Bed nucleus of the stria terminalis NMDA receptors and nitric oxide modulate contextual fear conditioning in rats

Hott, Sara C.; Gomes, Felipe V.; Uliana, Daniela L; Vale, Gabriel Tavares do; Tirapelli, Carlos Renato; Resstel, Leonardo Barbosa Moraes

doi:10.1016/j.neuropharm.2016.05.022

Cited by 23 publications

(26 citation statements)

References 55 publications

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“…BNST function in fear conditioning: stimulus modality and duration BNST lesions (whether permanent or temporary) do not universally blunt somatic, autonomic, or hormonal responses during fear conditioning. Rather, several studies have now demonstrated a necessary role for the BNST in the learning and/or expression of contextual-but not discretely cued-fear, as indexed by freezing, conditioned suppression, potentiated startle, and stress hormone release (LeDoux et al 1988;Hitchcock and Davis 1991;Lee and Davis 1997;Gewirtz et al 1998;Sullivan et al 2004;Waddell et al 2006;Resstel et al 2008;Duvarci et al 2009;Poulos et al 2010;Zimmerman and Maren 2011;Hott et al 2012Hott et al , 2017Sink et al 2013a;Davis and Walker 2014;Goode et al 2015b;Asok et al 2016). Relatedly, electrical stimulation of the BNST can either increase or decrease conditioned contextual fear (as assessed by freezing or startle amplitude), effects that depend on the location, intensity, and frequency of the stimulation (Luyck et al 2017; also, see Baas et al 2014;Luyck and Luyten 2015).…”

Section: Bnst Function In Response To Unconditioned Aversive Stimulimentioning

confidence: 99%

Role of the bed nucleus of the stria terminalis in aversive learning and memory

Goode

2017

Learn. Mem.

121

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Surviving threats in the environment requires brain circuits for detecting (or anticipating) danger and for coordinating appropriate defensive responses (e.g., increased cardiac output, stress hormone release, and freezing behavior). The bed nucleus of the stria terminalis (BNST) is a critical interface between the "affective forebrain"-including the amygdala, ventral hippocampus, and medial prefrontal cortex-and the hypothalamic and brainstem areas that have been implicated in neuroendocrine, autonomic, and behavioral responses to actual or anticipated threats. However, the precise contribution of the BNST to defensive behavior is unclear, both in terms of the antecedent stimuli that mobilize BNST activity and the consequent defensive reactions. For example, it is well known that the BNST is essential for contextual fear conditioning, but dispensable for fear conditioning to discrete conditioned stimuli (CSs), at least as indexed by freezing behavior. However, recent evidence suggests that there are circumstances in which contextual freezing may persist independent of the BNST. Furthermore, the BNST is involved in the reinstatement (or relapse) of conditioned freezing to extinguished discrete CSs. As such, there are critical gaps in understanding how the BNST contributes to fundamental processes involved in Pavlovian fear conditioning. Here, we attempt to provide an integrative account of BNST function in fear conditioning. We discuss distinctions between unconditioned stress and conditioned fear and the role of BNST circuits in organizing behaviors associated with these states. We propose that the BNST mediates conditioned defensive responses-not based on the modality or duration of the antecedent threat or the duration of the behavioral response to the threat-but rather as consequence the ability of an antecedent stimulus to predict when an aversive outcome will occur (i.e., its temporal predictability). We argue that the BNST is not uniquely mobilized by sustained threats or uniquely involved in organizing sustained fear responses. In contrast, we argue that the BNST is involved in organizing fear responses to stimuli that poorly predict danger will occur, no matter the duration, modality, or complexity of those stimuli. The concepts discussed in this review are critical to understanding the contribution of the human BNST to fear and anxiety disorders.

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Section: Bnst Function In Response To Unconditioned Aversive Stimulimentioning

confidence: 99%

Role of the bed nucleus of the stria terminalis in aversive learning and memory

Goode

2017

Learn. Mem.

121

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“…To further investigate whether Co-derived cells contributed to specific circuits, we focused on their contribution to the BNST, which organization and function has been recently investigated (Asok, Schulkin, & Rosen, 2016;Choi et al, 2007;Daldrup, Lesting, Meuth, Seidenbecher, & Pape, 2016;Dong, Petrovich, & Swanson, 2001;Geng et al, 2016;Hott et al, 2016;Kim et al, 2013). The BNST is a complex structure which comprise a large number of subdivisions that are difficult to identify on anatomical criterions (Bayer, 1987;Ju & Han, 1989).…”

Section: Co-derived Neurons Contribute To Nuclei That Mediate Anxiementioning

confidence: 99%

“…Indeed, even though the internal capsule is only present in mammals, cells with a molecular identity similar to Co cells have been also identified in avian and reptile embryos (Bielle, Marcos‐Mondejar, Keita, et al, ; Bielle, Marcos‐Mondéjar, Leyva‐Díaz, et al, 2011; Bupesh, Abellán, & Medina, ). Moreover, gene expression studies suggest contribution of LGE derivatives to the central and extended amygdala, evolutionarily conserved superstructures located in the subpallium that contain neurons of different developmental origin and are involved in fear and anxiety control (Hott et al, ; Ranjan et al, ) and anxiety (Geng et al, ; Morano, Bailey, Cahill, & Dumont, ; Ventura‐Silva et al, ). These observations raised the intriguing possibility that guidepost might be an acquired function for Co cells, which would have a distinct, evolutionary conserved role.…”

Section: Introductionmentioning

confidence: 99%

Tangential migration of corridor guidepost neurons contributes to anxiety circuits

Tinterri

Deck

Keita

et al. 2017

J of Comparative Neurology

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In mammals, thalamic axons are guided internally toward their neocortical target by corridor (Co) neurons that act as axonal guideposts. The existence of Co-like neurons in non-mammalian species, in which thalamic axons do not grow internally, raised the possibility that Co cells might have an ancestral role. Here, we investigated the contribution of corridor (Co) cells to mature brain circuits using a combination of genetic fate-mapping and assays in mice. We unexpectedly found that Co neurons contribute to striatal-like projection neurons in the central extended amygdala. In particular, Co-like neurons participate in specific nuclei of the bed nucleus of the stria terminalis, which plays essential roles in anxiety circuits. Our study shows that Co neurons possess an evolutionary conserved role in anxiety circuits independently from an acquired guidepost function. It furthermore highlights that neurons can have multiple sequential functions during brain wiring and supports a general role of tangential migration in the building of subpallial circuits.

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“…In particular, control of the cardiovascular responses induced by stress involves the BNST Resstel et al, 2008). Recent studies have indicated that nitrergic neurotransmission acting via activation of the neuronal isoform of the NOS enzyme (nNOS) is a prominent local neurochemical mechanism involved in the control of stress-evoked cardiovascular responses exerted by the BNST (Barretto- de-Souza et al, 2018;Hott et al, 2017). For instance, blockade of nNOS, as well as of signalling mechanisms related to NO effects such as soluble guanylyl cyclase (sGC) and PKG, within the BNST, enhanced tachycardia and decreased the drop in tail skin temperature evoked by acute restraint stress (Barretto-de-Souza et al, 2018).…”

Section: Introductionmentioning

confidence: 99%