Role of noradrenergic projections to the bed nucleus of the stria terminalis in the regulation of the hypothalamic–pituitary–adrenal axis

Forray, María Inés; Gysling, Katia

doi:10.1016/j.brainresrev.2004.07.011

Cited by 173 publications

(169 citation statements)

References 128 publications

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“…The role of norepinephrine in drug addiction is often overshadowed by that of dopamine (Weinshenker and Schroeder, 2007), despite evidence that medullary norepinephrine synthesis may be crucial for establishing morphine self-administration (Davis et al, 1975) and conditioned place preference (Olson et al, 2006). The vBNST receives dense noradrenergic projections from the NTS (Forray and Gysling, 2004), and thus is a likely downstream target for norepinephrine's actions in morphine reward. However, we did not detect norepinephrine release in the vBNST during morphine, although elevated norepinephrine in the BNST may develop following chronic drug exposure (Fuentealba et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Although few studies emphasize the noradrenergic component of drug use, norepinephrine in the bed nucleus of the stria terminalis (BNST) has been clearly implicated in drug withdrawal (Aston-Jones et al, 1999). The ventral BNST (vBNST) receives dense innervation from the nucleus of the solitary tract (NTS) (Forray and Gysling, 2004), the source of norepinephrine critical for withdrawal aversion , and chronic morphine treatment increases basal norepinephrine in the BNST (Fuentealba et al, 2000). However, no work addresses the effect of acute drug exposure or withdrawal on phasic release.…”

Section: Introductionmentioning

confidence: 99%

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Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

Fox

Rodeberg

Wightman

2016

Neuropsychopharmacol

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Dysregulated catecholamine signaling has long been implicated in drug abuse. Although much is known about adaptations following chronic drug administration, little work has investigated how a single drug exposure paired with withdrawal influences catecholamine signaling in vivo. We used fast-scan cyclic voltammetry in freely moving rats to measure real-time catecholamine overflow during acute morphine exposure and naloxone-precipitated withdrawal in two regions associated with the addiction cycle: the dopamine-dense nucleus accumbens (NAc) and norepinephrine-rich ventral bed nucleus of the stria terminalis (vBNST). We compared dopamine transients in the NAc with norepinephrine concentration changes in the vBNST, and correlated release with specific withdrawal-related behaviors. Morphine increased dopamine transients in the NAc, but did not elicit norepinephrine responses in the vBNST. Conversely, dopamine output was decreased during withdrawal, while norepinephrine was released in the vBNST during specific withdrawal symptoms. Both norepinephrine and withdrawal symptoms could be elicited in the absence of morphine by administering naloxone with an α 2 antagonist. The data support reciprocal roles for dopamine and norepinephrine signaling during drug exposure and withdrawal. The data also support the allostasis model and show that negative-reinforcement may begin working after a single exposure/withdrawal episode.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

Fox

Rodeberg

Wightman

2016

Neuropsychopharmacol

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“…The bed nucleus of the stria terminalis (BNST) is thought to be a key structure for mediating anxiety-like responses elicited by unconditioned or ethologically valid threats (Lee and Davis, 1997;Walker and Davis, 1997;Davis and Shi, 1999;Fendt et al, 2003), and is a key structure that relays and integrates limbic and autonomic information related to stress responses (Cullinan et al, 1993;Forray and Gysling, 2004;Herman et al, 2004). The BNST has also been identified as an area critical for stress-induced reinstatement of drug-seeking behaviors, and for the increased anxiety associated with protracted withdrawal (Erb and Stewart, 1999;Leri et al, 2002;Aston-Jones and Harris, 2004).…”

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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“…Several lines of evidence mark the BST as a major mediator of the HPA axis responses to stress (Casada and Dafny, 1991;Crane et al, 2003;Dunn, 1987;Feldman et al, 1990;Forray and Gysling, 2004;Gray et al, 1993;Zhu et al, 2001) raising the possibility that the BST may play a role in HPA axis disorders mediated by upstream limbic structures. The BST can be subdivided into a number of cytoarchitecturally distinct subnuclei with distinct afferent input and efferent targets (Swanson, 1998).…”

Section: Introductionmentioning

confidence: 99%

The role of the posterior medial bed nucleus of the stria terminalis in modulating hypothalamic–pituitary–adrenocortical axis responsiveness to acute and chronic stress

Choi¹,

Furay²,

Evanson³

et al. 2008

Psychoneuroendocrinology

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SummaryThe bed nucleus of the stria terminalis (BST) plays a prominent role in brain integration of acute responses to stressful stimuli. This study tests the hypothesis that the BST plays a complementary role in regulation of physiological changes associated with chronic stress exposure. Male SpragueDawley rats received bilateral ibotenate lesions or sham lesions of the posterior medial region of the BST (BSTpm), an area known to be involved in inhibition of HPA axis responses to acute stress. Chronic stress was induced by 14-day exposure to twice daily stressors in an unpredictable sequence (chronic variable stress (CVS)). On the morning after the end of CVS, stressed and nonstressed controls were exposed to a novel restraint stress challenge. As previously documented, CVS caused adrenal hypertrophy, thymic involution, and attenuated body weight gain. None of these endpoints were affected by BSTpm lesions. Chronic stress exposure facilitated plasma corticosterone responses to the novel restraint stress and elevated CRH mRNA. Lesions of the BSTpm increased novel stressor-induced plasma ACTH and corticosterone secretion and enhanced c-fos mRNA induction in the paraventricular nucleus of the hypothalamus (PVN). In addition, lesion of the BSTpm resulted in an additive increase in CVS-induced facilitation of corticosterone responses and PVN CRH expression. Collectively these data confirm that the BSTpm inhibits HPA responses to acute stress, but do not strongly support an additional role for this region in limiting HPA axis responses to chronic drive. The data further suggest that acute vs. chronic stress integration are subserved by different brain circuitry.

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Role of noradrenergic projections to the bed nucleus of the stria terminalis in the regulation of the hypothalamic–pituitary–adrenal axis

Cited by 173 publications

References 128 publications

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

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

The role of the posterior medial bed nucleus of the stria terminalis in modulating hypothalamic–pituitary–adrenocortical axis responsiveness to acute and chronic stress

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