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Related Experiment Videos

Angst and the amygdala.

Jay Schulkin1

  • 1Department of Physiology and Biophysics, Georgetown University, School of Medicine, Washington, DC, USA. jschulkin@acog.org

Dialogues in Clinical Neuroscience
|February 13, 2007
PubMed
Summary
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Excessive fear, linked to mental health issues, involves the amygdala and corticotropin-releasing hormone (CRH). Glucocorticoids amplify CRH, potentially causing anxious depression with sustained exposure.

Area of Science:

  • Neuroscience
  • Psychiatry
  • Endocrinology

Background:

  • Fear is an adaptive response to danger.
  • Excessive fear contributes to mental anguish and pathology.
  • The amygdala and corticotropin-releasing hormone (CRH) are implicated in adversity.
  • CRH is localized in the central nucleus of the amygdala.

Purpose of the Study:

  • To explore the neural mechanisms underlying excessive fear and anxiety.
  • To investigate the role of the amygdala and CRH in fear responses.
  • To understand the influence of glucocorticoids on CRH production and anxiety.

Main Methods:

  • Review of neurobiological and psychiatric literature.
  • Analysis of the role of the amygdala in fear processing.

Related Experiment Videos

  • Examination of the function of corticotropin-releasing hormone (CRH) in the central amygdala.
  • Investigation of glucocorticoid effects on CRH.

    • Main Results:

    • The amygdala is a key neural site for processing adversity.
    • Corticotropin-releasing hormone (CRH) is centrally localized within the amygdala.
    • Glucocorticoids enhance CRH production in the amygdala.
    • Sustained elevation of CRH may contribute to anxious depression.

    Conclusions:

    • The amygdala-CRH system plays a critical role in fear and anxiety.
    • Glucocorticoid regulation of amygdala CRH is a potential mechanism for anxiety disorders.
    • Understanding this pathway may inform treatments for anxious depression.