β1 Adrenergic Receptors in the Bed Nucleus of Stria Terminalis Mediate Differential Responses to Opiate Withdrawal

Cecchi, Marco; Capriles, Nancy; Watson, Stanley J.; Akil, Huda

doi:10.1038/sj.npp.1301140

Cited by 36 publications

(24 citation statements)

References 58 publications

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“…Of particular interest are findings from Delfs et al (2000) who found that intra-BNST infusions of a noradrenergic β1/β2 receptor antagonist cocktail (betaxolol + ICI 118,551), or of the non-selective β-receptor antagonist S -propranolol, or of the noradrenergic α2 agonist clonidine (which inhibits norepinephrine release via actions on presynaptic receptors (Forray et al , 1995; Forray et al , 1997) each block the development of withdrawal-induced place aversions with only modest (e.g., teeth chattering, eye twitching) or non-existent (e.g., wet dog shakes, jump escapes) effects on the acute somatic signs of withdrawal. Similar results have been reported by Cecchi et al (2007). The noradrenergic system was targeted in these studies because of the extraordinarily high levels of norepinephrine found in the BNST (e.g., Brownstein et al , 1974; Kilts and Anderson, 1986) and released during stress (Pacak et al , 1995; Pardon et al , 2002).…”

Section: Does Bnst Plasticity Mediate Stress-induced Anxiety?supporting

confidence: 78%

Selective participation of the bed nucleus of the stria terminalis and CRF in sustained anxiety-like versus phasic fear-like responses

Walker

Miles

Davis

2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

304

272

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The medial division of the central nucleus of the amygdala (CeA M ) and the lateral division of the bed nucleus of the stria terminalis (BNST L ) are closely related. Both receive projections from the basolateral amygdala (BLA) and both project to brain areas that mediate fear-influenced behaviors. In contrast to CeA M however, initial attempts to implicate the BNST in conditioned fear responses were largely unsuccessful. More recent studies have shown that the BNST does participate in some types of anxiety and stress responses. Here, we review evidence suggesting that the CeA M and BNST L are functionally complementary, with CeA M mediating short-but not long-duration threat responses (i.e., phasic fear) and BNST L mediating long-but not short-duration responses (sustained fear or 'anxiety'). We also review findings implicating the stress-related peptide corticotropin-releasing factor (CRF) in sustained but not phasic threat responses, and attempt to integrate these findings into a neural circuit model which accounts for these and related observations. Keywords anxiety; startle; amygdala; bed nucleus of the stria terminalis; corticotropin releasing factor A now-familiar and widely-adopted neural circuit model of fear places the amygdala in center stage and assigns different functions to different amygdala subdivisions (Fig. 1). Thus, the basolateral group (BLA) screens incoming sensory information for threat cues and, if such cues are detected, passes this information on to the central nucleus of the amygdala's medial subdivision (CeA M ), which mediates threat responses by way of its many projections to areas that mediate specific fear-influenced behaviors (c.f., Davis, 1992;Fanselow and LeDoux, 1999;Maren, 2001;Pare et al., 2004).In the following pages, we review evidence suggesting that this model is incomplete, and should be expanded to include the bed nucleus of the stria terminalis (specifically, it's lateral subdivision -BNST L ). In fact, by many criteria, the CeA and BNST are closely related (Alheid © 2009 Elsevier Inc. All rights reserved.Correspondence should be addressed to: David L. Walker, Emory University School of Medicine, 954 Gatewood Road NE, Yerkes Neurosci Bldg -Rm 5214, Atlanta, GA 30329, Ph: (404) Fax: (404) 727-8070, dlwalke@emory.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptProg Neuropsychopharmacol Biol Psychiatry. Author manuscript; available in PMC 2010 November 13. Published in final edited form as:Prog Neuropsychopharmacol Biol Psychiatry. Alheid and Heimer, 1988;Johnston, 1923). Of par...

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Section: Does Bnst Plasticity Mediate Stress-induced Anxiety?supporting

confidence: 78%

Selective participation of the bed nucleus of the stria terminalis and CRF in sustained anxiety-like versus phasic fear-like responses

Walker

Miles

Davis

2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

304

272

View full text Add to dashboard Cite

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“…The BNST has one of the highest concentrations of norepinephrine in the brain, and opiate withdrawal activates BNST-projecting cells in the A1 and A2 noradrenergic cell groups of the caudal medulla. Lesions of the ventral noradrenergic bundle, which interrupt the projection of these cell groups to the BNST, reduce opiate-withdrawal-induced place aversion, as do injections of b-adrenergic-receptor antagonists into the BNST itself, even though these same manipulations have little effect on the somatic symptoms of withdrawal (Aston-Jones et al 1999;Delfs et al 2000; and see also Cecchi et al 2007).…”

Section: Role Of the Cea And Bnst In Drug Withdrawalmentioning

confidence: 96%

Role of the extended amygdala in short-duration versus sustained fear: a tribute to Dr. Lennart Heimer

2008

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The concept of the "extended amygdala", developed and explored by Lennart Heimer, Jose de Olmos, George Alheid, and their collaborators, has had an enormous impact on the field of neuroscience and on our own work. Measuring fear-potentiated startle test using conditioned stimuli that vary in length we suggest that the central nucleus of the amygdala (CeA) and the lateral division of the bed nucleus of the stria terminalis (BNST(L)) are involved in short-term versus long-term fear responses we call phasic versus sustained fear, respectively. Outputs from the basolateral amygdala (BLA) activate the medial division of the CeA (CeA(M)) to very rapidly elicit phasic fear responses via CeA(M) projections to the hypothalamus and brainstem. The BLA also projects to the BNST(L), which together with other BNST(L) inputs from the lateral CeA (CeA(L)) initiate a slower developing, but sustained fear response, akin to anxiety. We hypothesize this occurs because the CeA(L) releases the peptide corticotropin releasing hormone (CRF) into the BNST(L) which facilitates the release of glutamate from BLA terminals. This activates the BNST(L) which projects to hypothalamic and brainstem areas similar to those innervated by the CeA(M) that mediate the specific signs of fear and anxiety. The generality of this idea is illustrated by selective studies looking at context conditioning, social defeat, drug withdrawal and stress induced reinstatement.

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“…Blocking both β 1 -AR and β 2 -ARs abolishes withdrawal-induced place aversion (Aston-Jones et al, 1999). A selective β 1 -AR antagonist in the dBNST blocks withdrawal-induced aversion and attenuates opiate-withdrawal symptoms in rats with high reactivity to novelty (Cecchi et al, 2007).…”

Section: Norepinephrinementioning

confidence: 99%

Stress Modulation of Opposing Circuits in the Bed Nucleus of the Stria Terminalis

Daniel

Rainnie

2015

Neuropsychopharmacol

182

191

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The anterior bed nucleus of the stria terminalis (BNST) has been recognized as a critical structure in regulating trait anxiety, contextual fear memory, and appetitive behavior, and is known to be sensitive to stress manipulations. As one of the most complex structures in the central nervous system, the intrinsic circuitry of the BNST is largely unknown; however, recent technological developments have allowed researchers to begin to untangle the internal connections of the nucleus. This research has revealed the possibility of two opposing circuits, one anxiolytic and one anxiogenic, within the BNST, the relative strength of which determines the behavioral outcome. The balance of these pathways is critical in maintaining a normal physiological and behavioral state; however, stress and drugs of abuse can differentially affect the opposing circuitry within the nucleus to shift the balance to a pathological state. In this review, we will examine how stress interacts with the neuromodulators, corticotropin-releasing factor, norepinephrine, dopamine, and serotonin to affect the circuitry of the BNST as well as how synaptic plasticity in the BNST is modulated by stress, resulting in long-lasting changes in the circuit and behavioral state.

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β1 Adrenergic Receptors in the Bed Nucleus of Stria Terminalis Mediate Differential Responses to Opiate Withdrawal

Cited by 36 publications

References 58 publications

Selective participation of the bed nucleus of the stria terminalis and CRF in sustained anxiety-like versus phasic fear-like responses

Selective participation of the bed nucleus of the stria terminalis and CRF in sustained anxiety-like versus phasic fear-like responses

Role of the extended amygdala in short-duration versus sustained fear: a tribute to Dr. Lennart Heimer

Stress Modulation of Opposing Circuits in the Bed Nucleus of the Stria Terminalis

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