The CRF peptide family and their receptors: yet more partners discovered

Dautzenberg, Frank M.; Hauger, Richard L.

doi:10.1016/s0165-6147(02)01946-6

Cited by 498 publications

(413 citation statements)

References 58 publications

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“…Thus, CRF given centrally induces anxiogenic behaviors in various animal models, such as open field (Britton et al, 1982;Liang and Lee, 1988;Takahashi et al, 1989), EPM (Baldwin et al, 1991), conflict test (Britton et al, 1985), social interaction (SI) (Dunn and File, 1987), acoustic startle (Swerdlow et al, 1986;Liang et al, 1992), and conditioned fear response (Cole and Koob, 1988). So far, two CRF receptor subtypes, CRF 1 and CRF 2 , have been identified (De Souza et al, 1985;Chalmers et al, 1995;Perrin and Vale, 1999;Dautzenberg and Hauger, 2002). CRF 1 is widely distributed throughout central nervous system, whereas CRF 2 has more restricted distribution, primarily to subcortical regions (Chalmers et al, 1995;Van Pett et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

Lee

Fitz

Johnson

et al. 2008

Neuropsychopharmacol

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Increased extra-hypothalamic corticotrophin-releasing factor (CRF) neurotransmission has been suggested as one putative factor in the pathophysiology of anxiety disorders. We have previously reported that administering repeated subanxiogenic doses (termed 'priming') of the CRF receptor agonist urocortin 1 (Ucn1) into the basolateral amygdala (BLA) of rats elicited long-lasting behavioral changes in social interaction (SI) and elevated plus maze (EPM) tests of anxiety. Although substantial similarity exists, the bed nucleus of the stria terminals (BNST) and the amygdala are thought to play distinct roles in anxiety responses. Rats primed with Ucn1 in the BLA not only demonstrated increased anxiety-like behaviors, but also physiological sensitivity to intravenous sodium lactate infusions, which is seen in subjects with panic or posttraumatic stress disorders, but not social or generalized anxiety disorders. In the present study, we tested if similar priming with subanxiogenic doses of Ucn1 in the BNST of rats will induce either chronic anxiety or sensitivity to sodium lactate. After determining the dose of Ucn1 that is subanxiogenic when injected into the BNST, repeated intra-BNST injections of this subanxiogenic dose of Ucn1 (6 fmol/100 nl) elicited persistent (present even after 4 weeks) anxiety-like responses in the SI but not EPM test. Prior local injection of a CRF receptor antagonist, astressin, into the BNST blocked this effect. Unlike Ucn1 priming in the BLA, rats primed in the BNST showed no cardiovascular changes following lactate infusion. Thus, BNST priming appears to selectively model the pathophysiology of subjects with anxiety syndromes like social anxiety, which are not lactate sensitive.

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Section: Introductionmentioning

confidence: 99%

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

Lee

Fitz

Johnson

et al. 2008

Neuropsychopharmacol

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“…Both CRH and CRH-related neuropeptides exert their influence on CRH 1 and CRH 2 (Lovenberg et al, 1995;Van Pett et al, 2000;Dautzenberg and Hauger, 2002). CRH is relatively selective for the CRH 1 receptor with moderate affinity to the CRH 2 receptor (Timpl et al, 1998) whereas Ucn1 has high affinity to both CRH 1 and CRH 2 receptors (Timpl et al, 1998), but relatively greater affinity for CRH 2 receptors Reyes et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Mouse strain differences in the effects of corticotropin releasing hormone (CRH) on sleep and wakefulness

et al. 2008

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Corticotropin releasing hormone (CRH) plays a major role in central nervous system responses to stressors and has been implicated in stress-induced alterations in sleep. In the absence of stressors, CRH contributes to the regulation of spontaneous waking. We examined the effects of CRH and astressin (AST), a non-specific CRH antagonist, on wakefulness and sleep in two mouse strains with differential responsiveness to stress to determine whether CRH might also differentially affect undisturbed sleep and activity. Less reactive C57BL/6J (n=7) and high reactive BALB/cJ (n=7) male mice were implanted with a transmitter for determining sleep via telemetry and with a guide cannula aimed into a lateral ventricle. After recovery from surgery and habituation to handling, ICV microinjections of CRH (0.04, 0.2, and 0.4 μg), AST (0.1, 0.4, and 1.0 μg) or vehicle alone (pyrogenfree saline, 0.2 μl) were administered during the fourth h after lights on and sleep was recorded for the subsequent 8 h. Comparisons of wakefulness and sleep were conducted across conditions and across strains. In C57BL/6J mice, REM was significantly decreased after microinjections of CRH (0.2 μg) and CRH (0.4 μg), and NREM and total sleep were decreased after microinjections of CRH (0.4 μg ). CRH (0.4 μg) and AST did not significantly change wakefulness or sleep. In BALB/cJ mice, CRH (0.4 μg) increased wakefulness and decreased NREM, REM and total sleep. AST decreased active wakefulness and significantly increased REM at the low and high dosages. These findings demonstrate that CRH produces changes in arousal when given to otherwise undisturbed mice. Strain differences in the effects of CRH and AST may be linked to the relative responsiveness of C57BL/6J and BALB/cJ mice to stressors and to underlying differences in the CRH system.

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“…Duas variantes dos rCRH têm sido descritas nos animais vertebrados, nos peixes e nos anfíbios: O rCRH-1 e o rCRH-2 (11,12). Ambos pertencem ao grupo dos receptores de membrana, acoplados à proteína G. O rCRH-1 e o rCRH-2 apresentam 70% de homologia estrutural.…”

Section: Receptores Do Crhunclassified

“…Ambos pertencem ao grupo dos receptores de membrana, acoplados à proteína G. O rCRH-1 e o rCRH-2 apresentam 70% de homologia estrutural. A distribuição anatômica destes receptores é heterogênea, e varia consideravelmente entre as espécies (11,13). O rCRH-1 predomina no SNC, enquanto que os rCRH-2, na periferia.…”

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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The CRF peptide family and their receptors: yet more partners discovered

Cited by 498 publications

References 58 publications

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

Mouse strain differences in the effects of corticotropin releasing hormone (CRH) on sleep and wakefulness

Antagonistas do hormônio liberador da corticotrofina: atualização e perspectivas

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