Lesions in the bed nucleus of the stria terminalis disrupt corticosterone and freezing responses elicited by a contextual but not by a specific cue-conditioned fear stimulus

Sullivan, Gregory M.; Apergis, John; Bush, David E.; Johnson, Luke R.; Hou, Mian; LeDoux, Joseph E.

doi:10.1016/j.neuroscience.2004.06.015

Cited by 308 publications

(282 citation statements)

References 43 publications

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“…As already indicated, the BNST is not involved in the expression of fearpotentiated startle to CS lasting 3.7 sec (Campeau and Davis 1995;Hitchcock and Davis 1986;Sananes and Davis 1992). It is also not required for freezing to a 20-sec discrete cue, but it is necessary for freezing to context (Sullivan et al 2004). Further, BNST lesions do not affect conditioned suppression of bar-pressing behavior to a 1-min discrete CS but greatly reduces conditioned suppression to a 10-min discrete CS (Waddell et al 2006).…”

Section: Discussionmentioning

confidence: 82%

“…As mentioned earlier, animal data show that the BNST is involved in context conditioning, but not in cued fear conditioning (Sullivan et al 2004). Another structure that differentiates between cued and context conditioning is the hippocampus (Kim and Fanselow 1992;Pentkowski et al 2006;Phillips and LeDoux 1992;Richmond et al 1999).…”

Section: Context Conditioningmentioning

confidence: 87%

“…There is currently not clear response to this question, in part because very few studies have compared the influence of the amygdala and of the BNST on short-and long-duration threat. The BNST is clearly involved in the effect of stressors that last several minute (Sullivan et al 2004;Waddell et al 2006;Walker and Davis 1997a) to hours or days (Bangasser et al 2005;Hammack et al 2004). The earliest time of BNST involvement is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, phasic startle potentiation (i.e., fear-potentiated startle) is obtained in aversive conditioning studies, whereas light-enhanced startle, shock sensitization of startle, and CRH-enhanced startle are unconditioned responses. However, recent studies relying on measures of anxiety other than startle have also demonstrated the role of BNST in sustained forms of aversive conditioning such as context conditioning (Sullivan et al 2004) and long-duration conditioned stimuli (Waddell et al 2006), suggesting that the BNST is involved in sustained aversive states rather than unconditioned responses per se.…”

Section: Preclinical Evidence For Dissociated Neural Systems Of Fear mentioning

confidence: 99%

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Models and mechanisms of anxiety: evidence from startle studies

2007

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Rationale-Preclinical data indicates that threat stimuli elicit two classes of defensive behaviors, those that are associated with imminent danger and are characterized by avoidance or fight (fear), and those that are associated with temporally uncertain danger and are characterized by sustained apprehension and hypervigilance (anxiety).Objective-To 1) review evidence for a distinction between fear and anxiety in animal and human experimental models using the startle reflex as an operational measure of aversive states, 2) describe experimental models of anxiety, as opposed to fear, in humans, 3) examine the relevance of these models to clinical anxiety.Results-The distinction between phasic fear to imminent threat and sustained anxiety to temporally uncertain danger is suggested by psychopharmacological and behavioral evidence from ethological studies and can be traced back to distinct neuroanatomical systems, the amygdala and the bed nucleus of the stria terminalis. Experimental models of anxiety, not fear, are relevant to nonphobic anxiety disorders.Conclusions-Progress in our understanding of normal and abnormal anxiety is critically dependent on our ability to model sustained aversive states to temporally uncertain threat.

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Section: Discussionmentioning

confidence: 82%

Section: Context Conditioningmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Preclinical Evidence For Dissociated Neural Systems Of Fear mentioning

confidence: 99%

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Models and mechanisms of anxiety: evidence from startle studies

2007

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“…To date, lesions (reversible or irreversible) or pharmacological manipulations of the BST suggest roles in the physiology of fear, food intake, social behaviours, pain, and goal-directed behaviours and the associated pathophysiological states such as anxiety, anorexia, and addiction (Ciccocioppo et al, 2003;Colussi-Mas et al, 2005;Crown et al, 2000;Delfs et al, 2000;Deyama et al, 2007Deyama et al, , 2008Deyama et al, , 2009Dumont et al, 2005;Dunn and Williams, 1995;Epping-Jordan et al, 1998;Erb and Stewart,1999;Fendt et al, 2003;Gewirtz et al,1998;Jasnow et al, 2004;Lee and Davis, 1997;Leri et al, 2002;Liu et al, 2009;Nakagawa et al, 2005;Sajdyk et al, 2008;Sullivan et al, 2004;Walker and Davis, 1997;Walker et al, 2000;Wang et al, 2001). …”

mentioning

confidence: 99%

What is the bed nucleus of the stria terminalis?

Dumont

2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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What exactly is this bed nucleus of the stria terminalis? This is a question that I, and possibly all of my colleague neuroscientists with interest in this region of the brain, get on a regular basis. Unfortunately, the simplest questions are often the most difficult to answer.Firstly, what's in a name? Researchers have failed to reach consensus on whether "BST" or "BNST" is the most effective acronym for their structure of interest. It seems there is little hope for clarification, as there is no scientific or grammatical justification using which we might choose one or the other. To our chagrin, both will probably continue to be commonly used. A description of the BST [sic] should start by reporting that it is a cluster of about 12 nuclei surrounding the caudal part of the anterior commissure, deep in the cerebral hemispheres. The exact number of BST nuclei varies depending on the criteria used, which are, at the moment, mostly anatomical. This may change in the future with more precise and localized permanent or reversible lesion approaches.The BST is so named because it is located at one extremity of the stria terminalis, a bundle of axons that connects it with the amygdaloid nuclei. Although work is still needed to fully understand the function (s) of the BST, extensive anatomical studies of its connectivity suggest that it is a relay center within neurocircuits coordinating the activity of autonomic, neuroendocrine, and somatic motor systems into fully organized physiological functions and behaviours (Dong et al., 2001a,b;Dong and Swanson, 2003, 2004a, b, 2006aHasue and Shammah-Lagnado, 2002;Li and Kirouac, 2008;McDonald et al.,1999;Prewitt and Herman, 1998;Rodaros et al., 2007;Saggu and Lundy, 2007;Shin et al., 2008;Wood and Swann, 2005). Altogether, the BST seems to be a coordinating and relay center where descending cortical information meets ascending interoceptive and exteroceptive information regarding homeostatic states or potential changes in homeostasis. Information likely flows into the BST from exteroceptive (main and accessory olfactory, touch and nociception, gustatory) or interoceptive (energy and fluid levels, tissue damage, sexual hormone levels) sources through all central nervous system levels (from cortical to brain stem and spinal cord). The BST then has widespread descending projections to motor regions of the hindbrain that may trigger or contribute to the elaboration of coordinated physiological and behavioural responses necessary for a well-balanced homeostasis.The BST can be roughly divided into anterior and posterior subdivisions, each containing several nuclei, which can be identified based on their projection pattern and neurochemical identity (Cassell et al., 1986;Day et al

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