Effect of centrally administered corticotropin releasing factor (CRF) on multiple feeding paradigms

Levine, Allen S.; Rogers, Bernetta; Kneip, J.; Grace, Martha K.; Morley, John E.

doi:10.1016/0028-3908(83)90249-6

Cited by 140 publications

(35 citation statements)

References 18 publications

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“…CRH given ICV is known to influence metabolism by eliciting an increase in plasma concentration of glucagon and glucose and a decrease in plasma insulin levels (Brown, 1986;Brown et al, 1982), which in turn results in a decrease in feeding behaviour (Bray, 1992;Dunn & Berridge, 1990;Glowa & Gold, 1991;Gosnell et al, 1983;Levine et al, 1983;Morley & Levine, 1982Morley et al, 1985). On the other hand, ICV injection of the CRH receptor antagonist partially reversed the CRH-or stress-induced anorexic effects.…”

Section: Discussionmentioning

confidence: 99%

Behavioural activation produced by crh but not α-helical CRH (CRH-receptor antagonist) when microinfused into the central nucleus of the amygdala under stress-free conditions

Wiersma

Baauw

Bohus

et al. 1995

Psychoneuroendocrinology

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SUMMARYThe central nucleus of the amygdala (CeA) is known to be involved in the regulation of autonomic, neuroendocrine, and behavioural responses in stress situations. The CeA contains large numbers of corticotropin-releasing hormone (CRH)-containing cell bodies and terminals. In the present study we examined (by continuous behaviour observations) the effects of a high close of CRH (150 rig) and two doses of the CRH-receptor antagonist (a-hCRH: 1.0 and 0.1 p,g) after microinfusion into the CeA in freely moving male Wistar rats under stress-flee conditions. In comparison with control, a-hCRH infusion did not cause any behavioural activation. In contrast CRH-infusion revealed a long-lasting increase in grooming and exploration with a concomitant decrease in behaviours specified as resting. These results indicate that the CRH system in the CeA does not seem to be activated in stress-free conditions, but its activation is of importance for active behavioural responses.Keywords--Central nucleus of the amygdala (CeA); Stress-free conditions; Corticotropin-releasing hormone (CRH); a-Helical CRH (CRH-receptor antagonist).

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Section: Discussionmentioning

confidence: 99%

Behavioural activation produced by crh but not α-helical CRH (CRH-receptor antagonist) when microinfused into the central nucleus of the amygdala under stress-free conditions

Wiersma

Baauw

Bohus

et al. 1995

Psychoneuroendocrinology

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“…CRF is widely distributed in the brain and has been identified in a number of hypothalamic centres known to function in the control of energy balance (Brown et al 1982). CRF given intracerebroventricularly (icv), either acutely or chronically, suppresses food intake (Levine et al 1983; Arase et al 1988), enhances sympathetic activity (Brown & Fisher, 1985;Arase et al 1988) and depresses parasympathetic activity (Tache & Gunion, 1985). A lack of CRF function would provide an attractive hypothesis to explain the defects in a number of obese models and the restoration of normal energetic efficiency and BAT function after adrenalectomy.…”

Section: Corticosteroid Inhibition Of Thennogenesis In Obese Animalsmentioning

confidence: 99%

Corticosteroid inhibition of thermogenesis in obese animals

York

1989

Proc. Nutr. Soc.

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“…A number ofthese limbic system-mediated responses can be mimicked by central administration of CRF. Intracerebroventricular injection of CRF in rat, dog, and monkey results in behavioral changes and activation of the hypothalamic-pituitary-adrenal axis (1,4,31,32) and the sympathetic nervous system with the subsequent visceral and metabolic responses (1,(32)(33)(34)(35). In chair-restrained monkeys, administration of CRF into the brain causes an increase in arousal consistent with limbic activation (31 (41).…”

Section: Methodsmentioning

confidence: 99%

Distribution of corticotropin-releasing factor receptors in primate brain.

Millán¹,

Jacobowitz²,

Hauger³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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The distribution and properties of receptors for corticotropin-releasing factor (CRF) were analyzed in the brain of cynomolgus monkeys. Binding of [125I]tyrosine-labeled ovine CRF to frontal cortex and amygdala membrane-rich fractions was saturable, specific, and time-and temperaturedependent, reaching equilibrium in 30 min at 23TC. Scatchard analysis of the binding data indicated one class of high-affinity sites with a Kd of 1 nM and a concentration of 125 fmol/mg (,30% of the receptor number in monkey anterior pituitary membranes). As in the rat pituitary and brain, CRF receptors in monkey cerebral cortex and amygdala were coupled to adenylate cyclase. Autoradiographic analysis of specific CRF binding in brain sections revealed that the receptors were widely distributed in the cerebral cortex and limbic system. Receptor density was highest in the pars tuberalis of the pituitary and throughout the cerebral cortex, specifically in the prefrontal, frontal, orbital, cingulate, insular, and temporal areas, and in the cerebellar cortex. A very high binding density was also present in the hippocampus, mainly in the dentate gyrus, and in the arcuate nucleus and nucleus tuberis lateralis. A high binding density was present in the amygdaloid complex and mammary bodies, olfactory tubercle, and medial portion of the dorsomedial nucleus of the thalamus. A moderate binding density was found in the nucleus accumbens, claustrum, caudate-putamen, paraventricular and posterior lateral nuclei of the thalamus, inferior colliculus, and dorsal parabrachial nucleus. A low binding density was present in the superior colliculus, locus coeruleus, substantia gelatinosa, preoptic area, septal area, and bed nucleus of the stria terminalis. These data demonstrate that receptors for CRF are present within the primate brain at areas related to the central control of visceral function and behavior, suggesting that brain CRF may serve as a neurotransmitter in the coordination of endocrine and neural mechanisms involved in the response to stress.In addition to its role as a major regulator of corticotropin (ACTH) release from the anterior pituitary (1), corticotropinreleasing factor (CRF) also exerts direct actions within the central nervous system in several animal species. Intracerebroventricular administration of CRF in experimental animals results in altered behavior and activates the hypothalamic-pituitary adrenal axis and the sympathetic nervous system, similar to the changes observed during stress (1-4). Immunoreactive CRF has been found in several extrahypothalamic sites in the brain, including many parts of the limbic system and centers known to control the autonomic nervous system (1, 5-7). These findings suggest that the peptide acts as a neurotransmitter in the brain to modulate the integrated responses to stress. This view is supported by the demonstration that CRF receptors are present in the rat brain, with a distribution corresponding to the components of the limbic system and cerebral cortex (8). There is evidence indic...

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Effect of centrally administered corticotropin releasing factor (CRF) on multiple feeding paradigms

Cited by 140 publications

References 18 publications

Behavioural activation produced by crh but not α-helical CRH (CRH-receptor antagonist) when microinfused into the central nucleus of the amygdala under stress-free conditions

Behavioural activation produced by crh but not α-helical CRH (CRH-receptor antagonist) when microinfused into the central nucleus of the amygdala under stress-free conditions

Corticosteroid inhibition of thermogenesis in obese animals

Distribution of corticotropin-releasing factor receptors in primate brain.

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