Central Actions of Corticotropin-Releasing Hormone (CRH) on Behavioral, Neuroendocrine, and Cardiovascular Regulation: Brain Corticoid Receptor Involvement

Korte, S. Mechiel; Bouws, G.A.H.; Bohus, B.

doi:10.1006/hbeh.1993.1013

Cited by 71 publications

(33 citation statements)

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“…To the best of our knowledge, the present studies are the first to specifically characterize and quantify the burying response to i.c.v. CRF administration, though this response has been previously reported in mice (Litvin et al 2007) and rats (Korte et al 1993;Price et al 1998;Wiersma et al 1995) and could only be seen if bedding material were present. Although the burying response evoked by CRF appeared almost identical to behaviors directed towards the electrified probe in the defensive burying response, the occurrence of burying in the absence of a specific aversive stimulus made the behavior appear spontaneous as reported following muscimol injected into the nucleus accumbens (Reynolds and Berridge, 2001).…”

Section: Characterization Of Crf-evoked Behaviorsmentioning

confidence: 75%

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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Section: Characterization Of Crf-evoked Behaviorsmentioning

confidence: 75%

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

et al. 2008

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“…Independent of its adrenocorticotropic properties, numerous studies on the effects of intracerebroventricular (ICV) CRH injections reveal overall increases in blood pressure, heart rate (Brown & Fisher, 1985 (Brown, 1986;Brown et al, 1982), as well as increases in emotionality, fear, and behavioural activity (Cole & Koob, 1991;Diamant & De Wied, 1991;Dunn & Berridge, 1990;Koob et al, 1992;Korte et al, 1993;Morley & Levine, 1982;Thatcher-Britton et al, 1986), and decreases in feeding behaviour in different species (Bray, 1992;Dunn & Berridge, 1990;Glowa & Gold, 1991;Gosnell et al, 1983;Morley & Levine, 1982Morley et al, 1985). Despite these numerous studies, the exact anatomical sites responsible for the CRH (ICV)-induced actions are less understood.…”

Section: Corticotropin-releasing Hormone (Crh)mentioning

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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“…Os (17). Este efeito não é observado após administração sistêmica (parenteral) de CRH, e não é mitigado pela hipofisectomia ou por supressão do eixo HHA com glicocorticóides (18).…”

Section: Receptores Do Crhunclassified

Antagonistas do hormônio liberador da corticotrofina: atualização e perspectivas

Ayala¹

2002

Arq Bras Endocrinol Metab

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RESUMOModelos genéticos e estudos epidemiológicos têm contribuído para a compreensão da fisiopatologia das doenças relacionadas ao estresse. O hormônio liberador da corticotrofina (CRH) pertence à família dos chamados peptídeos relacionados ao CRH, junto com a urocortina, urocortina II (ou peptídeo relacionado à estressecopina) e urocortina III (ou estressecopina). O CRH é o maior estimulador da secreção hipofisária de ACTH em humanos, e tem um papel importante na resposta fisiológica ao estresse. O CRH e seus receptores (tipos 1 e 2) estão difusamente distribuí -dos em todo o sistema nervoso central (SNC) e, em menor proporção, em tecidos periféricos. A distribuição dos receptores no SNC mostra ampla variabilidade entre as espécies. Os neurônios do CRH modulam a função autonômica e do sistema límbico. O CRH tem importantes efeitos, também, nos sistemas cardiovascular, metabólico e comportamental. As ações regionais deste peptídeo no SNC e na periferia são vários e apenas parcialmente conhecidos. Ações aberrantes do CRH estão implicadas em algumas condições psiquiátricas, incluindo depressão e ansiedade. Esta teoria tem sido corroborada por dados em ratos transgênicos que não expressam CRH e estudos pré-clínicos envolvendo a administração de antagonistas do CRH em macacos Rhesus. Embora ainda não disponível para uso clínico de rotina, dados preliminares de estudos conceituais envolvendo a administração oral de antagonistas do CRH em humanos são encorajadores. Entretanto, ainda permanece um desafio o desenvolvimento de antagonistas não peptídicos seletivos do receptor de CRH. Além disso, são extremamente necessários testes com estudos clíni -cos randomizados, que deverão trazer novas luzes sobre esta área. Genetic models and epidemiological studies have contributed to our understanding of the pathophysiology of stress-related disorders. Corticotropin-releasing hormone (CRH) belongs to the family of the so-called CRH related peptides along with Urocortin, Urocortin II (or Stresscopin Related Peptide) and Urocortin III (or Stresscopin). CRH is the major stimulus for pituitary ACTH secretion in humans and plays a major role in the physiologic response to stress. CRH and its receptors (type 1 and 2) are widely distributed throughout the central nervous system and to a lesser extent in peripheral tissues. The receptor distribution in the CNS exhibits a wide inter-species variability. The CRH neurons modulate autonomic and limbic system function. CRH affects a wide array of cardiovascular, metabolic and behavioral effects. The regional actions of this peptide in the CNS and in the periphery are varied and only partially understood. Aberrant CRH action is implicated in psychiatric disorders including depression and anxiety. Data from transgenic mice lacking over expressing CRH and pre-clinical studies involving CRH antagonist administration to Rhesus monkeys have substantiated this theory.Although not yet available for routine clinical use, preliminary proofs of concept studies revisão

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Central Actions of Corticotropin-Releasing Hormone (CRH) on Behavioral, Neuroendocrine, and Cardiovascular Regulation: Brain Corticoid Receptor Involvement

Cited by 71 publications

References 0 publications

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

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

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

Antagonistas do hormônio liberador da corticotrofina: atualização e perspectivas

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