The neuronal organization of the supracapsular part of the stria terminalis in the rat: The dorsal component of the extended amygdala

Alheid, George F.; Beltramino, C.; Olmos, J.S. de; Forbes, Michael S.; Swanson, D.J.; Heimer, Lennart

doi:10.1016/s0306-4522(97)00560-5

Cited by 107 publications

(115 citation statements)

References 68 publications

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“…Work from several other laboratories has shown that reinstatement of drugseeking is dependent on the extended amygdala. The extended amygdala consists of the BNST, CeA, and shell of the NAc (Alheid et al, 1998). This system is important in several stress-related components of drug withdrawal (Smith and Aston-Jones, 2008), and inactivation of CeA, BNST, shell of the NAc, or VTA has been shown to block footshock-induced reinstatement of cocaine-seeking (McFarland et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Mifepristone in the Central Nucleus of the Amygdala Reduces Yohimbine Stress-Induced Reinstatement of Ethanol-Seeking

Simms

Haass‐Koffler

Bito-Onon

et al. 2011

Neuropsychopharmacol

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Chronic ethanol exposure leads to dysregulation of the hypothalamic-pituitary-adrenal axis, leading to changes in glucocorticoid release and function that have been proposed to maintain pathological alcohol consumption and increase vulnerability to relapse during abstinence. The objective of this study was to determine whether mifepristone, a glucocorticoid receptor antagonist, plays a role in ethanol self-administration and reinstatement. Male, Long-Evans rats were trained to self-administer either ethanol or sucrose in daily 30 min operant self-administration sessions using a fixed ratio 3 schedule of reinforcement. Following establishment of stable baseline responding, we examined the effects of mifepristone on maintained responding and yohimbine-induced increases in responding for ethanol and sucrose. Lever responding was extinguished in separate groups of rats and animals were tested for yohimbine-induced reinstatement and corticosterone release. We also investigated the effects of local mifepristone infusions into the central amygdala (CeA) on yohimbine-induced reinstatement of ethanol-and sucrose-seeking. In addition, we infused mifepristone into the basolateral amygdala (BLA) in ethanol-seeking animals as an anatomical control. We show that both systemic and intra-CeA (but not BLA) mifepristone administration suppressed yohimbine-induced reinstatement of ethanol-seeking, while only systemic injections attenuated sucroseseeking. In contrast, baseline consumption, yohimbine-induced increases in responding, and circulating CORT levels were unaffected. The data indicate that the CeA plays an important role in the effects of mifepristone on yohimbine-induced reinstatement of ethanolseeking. Mifepristone may be a valuable pharmacotherapeutic strategy for preventing relapse to alcohol use disorders and, as it is FDA approved, may be a candidate for clinical trials in the near future.

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Section: Discussionmentioning

confidence: 99%

Mifepristone in the Central Nucleus of the Amygdala Reduces Yohimbine Stress-Induced Reinstatement of Ethanol-Seeking

Simms

Haass‐Koffler

Bito-Onon

et al. 2011

Neuropsychopharmacol

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“…Some (see Refs. 528, 620) but certainly not all fear responses (337) include the bed nucleus of the stria terminalis (BNST), a part of the so-called extended amygdala (13,646), among the projections of the CE that mediate the behavioral responses to fear.…”

Section: Hippocampus Amygdala Infralimbic Ventromedial Prefrontmentioning

confidence: 99%

Fear Memory

Izquierdo

Furini

Myskiw

2016

Physiological Reviews

339

241

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Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre-and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.

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“…The BNST is adjacent to the anterior commissure in the basal forebrain and makes up the rostral portion of the neural continuum known as the extended amygdala. The BNST resembles the amygdala in terms of cell morphology and neurotransmitters (Alheid et al 1998). Both the central nucleus of the amygdala (CeA) and the BNST receive highly processed information from the basolateral nuclei of the amygdala and send similar downstream connections to brain structures that mediate the expression of fear and anxiety (Walker et al 2003).…”

Section: Preclinical Evidence For Dissociated Neural Systems Of Fear mentioning

confidence: 99%

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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The neuronal organization of the supracapsular part of the stria terminalis in the rat: The dorsal component of the extended amygdala

Cited by 107 publications

References 68 publications

Mifepristone in the Central Nucleus of the Amygdala Reduces Yohimbine Stress-Induced Reinstatement of Ethanol-Seeking

Mifepristone in the Central Nucleus of the Amygdala Reduces Yohimbine Stress-Induced Reinstatement of Ethanol-Seeking

Fear Memory

Models and mechanisms of anxiety: evidence from startle studies

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