Effect of corticotropin-releasing factor antagonist on behavioral and neuroendocrine responses during exposure to defensive burying paradigm in rats

Korte, S.M.; Korte-Bouws, G.A.H.; Bohus, B.; Koob, George F.

doi:10.1016/0031-9384(94)90268-2

Cited by 60 publications

(34 citation statements)

References 27 publications

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“…The CRF receptor antagonist also significantly decreased total time spent burying the probe [F(3,28)ϭ8.0, p Ͻ .0005], with the 20 mg/kg dose producing a significant (Schéffe test, p Ͻ .005) decline relative to vehicle-treated controls (Table 2). Such results are consistent with those produced by central administration of a peptide CRF receptor antagonist in this paradigm (Korte et al 1994).…”

Section: Resultssupporting

confidence: 80%

Brain Penetrance, Receptor Occupancy and Antistress In Vivo Efficacy of a Small Molecule Corticotropin Releasing Factor Type I Receptor Selective Antagonist

Heinrichs

Souza

Schulteis

et al. 2002

Neuropsychopharmacology

143

112

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The widely distributed brain corticotropin-releasing factor Type 1 (CRF 1 ) receptor has been strongly implicated in the increased emotionality accompanying exposure to environmental stressors (Steckler and Holsboer 1999). First, exogenous administration of a mixed CRF receptor agonist such as CRF or urocortin in testing models of anxiety produces anxiogenic-like behavior and potentiates the effects of stressor exposure (Koob and Heinrichs 1999;Moreau et al. 1997). Second, limbic and brain stem regions thought to subserve arousal and fear-like behaviors are enriched with CRF 1 receptors (Chalmers et al.

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Section: Resultssupporting

confidence: 80%

Brain Penetrance, Receptor Occupancy and Antistress In Vivo Efficacy of a Small Molecule Corticotropin Releasing Factor Type I Receptor Selective Antagonist

Heinrichs

Souza

Schulteis

et al. 2002

Neuropsychopharmacology

143

112

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“…Intracerebroventricular (icv) administration of corticotropin-releasing factor (CRF) is anxiogenic and potentiates the acoustic startle (Swerdlow et al, 1986), and icv administration of CRF receptor antagonist can suppress both light-enhanced startle (de Jongh et al, 2003) and indices of anxiety (Korte et al, 1994;Koob and Heinrichs, 1999), suggesting that CRF is involved in both light-enhanced startle and anxiety. It has been demonstrated (Walker and Davis, 2006) that light-enhanced startle is mediated by the bed nucleus of the stria terminalis, which also mediates anxiety and CRF-enhanced startle Walker and Davis, 1997b).…”

Section: Discussionmentioning

confidence: 99%

Acoustic startle amplitude predicts vulnerability to develop post-traumatic stress hyper-responsivity and associated plasma corticosterone changes in rats

Rasmussen

Crites

Burke

2008

Psychoneuroendocrinology

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SummaryFollowing exposure to trauma, a vulnerable sub-population of individuals develop post-traumatic stress disorder (PTSD) with characteristic persistent autonomic hyper-responsivity, associated increased startle response, and commonly altered hypothalamo-pituitary-adrenal regulation. A goal of this investigation was to identify a predictive marker for this vulnerability. Previous investigators have developed a model for PTSD in which male mice were exposed to a single brief episode of inescapable footshock followed by one-minute contextual reminders of this trauma at weekly intervals for six weeks. Exposure to these reminders induced a progressive and persistent increase in the amplitude of acoustic startle consistent with the persistently increased acoustic startle of individuals exhibiting PTSD. We adapted this model to adult male Wistar rats, with added characterization of initial (pre-trauma) startle response. After one episode of inescapable footshock (10 second, 2 mA) or control treatment followed by six weekly one-minute contextual reminders, acoustic startle was re-tested. Data were analyzed after dividing rats within each treatment into LOW vs MID vs HIGH (33% in each group) pre-treatment startle responders. Rats which exhibited pretreatment LOW-and MID-range acoustic startle responses did not develop increased acoustic startle responses following subsequent traumatic stress + reminders ([TS+R]) treatment. However, rats which exhibited HIGH pre-treatment startle responses exhibited further significant (p<0.01) [TS+R]-induced persistent enhancement of this already elevated startle response. Furthermore, rats exhibiting HIGH pre-treatment startle responses were also the only subgroup which exhibited increased basal plasma corticosterone levels following [TS+R] treatment. These results suggest that initial pre-stress acoustic startle response can identify subgroups of rats which are predisposed to, or resistant to, developing a PTSD-like syndrome following subsequent trauma.

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“…No differences in the latency to contact the probe were observed between DSP-4-treated and control animals, indicating that the attenuation of burying was not due to an overall decrease in locomotion or exploratory activity. CRF administration has been shown to increase probe burying, while this behavior was blocked by CRF antagonists (Basso et al 1999;Diamant et al 1992;Korte et al 1994). Furthermore, shock-probe burying is accompanied by increases in NE transmission (Bondi et al 2007;Korte et al 1992) and attenuated by pretreatment with noradrenergic antagonists (Morilak et al 2005).…”

Section: Burying Behavior Is Mediated By Forebrain Nementioning

confidence: 99%

“…and site-specific administration of CRF mimics behavioral responses to stressful stimuli (Campbell et al 2004;Liang et al 1992) and produces anxiogenic effects in a number of behavioral tests of anxiety (Dunn and File 1987;Zorrilla et al 2002). Furthermore, CRF receptor antagonists are effective in blocking many of the behavioral effects of CRF, and reverse the suppression and activation of behaviors observed in response to stress (Basso et al 1999;Heinrichs et al 1992;Korte et al 1994;Takahashi 2001;Zorrilla et al 2002). Clinical findings have also implicated increased central CRF drive in the etiology of anxiety and affective disorders and suggest significant potential for CRF receptor antagonists in the treatment of anxiety disorders (Nemeroff 2004;Zobel et al 2000).…”

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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Effect of corticotropin-releasing factor antagonist on behavioral and neuroendocrine responses during exposure to defensive burying paradigm in rats

Cited by 60 publications

References 27 publications

Brain Penetrance, Receptor Occupancy and Antistress In Vivo Efficacy of a Small Molecule Corticotropin Releasing Factor Type I Receptor Selective Antagonist

Brain Penetrance, Receptor Occupancy and Antistress In Vivo Efficacy of a Small Molecule Corticotropin Releasing Factor Type I Receptor Selective Antagonist

Acoustic startle amplitude predicts vulnerability to develop post-traumatic stress hyper-responsivity and associated plasma corticosterone changes in rats

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

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