Local circuit regulation of paraventricular nucleus stress integration

Herman, James P.; Tasker, Jeffrey G.; Ziegler, Dana R.; Cullinan, William E.

doi:10.1016/s0091-3057(01)00681-5

Cited by 245 publications

(174 citation statements)

References 95 publications

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“…The BNST acts as a conduit between the amygdala and the HPA axis, and, through tonic regulation of the PVN (Herman et al, 1994;Herman et al, 2002), mediates both the physiological (Choi et al, 2007) and the behavioralaffective response to stress (Cecchi et al, 2002;Davis and Shi, 1999). The aim of the present investigation was to explore the mechanisms mediating the sequalae of behavioral and endocrine phenotypes induced by chronic intermittent psychological stress.…”

Section: Discussionmentioning

confidence: 98%

Importance of CRF Receptor-Mediated Mechanisms of the Bed Nucleus of the Stria Terminalis in the Processing of Anxiety and Pain

Tran

Schulkin

Meerveld

2014

Neuropsychopharmacol

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Corticotropin-releasing factor (CRF)-mediated mechanisms in the bed nucleus of the stria terminalis (BNST) have a pivotal role in stressinduced anxiety and hyperalgesia. Although CRF is known to activate two receptor subtypes, CRF 1 and CRF 2 , attempts to delineate the specific role of each subtype in modulating anxiety and nociception have been inconsistent. Here we test the hypothesis that CRF 1 and CRF 2 receptor activation in the anteriolateral BNST (BNST AL ) facilitates divergent mechanisms modulating comorbid anxiety and hyperalgesia. Microinfusions of the specific antagonists CP376395 and Astressin 2 B into the BNST AL were used to investigate CRF 1 and CRF 2 receptor functions, respectively. We found that CRF 1 and CRF 2 receptors in the BNST AL had opposing effects on exploratory behavior in the elevated plus-maze, somatic mechanical threshold, and the autonomic and endocrine response to stress. However, CRF 1 or CRF 2 receptor antagonism in the BNST AL revealed complementary roles in facilitating the acoustic startle and visceromotor reflexes. Our results suggest that the net effect of CRF 1 and CRF 2 receptor activation in the BNST AL is pathway-dependent and provides important insight into the CRF receptor-associated circuitry that likely underpins stress-induced pathologies.

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Section: Discussionmentioning

confidence: 98%

Importance of CRF Receptor-Mediated Mechanisms of the Bed Nucleus of the Stria Terminalis in the Processing of Anxiety and Pain

Tran

Schulkin

Meerveld

2014

Neuropsychopharmacol

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“…Our findings of a higher HPA-system sensitivity in more anxious individuals after HF-rTMS applied over the right DLPFC might be especially germane in light of the therapeutic applications of rTMS as a treatment for anxiety disorders and/or posttraumatic stress disorder (PTSD) (Cohen et al, 2004;Pallanti and Bernardi, 2009;Zwanzger et al, 2009;Handwerger, 2009;Yue et al, in press). Because of the overwhelming evidence that GABAergic mechanisms regulate neuroendocrine stress responses (Herman et al, 2002;Herman et al, 2004;Kovács et al, 2004;Cullinan et al 2008;Radley et al, 2009) and the importance of GABA receptor involvement in the pathophysiology and treatment of anxiety disorders (Lydiard, 2003;Nemeroff, 2003;Kalueff and Nutt., 2007), it is tempting to assume that in our study the observed HPA-axis sensitivity to one HF-rTMS session in more anxious females was mediated by the GABA system.…”

Section: Discussionmentioning

confidence: 99%

Baseline ‘state anxiety’ influences HPA-axis sensitivity to one sham-controlled HF-rTMS session applied to the right dorsolateral prefrontal cortex

Baeken¹,

Vanderhasselt²,

Raedt³

2011

Psychoneuroendocrinology

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2 SummaryAlthough negative results have been reported, an important aspect of the physiology of repetitive Transcranial Magnetic Stimulation (rTMS) could be related to the endocrinological response of the hypothalamic-pituitaryadrenal (HPA) axis, such as cortisol secretion. Because endocrinological responses are influenced by anxiety states, this could influence the effect of rTMS in healthy individuals. In this sham-controlled, "single blind" crossover study, we examined whether one session of HF-rTMS could affect the HPA-system, when taking into account individual state anxiety scores based on the State-Trait Anxiety Inventory (STAI). Twenty-four healthy rTMS naïve females received one sham-controlled high frequency (HF)-rTMS session delivered on the right dorsolateral prefrontal cortex (DLPFC). The Profile of Mood States (POMS) questionnaire, together with salivary cortisol samples, was collected before, just after and 30 minutes post HF-rTMS. To examine whether state anxiety could influence endocrinological outcome measurements, we administered the STAI-state just before each HF-rTMS experiment started. Based on the POMS questionnaire, no mood changes were observed.Without taking individual state anxiety scores into account, one sham-controlled right-sided HF-rTMS session did not influence the HPA-system. When taking into account individual STAI-state scores, we found that healthy women scoring higher on the STAI-state displayed a significantly more sensitive HPA-system, resulting in salivary cortisol concentration increases after real HF-rTMS, compared to those scoring lower on this anxiety scale. Our results indicate that healthy women scoring high on state anxiety display a more sensitive HPAsystem when receiving one right-sided HF-rTMS session. Our findings suggest that the incorporation of individual anxiety states in experimental rTMS research could add further information about its neurobiological influences on the HPA-system.

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“…The MeA, which lies medial to the CeA, showed the largest increase in c-fos expression within the amygdala and is of interest because earlier studies associated it with fear and defensive responses (Kemble et al, 1984). The MeA projects to areas adjacent to the PVN and also links to neurons in the bed nucleus of the stria terminalis that project to the PVN (Herman et al, 2002). These linkages with the hypothalamus are consistent with the MeA being the amygdala region that has the greatest modulatory influence on stress-induced HPA activity.…”

Section: Discussionmentioning

confidence: 99%

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Roseboom

Nanda

Bakshi

et al. 2007

Psychoneuroendocrinology

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SummaryBehavioral inhibition (BI) is an adaptive defensive response to threat; however, extreme BI is associated with anxiety-related psychopathology. When rats are exposed to a natural predator they display stress-and anxiety-related behavioral alterations and physiological activation. To develop a preclinical rodent model to study mechanisms underlying human BI and anxiety, we examined the extent to which ferret exposure elicits anxiety-related BI and HPA and amygdala activation of the CRF system. In the first experiment, BI and other behaviors were assessed in the presence or absence of a ferret. In the second experiment, ferret-induced corticosterone release and changes in brain cfos expression were assessed. In the final experiment, gene chip and quantitative real time-PCR analyses were performed on amygdala tissue from control and ferret-exposed rats. Ferret exposure increased BI and submissive posturing, as well as plasma corticosterone and the number of Fospositive cells in several brain regions including the amygdala. Gene expression analysis revealed increased amygdalar mRNA for CRF-binding protein, but not the CRF 1 receptor, CRF 2 receptor or CRF. In rodents, ferret exposure can be used to elicit anxiety-related BI, which is associated with HPA and amygdala activation. Since the amygdala and the CRF system have been implicated in adaptive and maladaptive anxiety responses in humans, these data support use of our rodent model to further investigate mechanisms underlying anxiety-related psychopathology in humans.

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Local circuit regulation of paraventricular nucleus stress integration

Cited by 245 publications

References 95 publications

Importance of CRF Receptor-Mediated Mechanisms of the Bed Nucleus of the Stria Terminalis in the Processing of Anxiety and Pain

Importance of CRF Receptor-Mediated Mechanisms of the Bed Nucleus of the Stria Terminalis in the Processing of Anxiety and Pain

Baseline ‘state anxiety’ influences HPA-axis sensitivity to one sham-controlled HF-rTMS session applied to the right dorsolateral prefrontal cortex

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

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