsal Raphe Nucleus Is Innervated By Cortimentioning

confidence: 99%

Effects of Corticotropin-Releasing Factor on Brain Serotonergic Activity

Price

Curtis

Kirby

et al. 1998

Neuropsychopharmacology

200

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The serotonergic dorsal raphe nucleus is innervated by corticotropin-releasing factor (CRF) and expresses CRF receptors, suggesting that endogenous CRF impacts on this system. The present study characterized interactions between CRF and the dorsal raphe serotonin (5-HT) system. The effects of intracerebroventricularly (i.c.v.) administered CRF on microdialysate concentrations of 5-HT in the lateralCorticotropin-releasing factor (CRF) is the hypothalamic neurohormone that initiates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary during stress (Vale et al. 1981). In addition, CRF is thought to function as a brain neurotransmitter that interacts with other neurotransmitter systems to coordinate autonomic and behavioral components of the stress response (Dunn and Berridge 1990;Owens and Nemeroff 1991;Valentino et al. 1993). This is supported by anatomical studies that have identified a widespread distribution of CRF-immunoreactive neurons and fibers outside of the hypothalamic-pituitary axis in brain regions that are not directly involved with endocrine responses to stress (Sakanaka et al. 1987;Swanson et al. 1983). This distribution far exceeds that required for CRF-evoked release of ACTH. Consistent with this widespread distribution of CRF-immunoreactive terminals, CRF receptor binding sites and CRF receptor mRNA are localized in diverse brain regions that are unrelated to their pituitary actions (Chalmers et al. 1995;De Souza 1987;Potter et al. 1994).Among the brain regions that are both innervated by CRF-immunoreactive fibers (Sakanaka et al. 1987;Swanson et al. 1983) and that contain mRNA for CRF receptors (Chalmers et al. 1995;Potter et al. 1994) are the dorsal and median raphe nuclei, the source nuclei of forebrain serotonergic innervation (Azmitia and Segal 1978;Kellar et al. 1977;Vertes 1991 dence for an impact of stress on forebrain 5-HT (Chaouloff 1993;De Souza and Van Loon 1986;Dunn 1988;Morgan et al. 1975;Pol et al. 1992;Tanaka et al. 1983), these anatomical findings lead to the speculation that CRF release within the raphe nucleus may mediate the effects of stress on this system. Nonetheless, there are few reports of the effects of CRF on measures of 5-HT function, and these have yielded equivocal results. For example, relatively high doses of CRF failed to alter levels of the 5-HT precursor, 5-hydroxytryptophan (Van Loon et al. 1982). Similarly, tissue levels of 5-HT or its catabolite 5-hydroxyindoleacetic acid (5-HIAA) were unaltered by CRF (Dunn and Berridge 1987). In contrast, CRF increased activity of tryptophan hydroxylase, the rate-limiting enzyme in the synthesis of 5-HT, in cortex and midbrain (Singh et al. 1991), and 5-HIAA levels, measured by microdialysis, in hypothalamus and prefrontal cortex (Lavicky and Dunn 1993). Each of these studies used relatively indirect measures of 5-HT activity. A recent study, using in vivo microdialysis to measure extracellular 5-HT levels in the hippocampus of freely-moving rats, found no change after long term administration of ...

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“…infusion of very high doses of CRF (30 pglkg). Also, Singh et al (1992) found that a high dose of CRF (3 pg) injected into the rat amygdala stimulated tryptophan hydroxylase activity assayed in vitro. However, Boadle-Biber (personal communication) failed to find any effect of CRF on 5-HIAA.…”

Section: Figmentioning

confidence: 99%

Corticotropin‐Releasing Factor Stimulates Catecholamine Release in Hypothalamus and Prefrontal Cortex in Freely Moving Rats as Assessed by Microdialysis

Lavický¹,

Dunn²

1993

Journal of Neurochemistry

167

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Abstract:In vivo microdialysis was used to measure changes in extracellular concentrations of catecholamines and indoleamines in freely moving rats in response to administration of corticotropin-releasing factor (CRF). Dialysis probes were placed stereotaxically in either the medial hypothalamus or the medial prefrontal cortex. We used a repeated-measures design in which each rat received artificial CSF or one dose of C R F 3-4 h apart, and each subject was retested with the same treatments in the reverse order 5-7 days later. With the dialysis probe in the hypothalamus, intracerebroventricular administration of C R F (17 or 330 pmol) dose-dependently increased dialysate concentrations of norepinephrine (NE), dopamine (DA), and all their measurable catabolites except normetanephrine. The effects on NE were substantially greater than those on DA. Dialysate concentrations of serotonin could not be measured reliably, but those of its catabolite, 5-hydroxyindoleacetic acid, were also elevated. Concentrations of NE and DA were elevated within the first one or two (20 min) collection periods, with a peak response at -1-2 h. Dialysate concentrations of catecholamines and metabolites normally returned to baseline within 3 h. Similar data were obtained with dialysis probes in the medial prefrontal cortex after intracerebroventricular administration of 17 or 167 pmol of CRF, except that the increases in DA exceeded those of NE in this region. lntraperitoneal administration ofCRF (1 nmol) similarly elevated dialysate concentrations of NE, DA, 5-hydroxyindoleacetic acid, and all catecholamine catabolites except normetanephrine in both medial hypothalamus and medial prefrontal cortex. These results support earlier neurochemical data suggesting that C R F administered both centrally and peripherally stimulates the release of both DA and NE in the brain.

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Increase in cortical and midbrain tryptophan hydroxylase activity by intracerebroventricular administration of corticotropin releasing factor: block by adrenalectomy, by RU 38486 and by bilateral lesions to the central nucleus of the amygdala

Cited by 36 publications

References 58 publications

Long-Term Intracerebroventricular Infusion of Corticotropin-Releasing Hormone Alters Neuroendocrine, Neurochemical, Autonomic, Behavioral, and Cytokine Responses to a Systemic Inflammatory Challenge

Long-Term Intracerebroventricular Infusion of Corticotropin-Releasing Hormone Alters Neuroendocrine, Neurochemical, Autonomic, Behavioral, and Cytokine Responses to a Systemic Inflammatory Challenge

Effects of Corticotropin-Releasing Factor on Brain Serotonergic Activity

Corticotropin‐Releasing Factor Stimulates Catecholamine Release in Hypothalamus and Prefrontal Cortex in Freely Moving Rats as Assessed by Microdialysis

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