Bed Nucleus of the Stria Terminalis Subregions Differentially Regulate Hypothalamic–Pituitary–Adrenal Axis Activity: Implications for the Integration of Limbic Inputs

Choi, Dennis C.; Furay, Amy R.; Evanson, Nathan K.; Ostrander, Michelle M.; Ulrich‐Lai, Yvonne M.; Herman, James P.

doi:10.1523/jneurosci.4301-06.2007

Cited by 343 publications

(324 citation statements)

References 52 publications

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“…In situ hybridization was performed as previous described (43). Antisense cRNA probes complementary to rat PPG (399 bp) labeled by in vitro transcription [ 35 S]UTP were applied for PPG mRNA analysis, and biotinlabeled hnRNA probes were used for PPG hnRNA analysis (see details in SI Materials and Methods).…”

Section: Regulation Of Ppg Gene Expression By Acute Stress Experimenmentioning

confidence: 99%

Glucocorticoid regulation of preproglucagon transcription and RNA stability during stress

Zhang¹,

Packard²,

Tauchi³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Stress elicits a synchronized response of the endocrine, sympathetic, and central nervous systems to preserve homeostasis and well-being. Glucagon-like peptide-1 (GLP-1), a primary posttranslational product of the preproglucagon (PPG) gene, activates both physical and psychological stress responses. The current study examined mechanisms regulating expression of PPG gene products in the hindbrain. Our results indicate that PPG mRNA decreases rapidly after exposure to acute stressors of multiple modalities. Reduced mRNA levels are accompanied by reduced GLP-1 immunoreactivity in the paraventricular nucleus of hypothalamus, suggesting release at PPG terminals. Stress-induced decrements in PPG mRNA were attenuated in adrenalectomized-corticosterone-replaced rats, suggesting that mRNA down-regulation is due at least in part to glucocorticoid secretion. In contrast, acute stress increased levels of PPG heteronuclear RNA (hnRNA) in a glucocorticoid-dependent manner, suggesting that decreases in PPG mRNA are due to increased degradation rather than reduced transcription. Glucocorticoid administration to unstressed rats is sufficient to cause decrements in PPG mRNA and increments in PPG hnRNA. These findings suggest that glucocorticoids deplete the pool of transcribed PPG mRNA and concurrently stimulate PPG gene transcription, with the latter allowing a mechanism for replenishment of PPG mRNA after stress cessation. The combination of rapid PPG mRNA depletion and initiation of PPG transcription within 30 min is consistent with a rapid action of glucocorticoids on GLP-1 bioavailability, resulting in a transient reduction in the capacity for neuropeptidergic excitation of stress responses.

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Section: Regulation Of Ppg Gene Expression By Acute Stress Experimenmentioning

confidence: 99%

Glucocorticoid regulation of preproglucagon transcription and RNA stability during stress

Zhang¹,

Packard²,

Tauchi³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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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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“…Similarly, the FU projects along approximately 4 distinct pathways that terminate in the central amygdala, hypothalamus (PVH), midbrain (ventral tegmental area) and lower brainstem (lateral periaque-ducal gray, raphe) (Dong et al, 2001b). Each of these descending pathways corresponds to important physiological functions triggered by nociceptive stimuli such as defensive behaviours, descending analgesia, autonomic control of breathings, cardiovascular responses, arousal, and activation of HPA axis (Choi et al, 2007;Dick and Coles, 2000;Rossi et al, 1994;Satoh and Fibiger, 1986;Vertes, 1991). Given this broad projection pattern of each BST sub-nuclei, noxious stimuli-induced activation of the BST should result in generalized physiological responses consistent with an emotional response.…”

Section: Significance Of Noxious Stimulation-induced Neuronal Activatmentioning

confidence: 99%

Nuclei-and condition-specific responses to pain in the bed nucleus of the stria terminalis

Morano

Bailey

Cahill

et al. 2008

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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The bed nucleus of the stria terminalis (BST) is a basal forebrain structure considered to be part of a cortico-striato-pallidal system that coordinates autonomic, neuroendocrine and behavioural physiological responses.Recent evidence suggests that the BST plays a role in the emotional aspect of pain. The objective of the present study was to further understand the neurophysiological bases underlying the involvement of the BST in the pain experience, in both acute and chronic pain conditions. Using c-Fos as an indicator of neuronal activation, the results demonstrated that a single toe-pinch in rats produced nuclei-and condition-specific neuronal responses within the anterior region of the BST (antBST). Specifically, acute noxious stimulation increased c-Fos in the dorsal medial (dAM) and fusiform (FU) nuclei. Chronic neuropathic pain induced by chronic constriction injury (CCI) of the sciatic nerve decreased the number of c-Fos positive cells following acute mechanical stimulation in the dAM and FU nuclei, and increased c-Fos immunoreactivity in the ventral medial (vAM) aspect of the BST. In addition, the results revealed a nuclei-specific sensitivity to the surgical procedure. Following noxious stimulation to animals that received a sham surgery, c-Fos immunoreactivity was blunted in the FU nucleus while it increased in the oval (OV) nucleus of the BST.Altogether, this study demonstrates that pain induces nuclei-and condition-specific neuronal activation in the BST revealing an intriguing supraspinal neurobiological substrate that may contribute to the physiology of acute nociception and the pathophysiology of chronic pain.

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Bed Nucleus of the Stria Terminalis Subregions Differentially Regulate Hypothalamic–Pituitary–Adrenal Axis Activity: Implications for the Integration of Limbic Inputs

Cited by 343 publications

References 52 publications

Glucocorticoid regulation of preproglucagon transcription and RNA stability during stress

Glucocorticoid regulation of preproglucagon transcription and RNA stability during stress

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

Nuclei-and condition-specific responses to pain in the bed nucleus of the stria terminalis

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