scholarly journals Amygdala and bed nucleus of the stria terminalis: differential roles in fear and anxiety measured with the acoustic startle reflex

1997 ◽  
Vol 352 (1362) ◽  
pp. 1675-1687 ◽  
Author(s):  
◽  
Michael Davis ◽  
David L. Walker ◽  
Younglim Lee
Keyword(s):  
Excitatory Amino Acid ◽  
Conditioned Fear ◽  
Acoustic Startle ◽  
Acoustic Startle Reflex ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Amino Acid Receptors ◽  
Sensory Modalities ◽  
Behavioural Tests ◽  
Fear And Anxiety

Neural stimuli associated with traumatic events can readily become conditioned so as to reinstate the memory of the original trauma. These conditioned fear responses can last a lifetime and may be especially resistant to extinction. A large amount of data from many different laboratories indicate that the amygdala plays a crucial role in conditioned fear. The amygdala receives information from all sensory modalities and projects to a variety of hypothalamic and brainstem target areas known to be critically involved in specific signs that are used to define fear and anxiety. Electrical stimulation of the amygdala elicits a pattern of behaviours that mimic natural or conditioned states of fear. Lesions of the amygdala block innate or conditioned fear and local infusion of drugs into the amygdala have anxiolytic effects in several behavioural tests. Excitatory amino acid receptors in the amygdala are critical for the acquisition, expression and extinction of conditioned fear.

scholarly journals Bed nucleus of the stria terminalis regulates fear to unpredictable threat signals

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Travis D Goode ◽  
Reed L Ressler ◽  
Gillian M Acca ◽  
Olivia W Miles ◽  
Stephen Maren
Keyword(s):  
Conditioned Fear ◽  
Stria Terminalis ◽  
Conditioned Stimuli ◽  
Variable Intensity ◽  
Reversible Inactivation ◽  
Bed Nucleus ◽  
Defensive Behaviors ◽  
The Us ◽  
Specific Factors ◽  
Fear And Anxiety

The bed nucleus of the stria terminalis (BNST) has been implicated in conditioned fear and anxiety, but the specific factors that engage the BNST in defensive behaviors are unclear. Here we examined whether the BNST mediates freezing to conditioned stimuli (CSs) that poorly predict the onset of aversive unconditioned stimuli (USs) in rats. Reversible inactivation of the BNST selectively reduced freezing to CSs that poorly signaled US onset (e.g., a backward CS that followed the US), but did not eliminate freezing to forward CSs even when they predicted USs of variable intensity. Additionally, backward (but not forward) CSs selectively increased Fos in the ventral BNST and in BNST-projecting neurons in the infralimbic region of the medial prefrontal cortex (mPFC), but not in the hippocampus or amygdala. These data reveal that BNST circuits regulate fear to unpredictable threats, which may be critical to the etiology and expression of anxiety.

scholarly journals Bed nucleus of the stria terminalis regulates fear to unpredictable threat signals

2018 ◽  
Author(s):  
Travis D. Goode ◽  
Reed L. Ressler ◽  
Gillian M. Acca ◽  
Olivia W. Miles ◽  
Stephen Maren
Keyword(s):  
Conditioned Fear ◽  
Stria Terminalis ◽  
Variable Intensity ◽  
Reversible Inactivation ◽  
Bed Nucleus ◽  
Defensive Behaviors ◽  
The Us ◽  
Specific Factors ◽  
Fear And Anxiety ◽  
Pathological Anxiety

ABSTRACTThe bed nucleus of the stria terminalis (BNST) has been implicated in conditioned fear and anxiety, but the specific factors that engage the BNST in defensive behaviors are unclear. Here we examined whether the BNST mediates freezing to conditioned stimuli (CSs) that poorly predict the onset of aversive unconditioned stimuli (USs) in rats. Reversible inactivation of the BNST selectively reduced freezing to CSs that poorly signaled US onset (e.g., a backward CS that followed the US), but did not eliminate freezing to forward CSs even when they predicted USs of variable intensity. Additionally, backward (but not forward) CSs selectively increased Fos in the ventral BNST and in BNST-projecting neurons in the infralimbic region of the medial prefrontal cortex (mPFC), but not in the hippocampus or amygdala. These data reveal that BNST circuits regulate fear to unpredictable threats, which may be critical to the etiology and expression of anxiety.IMPACT STATEMENTThe bed nucleus of the stria terminalis (BNST) is required for the expression of defensive behavior to unpredictable threats, a function that may be central to pathological anxiety.

scholarly journals CART neuropeptide modulates the extended amygdalar CeA-vBNST circuit to gate expression of innate fear

2016 ◽  
Author(s):  
Abhishek Rale ◽  
Ninad Shendye ◽  
Devika S Bodas ◽  
Nishikant Subhedar ◽  
Aurnab Ghose
Keyword(s):  
Conditioned Fear ◽  
Stria Terminalis ◽  
Fear Response ◽  
Bed Nucleus ◽  
Freezing Response ◽  
Central Processing ◽  
Panic Disorders ◽  
Local Levels ◽  
Innate Fear ◽  
Excitatory Drive

ABSTRACTInnate fear is critical for the survival of animals and is under tight homeostatic control. Deregulation of innate fear processing is thought to underlie pathological phenotypes including, phobias and panic disorders. Although central processing of conditioned fear has been extensively studied, the circuitry and regulatory mechanisms subserving innate fear remain relatively poorly defined.In this study, we identify cocaine- and amphetamine-regulated transcript (CART) neuropeptide signaling in the central amygdala (CeA) - ventral bed nucleus of stria terminalis (vBNST) axis as a key modulator of innate fear expression. 2,4,5-trimethyl-3-thiazoline (TMT), a component of fox faeces, induces a freezing response whose intensity is regulated by the extent of CART-signaling in the CeA neurons. Abrogation of CART activity in the CeA attenuates the freezing response and reduces activation of vBNST neurons. Conversely, ectopically elevated CART signaling in the CeA potentiates the fear response concomitant with enhanced vBNST activation. We show that local levels of CART signaling modulate the activation of CeA neurons by NMDA receptor-mediated glutamatergic inputs, in turn, regulating activity in the vBNST.This study identifies the extended amygdalar CeA-vBNST circuit as a CART modulated axis encoding innate fear. CART signaling regulates the glutamatergic excitatory drive in the CeA-vBNST circuit, in turn, gating the expression of the freezing response to TMT.

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