Corticotropin-Releasing Factor Receptors in Rat Forebrain: Autoradiographic Identification

Souza, EB De; Perrin, Marilyn H.; Tr, Insel; Rivier, Jean; Vale, W.; Kuhar, MJ

doi:10.1126/science.6328656

Cited by 196 publications

(62 citation statements)

References 34 publications

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“…Post et al, 1981;Charney et al, 1993), such effects might be amplified by stress-induced kindling of various limbic areas, including the amygdala and BNST. The amygdala and BNST show particularly dense concentrations of CRH cell bodies and receptors (Cummings et al, 1983;De Souza et al, 1984;Sawchenko and Swanson, 1985;Sakanaka et al, 1987;Chalmers et al, 1995;Lovenberg et al, 1995), and chronic stress increased CRH mRNA in the CeA and BNST (Mamalaki et al, 1992;Makino et al, 1994aMakino et al, ,b, 1995. Taken together, these data raise the possibility that stress may sensitize CRH systems in limbic structures, such as the amygdala and/or BNST, leading to a persistent increase in CRH transmission.…”

Section: Discussionmentioning

confidence: 99%

“…Canteras and Swanson, 1992;Cullinan et al, 1993;Amaral and Witter, 1995). Furthermore, both the ventral hippocampus and the BNST contain a moderate amount of CRH receptors (De Souza et al, 1984;Chalmers et al, 1995;Sawchenko and Swanson, 1985). Therefore, it is conceivable that CRH given intracerebroventricularly primarily binds to the ventral hippocampus and modulates startle amplitude via hippocampal-BNST connections.…”

Section: Abstract: Bed Nucleus Of the Stria Terminalis (Bnst ); Amygmentioning

confidence: 99%

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Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

1997

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Previously, we demonstrated that transection of the fimbria/ fornix blocked the excitatory effect of corticotropin-releasing hormone (CRH) on startle (CRH-enhanced startle), suggesting that the hippocampus and its efferent target areas that communicate via the fimbria may be critically involved in CRHenhanced startle. The bed nucleus of the stria terminalis (BNST) receives direct projections from the ventral hippocampus via the fimbria/fornix. Therefore, the role of the ventral hippocampus, the BNST, and the amygdala in CRH-enhanced startle was investigated. NMDA lesions of the BNST completely blocked CRH-enhanced startle, whereas chemical lesions of the ventral hippocampus and the amygdala failed to block CRH-enhanced startle. However, the same amygdala-lesioned animals showed a complete blockade of fear-potentiated startle, a conditioned fear response sensitive to manipulations of the amygdala. In contrast, BNST-lesioned rats had normal fear-potentiated startle. This indicates a double dissociation between the BNST and the amygdala in two different paradigms that enhance startle amplitude. Microinfusions of CRH into the BNST, but not into the ventral hippocampus, mimicked intracerebroventricular CRH effects. Furthermore, infusion of a CRH antagonist into the BNST blocked CRH-enhanced startle in a dose-dependent manner. Control studies showed that this blockade did not result from either leakage of the antagonist into the ventricular system or a local anesthetic effect caused by infusion of the antagonist into the BNST. The present studies strongly suggest that CRH in the CSF can activate the BNST, which could lead to activation of brainstem and hypothalamic BNST target areas involved in anxiety and stress responses. Key words: bed nucleus of the stria terminalis (BNST ); amygdala; hippocampus; corticotropin-releasing hormone (CRH); startle; anxiety; fearIntracerebroventricular inf usion of corticotropin-releasing hormone (CRH) elicits a constellation of behavioral, physiological, and endocrinological changes similar to those produced by natural stressors (cf. Dunn and Berridge, 1990). Thus far, however, the exact anatomical sites responsible for these behavioral and physiological actions of CRH after intracerebroventricular administration have not been identified. As part of an effort to delineate the neural circuitry underlying intracerebroventricular CRH effects, recently we investigated a possible involvement of the septum, using increased acoustic startle amplitude after CRH (CRH-enhanced startle) as a behavioral measure (Lee and Davis, 1997). Electrolytic lesions of the whole septum and the medial septum, but not the lateral septum, blocked CRH-enhanced startle. However, fiber-sparing chemical lesions of the medial septum failed to block CRH-enhanced startle, suggesting that the blockade seen with electrolytic lesions was probably caused by damage to fibers of passage, presumably the fornix. Supporting this conclusion, f unctional lesions of the fornix induced by knife cuts of the fimbria /fornix complete...

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Section: Discussionmentioning

confidence: 99%

Section: Abstract: Bed Nucleus Of the Stria Terminalis (Bnst ); Amygmentioning

confidence: 99%

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

1997

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“…Developmental regulation of stress-related [8,20] and other effects of CRH have been demonstrated [1,3]. Autoradiography and radioligand binding studies during early postnatal life in the rat have demonstrated changes in receptor number and regional distribution [5,6,11,12,15]. The two methods have yielded conflicting information regarding CRH receptor distribution in a number of brain regions [12,16,17].…”

Section: Introductionmentioning

confidence: 99%

Developmental profile of messenger RNA for the corticotropin-releasing hormone receptor in the rat limbic system

Avishai-Eliner

Baram

1996

Developmental Brain Research

101

110

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The ontogeny of corticotropin-releasing hormone (CRH) receptor messenger ribonucleic acid (mRNA) in rat brain, using in situ hybridization, is the focus of this study. The developmental profile of CRH receptor using binding assays and receptor autoradiography has been reported, but may be confounded by the presence of a binding protein. The recent cloning of the rat CRH receptor gene has permitted the use of in situ hybridization histochemistry to map the distribution of cells expressing CRH receptor mRNA in the developing brain. We used antisense 35 S-labeled oligodeoxynucleotide probes for the two reported splice-variants of the CRH receptor mRNA, which yielded essentially identical localization patterns. CRH receptor mRNA was clearly detectable in infant brain starting on the second postnatal day. Signal in hippocampal CA1, CA2 and CA3a increased to 300-600% of adult levels by postnatal day 6 with a subsequent gradual decline. In the amygdala, in contrast, CRH receptor mRNA abundance increased steadily between the second and the ninth postnatal days, to levels twice higher than those in the adult. In the cortex, CRH receptor mRNA levels were high on postnatal day 2 and decreased to adult levels by day 12. Transient signal over the hypothalamic paraventricular nucleus, observed on the second postnatal day, was not evident at older ages. These results demonstrate robust synthesis of CRH receptor as early as on the second postnatal day and unique region-specific developmental profiles for CRH receptor gene expression.

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“…Attempts to characterise the CRH receptor began shortly after the discovery of ovine CRH (Vale et al 1981). High-affinity CRH-binding sites were subsequently established in rat and human pituitary glands and brains (Wynn et al 1983, DeSouza et al 1984, as well as in the corticotroph cell line AtT20 (Rosendale et al 1987). Moreover, this receptor was shown to be associated with a cAMP-dependent signal transduction system A model for the CRH peptide and receptor co-evolution in chordates.…”

Section: Corticotrophinmentioning

confidence: 99%

MOLECULAR EVOLUTION OF GPCRS: CRH/CRH receptors

Lovejoy¹,

Chang²,

Lovejoy³

et al. 2014

Journal of Molecular Endocrinology

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Corticotrophin-releasing hormone (CRH) is the pivotal neuroendocrine peptide hormone associated with the regulation of the stress response in vertebrates. However, CRH-like peptides are also found in a number of invertebrate species. The origin of this peptide can be traced to a common ancestor of lineages leading to chordates and to arthropods, postulated to occur some 500 million years ago. Evidence indicates the presence of a single CRH-like receptor and a soluble binding protein system that acted to transduce and regulate the actions of the early CRH peptide. In vertebrates, genome duplications led to the divergence of CRH receptors into CRH1 and CRH2 forms in tandem with the development of four paralogous ligand lineages that included CRH; urotensin I/urocortin (Ucn), Ucn2 and Ucn3. In addition, taxon-specific genome duplications led to further local divergences in CRH ligands and receptors. Functionally, the CRH ligand-receptor system evolved initially as a molecular system to integrate early diuresis and nutrient acquisition. As multicellular organisms evolved into more complex forms, this ligand-receptor system became integrated with the organismal stress response to coordinate homoeostatic challenges with internal energy usage. In vertebrates, CRH and the CRH1 receptor became associated with the hypothalamo-pituitary-adrenal/interrenal axis and the initial stress response, whereas the CRH2 receptor was selected to play a greater role in diuresis, nutrient acquisition and the latter aspects of the stress response.

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Corticotropin-Releasing Factor Receptors in Rat Forebrain: Autoradiographic Identification

Cited by 196 publications

References 34 publications

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

Developmental profile of messenger RNA for the corticotropin-releasing hormone receptor in the rat limbic system

MOLECULAR EVOLUTION OF GPCRS: CRH/CRH receptors

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