The DOI matches its Crossref record; 94 of the 94 references it cites were found in a registry or an index.
Neural systems involved in fear and anxiety measured with fear-potentiated startle.
Abstract
A good deal is now known about the neural circuitry involved in how conditioned fear can augment a simple reflex (fear-potentiated startle). This involves visual or auditory as well as shock pathways that project via the thalamus and perirhinal or insular cortex to the basolateral amygdala (BLA). The BLA projects to the central (CeA) and medial (MeA) nuclei of the amygdala, which project indirectly to a particular part of the acoustic startle pathway in the brainstem. N-methyl-D-aspartate (NMDA) receptors, as well as various intracellular cascades in the amygdala, are critical for fear learning, which is then mediated by glutamate acting in the CeA. Less predictable stimuli, such as a long-duration bright light or a fearful context, activate the BLA, which projects to the bed nucleus of the stria terminalis (BNST), which projects to the startle pathway much as the CeA does. The anxiogenic peptide corticotropin-releasing hormone increases startle by acting directly in the BNST. CeA-mediated behaviors may represent stimulus-specific fear, whereas BNST-mediated behaviors are more akin to anxiety. NMDA receptors are also involved in extinction of conditioned fear, and both extinction in rats and exposure-based psychotherapy in humans are facilitated by an NMDA-partial agonist called D-cycloserine. ((c) 2006 APA, all rights reserved).
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Citations
Cites
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Self-citationA primary acoustic startle circuit: lesion and stimulation studies
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Self-citationRole of the bed nucleus of the stria terminalis versus the amygdala in fear, stress, and anxiety
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Self-citation
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Cuthbert, B. N., & Insel, T. R. (2013) · BMC Medicine · doi:10.1186/1741-7015-11-126 · Cited by 3,053
“For instance, much is now known about circuits for fear and defense [28], for various aspects of appetitive behavior such as learning to predict reward and moving toward reward [29], and cognitive functions such as working memory [30].”
BackgroundThe Neurocircuitry of Fear, Stress, and Anxiety Disorders
Shin, L. M., & Liberzon, I. (2010) · Neuropsychopharmacology · doi:10.1038/npp.2009.83 · Cited by 2,083
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Cisler, J. M., & Koster, E. H. W. (2010) · Clinical Psychology Review · doi:10.1016/j.cpr.2009.11.003 · Cited by 1,753
Neural Mechanisms of Extinction Learning and Retrieval
Quirk, G. J., & Mueller, D. (2008) · Neuropsychopharmacology · doi:10.1038/sj.npp.1301555 · Cited by 1,645
Cuthbert, B. N. (2014) · World Psychiatry · doi:10.1002/wps.20087 · Cited by 1,377
Metadata
- Authors
- Davis, M.
- Venue
- American Psychologist
- Published
- 2006-11
- Volume
- 61
- Issue
- 8
- Pages
- 741-756
- ISSN
- 0003-066X (ISSN-L)
- 1935-990X
- OpenAlex
- W2003956791
- Cited by
- 592
- References
- 94
- FWCI
- 14.13
- Type
- journal article
- Language
- en
- Open access
- closed
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