A role for corticotropin releasing factor and urocortin in behavioral responses to stressors

Koob, George F.; Heinrichs, Stephen C.

doi:10.1016/s0006-8993(99)01991-5

Cited by 499 publications

(334 citation statements)

References 109 publications

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“…There might also be a physiological pathway, in which low social participation and isolation may influence health and coronary heart disease, e.g. acute myocardial infarction, by increasing psychological stress which in turn activates the hypothalamic-pituitaryadrenocortical (HPA) axis by the release of corticotropic-releasing factor (CRF) from neuronal cell bodies of the paraventricular nucleus (Dallman 1993), which ultimately cause the release of cortisol (McEwen et al 1993;Koob et al 1993). Increasing the production of cortisol, stress causes various sympathetic changes, including increased blood pressure, heart rate (HR), and catecholamine production (Cacioppo 1994;Christensen 1994) and, ultimately, heart disease.…”

Section: Discussionmentioning

confidence: 99%

Social capital, the miniaturisation of community, traditionalism and first time acute myocardial infarction: A prospective cohort study in southern Sweden

Ali

Merlo

Rosvall

et al. 2006

Social Science & Medicine

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Section: Discussionmentioning

confidence: 99%

Social capital, the miniaturisation of community, traditionalism and first time acute myocardial infarction: A prospective cohort study in southern Sweden

Ali

Merlo

Rosvall

et al. 2006

Social Science & Medicine

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“…These same central CRF systems are well documented to contribute to behavioral responses to stressors Koob and Heinrichs, 1999). When injected intracerebroventricularly, CRF is aversive and produces place aversions (Cador et al, 1992) and taste aversions (Heinrichs et al, 1991) and raises brain stimulation reward thresholds (Macey et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Buprenorphine and a CRF1 Antagonist Block the Acquisition of Opiate Withdrawal-Induced Conditioned Place Aversion in Rats

Stinus

Cador

Zorrilla

et al. 2004

Neuropsychopharmacol

127

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Conditioned place aversion in rats has face validity as a measure of the aversive stimulus effects of opiate withdrawal that reflects an important motivational component of opiate dependence. The purpose of the present study was to validate conditioned place aversion as sensitive to medications that will alleviate the aversive stimulus effects of opiate withdrawal in humans, and to extend this model to the exploration of the neuropharmacological basis of the motivational effects of opiate withdrawal. Male Sprague-Dawley rats were implanted with two subcutaneous morphine pellets and 5 days later began place conditioning training following subcutaneous administration of a low dose of naloxone. Animals were subjected to three pairings of a low dose of naloxone (15 mg/kg, s.c.) to one arm of a three-chambered place conditioning apparatus. Buprenorphine administered prior to each pairing dose-dependently blocked the place aversion produced by precipitated opiate withdrawal. A corticotropin-releasing factor-1 (CRF 1 ) receptor antagonist (antalarmin) also reversed the place aversion produced by precipitated opiate withdrawal. Antalarmin did not produce a place preference or place aversion by itself in morphine-dependent rats. No effect was observed with pretreatment of the dopamine partial agonist terguride or the selective serotonin reuptake inhibitor fluoxetine. Also, chronic pretreatment with acamprosate (a glutamate receptor modulator used to prevent relapse in alcohol dependence) did not alter naloxone-induced place aversion. Buprenorphine by itself in dependent rats produced a mild place preference at low doses and a mild place aversion at higher doses. These results suggest that buprenorphine blocks the aversive stimulus effects of precipitated opiate withdrawal in rats and provides some validity for the use of place conditioning as a measure that is sensitive to potential opiate-dependence medications. In addition, these results suggest that CRF 1 antagonists can block the aversive stimulus effects of opiate withdrawal and may be potential therapeutic targets for opiate dependence.

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“…Given the multiple roles of CRF in the mediation of the stress response, it has been hypothesized that stress-related disorders may result from the exacerbated stimulation of one or more CRFregulated pathways (Koob and Heinrichs 1999;Owens and Nemeroff 1993;Risbrough and Stein 2006). In rats, intracerebroventricular (i.c.v.)…”

Section: Introductionmentioning

confidence: 99%

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

et al. 2008

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Rationale-Central administration of corticotropin-releasing factor (CRF) elicits a specific pattern of behavioral responses resembling a stress-like state, and is anxiogenic in rodent models of anxiety.Objectives-Specific behaviors evoked by the administration of CRF were measured. The roles of CRF receptor subtypes and that of serotonergic and noradrenergic systems in mediating these responses were studied.Methods-Burying, grooming and head shakes were quantified in rats following intracerebroventricular administration of CRF and urocortin II and after pretreatment with antagonists. The role of forebrain norepinephrine in the behavioral responses to CRF (0.3 μg) was examined following pretreatment with the neurotoxin DSP-4 and that of serotonin after depletion using systemic administration of para-chlorophenylalanine (p-CPA).Results-CRF at 0.3 and 3.0 μg caused robust increases in burying, grooming and head shakes, but urocortin II was ineffective. Pretreatment with either antalarmin or propranolol significantly attenuated the CRF-evoked behaviors. Destruction of forebrain NE pathways blocked spontaneous burying behavior elicited by CRF and conditioned burying directed towards an electrified shock probe. In contrast, depletion of 5-HT selectively attenuated CRF-evoked grooming.Conclusions-Overt behavioral responses produced by CRF, burying, grooming, and head shakes, appeared to be mediated through the CRF 1 receptor. Spontaneous burying behavior evoked by CRF or conditioned burying directed towards a shock probe were disrupted by lesion of the dorsal noradrenergic bundle and may represent anxiety-like behavior caused by CRF activation of the LC. In contrast, CRF-evoked increases in grooming were dependent on serotonin.

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A role for corticotropin releasing factor and urocortin in behavioral responses to stressors

Cited by 499 publications

References 109 publications

Social capital, the miniaturisation of community, traditionalism and first time acute myocardial infarction: A prospective cohort study in southern Sweden

Social capital, the miniaturisation of community, traditionalism and first time acute myocardial infarction: A prospective cohort study in southern Sweden

Buprenorphine and a CRF1 Antagonist Block the Acquisition of Opiate Withdrawal-Induced Conditioned Place Aversion in Rats

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

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