Advertisement
Commentary| Volume 73, ISSUE 11, P1043-1044, June 01, 2013

Fear and Anxiety Take a Double Hit From Vagal Nerve Stimulation

  • Michael S. Fanselow
    Correspondence
    Address correspondence to Michael S. Fanselow, Ph.D., Department of Psychology, 405 Hilgard Avenue, University of California, Los Angeles, California 90095-1563
    Affiliations
    Departments of Psychology and Psychiatry and Biobehavioral Sciences, UCLA Integrative Center for Learning and Memory, University of California, Los Angeles, California
    Search for articles by this author
      At the forefront of translational research to combat anxiety disorders is the idea of developing neuroscience-based adjuncts to traditional exposure-based treatment such as cognitive/behavioral therapy. The core concept of exposure therapy is Pavlovian extinction, in which an anxiety-triggering stimulus is repeatedly presented so that that the patient learns that the stimulus predicts no negative consequences. This new association acts to inhibit the anxiety normally provoked by the stimulus. On its own, such exposure is quite effective, but it has some limitations. After exposure therapy, fear of the extinguished stimulus may return because of a stressful experience, a long passage of time since encountering the stimulus, or confronting the fear-provoking stimulus in a novel environment (
      • Bouton M.E.
      Context, ambiguity, and unlearning: sources of relapse after behavioral extinction.
      ). Additionally in some anxiety disorders, notably posttraumatic stress disorder, extinction learning itself is compromised (
      • Myers K.M.
      • Davis M.
      Mechanisms of fear extinction.
      ). The idea of neuroscience-based adjuncts given during exposure treatment is to overcome this limitation by either strengthening the extinction learning itself or changing its nature. An example of the strengthening strategy is the use of d-cycloserine (DCS) to facilitate the N-methyl-D-aspartate–mediated plasticity that normally mediates memory formation (
      • Myers K.M.
      • Davis M.
      Mechanisms of fear extinction.
      ). To change the nature of extinction, researchers have administered extinction training during periods when the original fear memory lacks stability because it was very recently encoded or reactivated (
      • Myers K.M.
      • Davis M.
      Mechanisms of fear extinction.
      ,
      • Monfils M.-H.
      • Cowansage K.K.
      • Klann E.
      • LeDoux J.E.
      Extinction-reconsolidation boundaries: key to persistent attenuation of fear memories.
      ).
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Biological Psychiatry
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      Reference

        • Bouton M.E.
        Context, ambiguity, and unlearning: sources of relapse after behavioral extinction.
        Biol Psychiatry. 2002; 52: 976-986
        • Myers K.M.
        • Davis M.
        Mechanisms of fear extinction.
        Mol Psychiatry. 2007; 12: 120-150
        • Monfils M.-H.
        • Cowansage K.K.
        • Klann E.
        • LeDoux J.E.
        Extinction-reconsolidation boundaries: key to persistent attenuation of fear memories.
        Science. 2009; 324: 951-955
        • Peña D.F.
        • Engineer N.D.
        • McIntyre C.K.
        Rapid remission of conditioned fear expression with extinction training paired with vagus nerve stimulation.
        Biol Psychiatry. 2013; 73: 1071-1077
        • Berlau D.J.
        • McGaugh J.L.
        Enhancement of extinction memory consolidation: the role of the noradrenergic and GABAergic systems within the basolateral amygdala.
        Neurobiol Learn Mem. 2006; 86: 123-132
        • Cain C.K.
        • Blouin A.M.
        • Barad M.
        Adrenergic transmission facilitates extinction of conditional fear in mice.
        Learn Mem. 2004; 11: 179-187
        • Clem R.L.
        • Huganir R.L.
        Calcium-permeable AMPA receptor dynamics mediate fear memory erasure.
        Science. 2010; 330: 1108-1112
        • Woods A.M.
        • Bouton M.E.
        D-cycloserine facilitates extinction but does not eliminate renewal of the conditioned emotional response.
        Behav Neurosci. 2006; 120: 1159-1162
        • Orsini C.A.
        • Maren S.
        Neural and cellular mechanisms of fear and extinction memory formation.
        Neurosci Biobehav Rev. 2012; 36: 1773-1802
        • Zelikowsky M.
        • Hast T.A.
        • Bennett R.Z.
        • Merjanian M.
        • Nocera N.A.
        • Ponnusamy R.
        • Fanselow M.S.
        Cholinergic blockade frees fear extinction from its contextual dependency.
        Biol Psychiatry. 2013; 73: 345-352

      Linked Article

      • Rapid Remission of Conditioned Fear Expression with Extinction Training Paired with Vagus Nerve Stimulation
        Biological PsychiatryVol. 73Issue 11
        • Preview
          Fearful experiences can produce long-lasting and debilitating memories. Extinction of conditioned fear requires consolidation of new memories that compete with fearful associations. In human subjects, as well as rats, posttraining stimulation of the vagus nerve enhances memory consolidation. Subjects with posttraumatic stress disorder show impaired extinction of conditioned fear. The objective of this study was to determine whether vagus nerve stimulation (VNS) can enhance the consolidation of extinction of conditioned fear.
        • Full-Text
        • PDF