ORIGINAL ARTICLE Cold Pressor ‘‘Augmentation’’ Does Not Differentially Improve Treatment Response for Spider Phobia Norman B. Schmidt • J. Anthony Richey • Ann P. Funk • Melissa A. Mitchell Published online: 1 May 2010 Ó Springer Science+Business Media, LLC 2010 Abstract An emerging literature suggests that memory enhancement may augment the effects of learning-based treatments such as cognitive behavioral therapy. Release of stress hormones, such as cortisol, has been shown to enhance memory. In this report, we evaluated whether a cold pressor stressor (CPS), which reliably generates stress hormones, may also augment treatment for specific pho- bias. Spider phobics were randomly assigned to CPS or warm water bath following a standardized session of exposure therapy. Inconsistent with our hypothesis, the CPS condition showed no significant enhancement in fear reduction compared to the control condition. Keywords Spider phobia Á Cold pressor stress Á Fear Á Stress hormones Introduction Glucocorticoid stress hormones including cortisol have been shown to modulate the consolidation of memories immediately preceding and including the precipitating stressor (Abercrombie et al. 2003; Beckwith et al. 1986; Buchanan and Lovallo 2001; Andreano and Cahill 2006). A variety of methods for stimulating the release of endogenous glutocorticoids have been documented, including the administration of exogenous hormones (e.g. Stark et al. 2006), as well as behavioral stressors including the Trier Social Stress Test (McRae et al. 2006) and Cold Pressor Stressor (CPS; Lovallo 1975). The CPS is a brief but reliable method of stimulating the release of endoge- nous glucocorticoid stress hormones (Cahill et al. 2003), which has been shown to facilitate the consolidation of memory (Andreano and Cahill 2006). The current study tested the hypothesis that random assignment to the CPS (vs. warm water bath) immediately subsequent to suc- cessful exposure therapy for specific phobia would result in enhanced memory for the treatment event, and therefore augment the effect of exposure therapy. Recent evidence suggests that endogenous stress hor- mones including cortisol modulate the encoding and con- solidation of memory (Buchanan and Lovallo 2001; Cahill and Alkire 2003; Cahill et al. 2003; Wolf 2008) by stim- ulating the basolateral (BL) nucleus of the amygdala, a region known to modulate the consolidation of memory in conjunction with the stria terminalis (Roozendaal and McGaugh 1996; Tomaz et al. 1992). The BL projects directly into the hippocampus and entorhinal cortex (Amaral et al. 1992), placing it comparatively ‘‘upstream’’ of circuits known to act directly on the long-term storage of experiential memory. Early research showed that infusion of drugs and hormones directly into the BL region after training facilitated memory storage (Liang et al. 1986; McGaugh et al. 1988), and more recent evidence suggests that the endogenous activity of stress hormones represents a key modulator of memory consolidation for emotional experiences. In particular, results strongly suggest that cortisol enhances fear extinction (Cai et al. 2006). N. B. Schmidt (&) Á A. P. Funk Á M. A. Mitchell Department of Psychology, Florida State University, Tallahassee, FL 32306-4301, USA e-mail: schmidt@psy.fsu.edu J. Anthony Richey Neurodevelopmental Disorders Research Center, University of North Carolina, Chapel Hill, NC 27599, USA J. Anthony Richey Brain Imaging and Analysis Center, Duke University, Durham, NC 27705, USA 123 Cogn Ther Res (2010) 34:413–420 DOI 10.1007/s10608-010-9310-6