Rat Corticotropin-Releasing Hormone Gene: Sequence and Tissue-Specific Expression*

Thompson, Robert C.; Seasholtz, Audrey F.; Herbert, Edward

doi:10.1210/mend-1-5-363

Cited by 209 publications

(91 citation statements)

References 33 publications

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“…TRH mRNA was localized to rat pituitary somatotropes (Bruhn 1994a,b,c) and TRH of pituitary origin can modulate both the secretion of TSH and the biosynthesis of pituitary TRH respectively (Bruhn et al 1998). Similarly, CRF mRNA was localized to the corticotropes in the rat pituitary (Thompson 1987, Giraldi & Cavagnini 1998 and there is evidence for the regulation of ACTH secretion by CRF of pituitary origin (Giraldi & Cavagnini 1998).…”

Section: Discussionmentioning

confidence: 99%

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Manzon¹,

Denver²

2004

Journal of Endocrinology

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Several hypotheses have been proposed to explain the increase and sustained expression of pituitary thyrotropin (TSH) in the presence of elevated plasma thyroid hormone (TH) concentrations at metamorphic climax in amphibians. It has been proposed that the negative feedback of TH on TSH is inoperative until metamorphic climax, and that it is established at this time by the upregulation of pituitary deiodinase type II (DII); DII converts thyroxine (T 4 ) to 3,5,3 -triiodothyronine (T 3 ). However, earlier investigators, using indirect measures of TSH, reported that TH negative feedback on TSH was functional in premetamorphic tadpoles. In an effort to understand pituitary TSH regulation during amphibian metamorphosis, we analyzed multiple pituitary genes known or hypothesized to be involved in TSH regulation in tadpoles of Xenopus laevis. Tadpole pituitary explant cultures were used to examine direct negative feedback on TSH mRNA expression. Negative feedback is operative in the early prometamorphic tadpole pituitary and both T 3 and T 4 can downregulate TSH mRNA expression throughout metamorphosis. The expression of both DII and TH receptor A mRNAs increased during development and peaked at climax; however, these increases coincided with similar increases in deiodinase type III, which inactivates TH. Moreover, corticotropin-releasing factor (CRF) receptors, CRF binding protein and thyrotropin-releasing hormone receptor type 2 mRNA expression also peaked at climax. Our data suggest that the regulation of TSH is more complex than the timing of DII expression, and likely involves a balance between stimulation of TSH synthesis and secretion by neuropeptides (e.g. CRF) of hypothalamic or pituitary origin, increased pituitary sensitivity to neuropeptides through upregulation of their receptors, and intrapituitary TH levels.

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Section: Discussionmentioning

confidence: 99%

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Manzon¹,

Denver²

2004

Journal of Endocrinology

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“…In situ hybridization histochemistry for CRF was performed on sections from both experiments 1 and 2 using a 48-mer cDNA oligoprobe corresponding to amino acids 22-37 of preprocorticotropin-releasing hormone (Thompson et al, 1987). In situ hybridization for AVP was performed on sections from experiment 2 using a 27-mer (AVP) directed against amino acids 110 -118 of rat prepropressophysin (Schmale et al, 1983).…”

Section: Methodsmentioning

confidence: 99%

Chronic Social Stress Alters Levels of Corticotropin-Releasing Factor and Arginine Vasopressin mRNA in Rat Brain

et al. 1997

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In the visible burrow system model of chronic social stress, male rats housed in mixed-sex groups quickly form a dominance hierarchy in which the subordinates appear to be severely stressed. A subgroup of subordinates have an impaired corticosterone response after presentation of a novel restraint stressor, leading to their designation as nonresponsive subordinates. To examine the mechanism underlying the blunted corticosterone response in these animals, in situ hybridization histochemistry was used to quantify corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) mRNA expression in the brain. In two separate visible burrow system experiments, the nonresponsive subordinates expressed a significantly lower average number of CRF mRNA grains per cell in the paraventricular hypothalamic nucleus compared with stress-responsive subordinates, dominants (DOM), or cage-housed control (CON) rats. The number of CRF mRNA labeled cells was also significantly lower in nonresponders than in responsive subordinates or DOM. In the central amygdala, CRF mRNA levels were increased in both groups of subordinates compared with CON rats, whereas responsive subordinates exhibited higher levels than the DOM rats as well. AVP mRNA levels did not vary with behavioral rank in any subdivision of the paraventricular hypothalamic nucleus. In the medial amygdala, the number of cells expressing AVP mRNA was significantly greater in CON rats compared with both groups of subordinates, although the average number of AVP mRNA grains per cell did not vary with rank. In addition, the number of AVP-positive cells significantly correlated with plasma testosterone level.

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“…Briefly, the CRF transgene was composed of the complete coding sequence of rat CRF cDNA (0.6 kb fragment; Thompson et al, 1987), which was inserted into a 8.2 kb genomic DNA fragment encompassing the murine Thy-1.2 gene, including regulatory regions and polyadenylation signal sequence (Aigner et al, 1995). The Thy-1 regulatory sequences drive constitutive transgene expression in postnatal and adult neurons (Morris and Grosveld, 1989;Vidal et al, 1990;Moechars et al, 1996;Lüthi et al, 1997;Wiessner et al, 1999).…”

Section: Animalsmentioning

confidence: 99%

Reversal of Startle Gating Deficits in Transgenic Mice Overexpressing Corticotropin-Releasing Factor by Antipsychotic Drugs

Dirks

Groenink

Westphal

et al. 2003

Neuropsychopharmacol

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Chronically elevated levels of corticotropin-releasing factor (CRF) in transgenic mice overexpressing CRF in the brain (CRF-OE) appear to be associated with alterations commonly associated with major depressive disorder, as well as with sensorimotor gating deficits commonly associated with schizophrenia. In the present study, we tested the hypothesis that antipsychotics may be effective in normalizing prepulse inhibition (PPI) of acoustic startle in CRF-OE mice, which display impaired sensorimotor gating compared to wildtype (WT) mice. The typical antipsychotic haloperidol and atypical antipsychotic risperidone improved PPI in the CRF-OE mice, but were ineffective in WT mice. The atypical antipsychotic clozapine did not influence PPI in CRF-OE mice, but reduced gating in WT mice. This effect of clozapine in the CRF-OE mice may thus be regarded as a relative improvement, consistent with the observed effect of haloperidol and risperidone. As expected, the anxiolytic, nonantipsychotic chlordiazepoxide was devoid of any effect. All four compounds dose-dependently reduced the acoustic startle response irrespective of genotype. These results indicate that antipsychotic drugs are effective in improving startle gating deficits in the CRF-OE mice. Hence, the CRF-OE mouse model may represent an animal model for certain aspects of psychotic depression, and could be a valuable tool for research addressing the impact of chronically elevated levels of CRF on information processing.

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Rat Corticotropin-Releasing Hormone Gene: Sequence and Tissue-Specific Expression*

Cited by 209 publications

References 33 publications

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Chronic Social Stress Alters Levels of Corticotropin-Releasing Factor and Arginine Vasopressin mRNA in Rat Brain

Reversal of Startle Gating Deficits in Transgenic Mice Overexpressing Corticotropin-Releasing Factor by Antipsychotic Drugs

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