Corticotropin-releasing factor in posttraumatic stress disorder (PTSD) with secondary psychotic symptoms, nonpsychotic PTSD, and healthy control subjects

Sautter, Frederic J.; Bissette, Garth; Wiley, Justin; Manguno-Mire, Gina M.; Schoenbachler, Benjamin; Myers, Leann; Johnson, Janet Elise; Cerbone, Arleen; Malaspina, Dolores

doi:10.1016/s0006-3223(03)00571-7

Cited by 149 publications

(91 citation statements)

References 39 publications

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“…Although it could also be argued that PD subjects, who score higher on measures of stress reactivity such as neuroticism, are more sensitive than other subjects to the psychological stress of lumbar puncture. Mean CRF concentration in the PD group (39.9727.8 pg/ml) was comparable to those reported previously in clinical populations with depression (Carpenter et al, 2004), anxiety disorder (Fossey et al, 1996), acute alcohol withdrawal (Adinoff et al, 1996), schizophrenia (Nishino et al, 1998), in PTSD with and without psychosis (Sautter et al, 2003), and as measured by serial sampling in PTSD (Baker et al, 1999). It is of interest that CRF values in our normal controls (27.1713.2 pg/ml) are comparable to those reported by Carpenter et al (2004) (24.978.6 pg/ml).…”

Section: Discussionsupporting

confidence: 85%

CSF Corticotropin-Releasing Factor in Personality Disorder: Relationship with Self-Reported Parental Care

Lee

Gollan

Kasckow

et al. 2006

Neuropsychopharmacol

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This cross-sectional investigation tests the relationship between the level of self-reported childhood parental care and cerebrospinal fluid (CSF) corticotropin-releasing factor (CRF) concentration in adults with and without personality disorder (PD). Based on preclinical models of the lasting effect of post-natal parental care on central CRF function, the primary hypothesis was that childhood parental care, as reflected by the parental bonding inventory (PBI) care and involvement subscale, is inversely correlated with adult CSF CRF levels. The sample includes cerebrospinal fluid CRF samples from 19 subjects who were included in a previously published report on the relationship between CRF level and Childhood Trauma Questionnaire score. Parental bonding was measured retrospectively with the PBI in 54 medication-free male and female subjects, 37 of whom were diagnosed with a DSM-IV PD, 17 of whom were normal controls free of Axis I and II psychopathology. CSF CRF level as measured by lumbar puncture was entered into a model as the dependent variable, with the independent variables of PBI Parental Care and Involvement, diagnostic category, age, and gender. The model predicting CSF CRF level was significant, with PBI parental care and involvement negatively correlated with CSF CRF level. PD subjects with higher than median PBI parental care and involvement score had significantly lower CSF CRF levels than both normal controls and PD subjects with lower than median PBI parental care and involvement. Higher levels of self-report parental care predict lower CSF CRF levels in PD subjects, consistent with a beneficial effect of parental care on decreased stress reactivity, and consistent with previous reports in humans. The cross-sectional design of the study, however, limits causal inferences.

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Section: Discussionsupporting

confidence: 85%

CSF Corticotropin-Releasing Factor in Personality Disorder: Relationship with Self-Reported Parental Care

Lee

Gollan

Kasckow

et al. 2006

Neuropsychopharmacol

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“…Posttraumatic stress disorder (PTSD) patients have been shown to exhibit excess CRF CSF concentrations (Baker et al, 1999;Bremner et al, 1997;Sautter et al, 2003). The two initial studies of CRF hypersecretion yielded mixed results in terms of any associations with depression or anxiety symptoms.…”

Section: Anxietymentioning

confidence: 99%

“…They did find a significant negative correlation, however, between 24-hour urinaryfree cortisol excretion and PTSD symptoms. Sautter et al (2003) reported that CRF elevations were specifically linked to psychotic symptoms in PTSD patients and suggested that excess CRF release may be unique to a more severely affected subclass of PTSD patients. Although it is generally presumed that the observed CRF hypersecretion in PTSD patients occurs only after trauma, this assumption has yet to be tested.…”

Section: Anxietymentioning

confidence: 99%

“…This same group of researchers, in showing that the HPA response to a pharmacological agent in patients with panic disorder can be cognitively modulated, has suggested that HPA disturbances in panic disorder may be secondary to manipulable cognitive/emotional sensitivities (Abelson et al, 2005). Thus, the present consensus seems to be that the HPA axis abnormalities in panic disorder are subtle, reflecting altered responses to certain kinds of stress which, presumably, have as their origin differences in CRF secretion or altered CRF receptor signaling.Posttraumatic stress disorder (PTSD) patients have been shown to exhibit excess CRF CSF concentrations (Baker et al, 1999;Bremner et al, 1997;Sautter et al, 2003). The two initial studies of CRF hypersecretion yielded mixed results in terms of any associations with depression or anxiety symptoms.…”

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confidence: 99%

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Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

Risbrough

Stein

2006

Hormones and Behavior

211

139

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Anxiety disorders are a group of mental disorders that include generalized anxiety disorder (GAD), panic disorder, phobic disorders (e.g., specific phobias, agoraphobia, social phobia) and posttraumatic stress disorder (PTSD). Anxiety disorders are among the most common of all mental disorders and, when coupled with an awareness of the disability and reduced quality of life they convey, they must be recognized as a serious public health problem. Over 20 years of preclinical studies point to a role for the CRF system in anxiety and stress responses. Clinical studies have supported a model of CRF dysfunction in depression and more recently a potential contribution to specific anxiety disorders (i.e., panic disorder and PTSD). Much work remains in both the clinical and preclinical fields to inform models of CRF function and its contribution to anxiety. First, we will review the current findings of CRF and HPA axis abnormalities in anxiety disorders. Second, we will discuss startle reflex measures as a tool for translational research to determine the role of the CRF system in development and maintenance of clinical anxiety. KeywordsCRH; CRF; Posttraumatic stress disorder; Anxiety; Panic disorder; Startle Overview of CRF neuroendocrine effects and its effects on G-protein-coupled receptorsCorticotropin releasing factor (CRF; also termed "CRH" for corticotropin releasing hormone) was first described in Science by Vale et al. (1981). They reported the discovery of a hypothesized hypothalamic factor, CRF, a 41 amino acid peptide which selectively and potently activated pituitary corticotropin (or adrenal corticotropin releasing hormone, ACTH) secretion. They predicted that this peptide could be "a key signal in mediating and integrating an organism's endocrine, visceral and behavioral response to stress" (Vale et al., 1981(Vale et al., p. 1397). More than 20 years of subsequent animal research and clinical studies have confirmed this hypothesis, supporting a role for CRF, and its more recently discovered ligand family Urocortin 1, 2 and 3, in anxiety and stress responses Reyes et al., 2001;Spina et al., 1996). In this review, we will focus on the current state of knowledge of CRF system dysregulation in clinical anxiety and discuss future avenues of translational research on the role of CRF in startle phenotypes observed in some anxiety disorders. CRF mediation of the neuroendocrine response to stressIn response to stress, CRF is released from the median eminence of the hypothalamus, where it subsequently binds to receptors at the anterior pituitary and increases ACTH release into the * Corresponding author. 8950 Villa La Jolla Drive, Suite B-218, La Jolla, CA 92037, USA. E-mail address: mstein@ucsd.edu (M.B. Stein). bloodstream. ACTH consequently acts at the adrenal cortex to facilitate release of glucocorticoids such as cortisol. This system, known as the hypothalamic-pituitary-adrenal axis (HPA), is an important component of the response to stress and has been shown to be dysregulated in both anxiety and de...

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“…CRF is a neuropeptide that is released in the brain in response to stress (Koob, 1999). Administration of CRF produces many of the same physiological and behavioral effects as stress in people and laboratory animals (Hauger et al, 2009), and people with stress-related psychiatric illness have higher levels of CRF in cerebrospinal fluid (CSF) and blood (Bremner et al, 1997;Sautter et al, 2003;de Kloet et al, 2008). Although much is known about the neural mechanisms by which CRF regulates stress (Bangasser and Valentino, 2012), it has remained difficult to develop clinically effective antistress agents that act directly at CRF receptors (Zorrilla and Koob, 2010).…”

Section: Introductionmentioning

confidence: 99%

Corticotropin-Releasing Factor (CRF)-Induced Disruption of Attention in Rats Is Blocked by the κ-Opioid Receptor Antagonist JDTic

Veer

Yano

Carroll

et al. 2012

Neuropsychopharmacol

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Stress often disrupts behavior and can lead to psychiatric illness. Considerable evidence suggests that corticotropin-releasing factor (CRF) plays an important role in regulating the effects of stress. CRF administration produces stress-like effects in humans and laboratory animals, and CRF levels are elevated in individuals with stress-related illness. Recent work indicates that k-opioid receptor (KOR) antagonists can block CRF effects, raising the possibility that at least some of the effects of stress are mediated via KORs. Here we examined the effects of CRF on performance in the 5-choice serial reaction time task (5CSRTT), a test used to quantify attention in rodents, as well as functional interactions between CRF and KORs. Male Sprague-Dawley rats were trained in the 5CSRTT and then each was implanted with an intracerebroventricular (ICV) cannula. After recovery and restabilization of performance, they received a single intraperitoneal (IP) injection of vehicle or JDTic (10 mg/kg), a KOR antagonist with long-lasting (414 days) effects. In subsequent sessions, rats received ICV infusions of CRF (0.25-1.0 mg) or vehicle and were tested 60 min later. CRF dose-dependently disrupted performance as reflected by decreases in correct responding, increases in omission errors, increases in latencies to respond correctly, and increases in time to complete the session. JDTic attenuated each of these CRF-induced deficits while having no effects on its own. The persistent ability of JDTic to disrupt KOR function was confirmed using the tail immersion assay. These findings indicate that KOR antagonists can prevent acute stress-related effects that degrade performance in tasks requiring attention.

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Corticotropin-releasing factor in posttraumatic stress disorder (PTSD) with secondary psychotic symptoms, nonpsychotic PTSD, and healthy control subjects

Cited by 149 publications

References 39 publications

CSF Corticotropin-Releasing Factor in Personality Disorder: Relationship with Self-Reported Parental Care

CSF Corticotropin-Releasing Factor in Personality Disorder: Relationship with Self-Reported Parental Care

Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

Corticotropin-Releasing Factor (CRF)-Induced Disruption of Attention in Rats Is Blocked by the κ-Opioid Receptor Antagonist JDTic

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