The Effect of Emotional Content on Visual Recognition Memory: A PET Activation Study 1 Stephan F. Taylor,* ,2 Israel Liberzon,* , † Lorraine M. Fig,‡ Laura R. Decker,* Satoshi Minoshima,§ and Robert A. Koeppe§ *Department of Psychiatry and §Internal Medicine Division of Nuclear Medicine, University of Michigan, Ann Arbor, Michigan 48109; and †Department of Psychiatry and ‡Department of Nuclear Medicine Services, Veterans Administration Medical Center, Ann Arbor, Michigan 48109 Received November 25, 1997 The emotional content of stimuli can enhance memory for those stimuli. This process may occur via an interaction with systems responsible for perception and memory or via the addition of distinct brain regions specialized for emotion which augment mne- monic processing. We performed an 15 O PET study to identify neuroanatomical systems which encode vi- sual stimuli with strong negative emotional valence compared to stimuli with neutral valence. Subjects also performed a recognition memory task for these same images, mixed with distracters of similar emo- tional valence. The experimental design permitted us to independently test effects of emotional content and recognition memory on regional activity. We found activity in the left amygdaloid complex associated with the encoding of emotional stimuli, although this activation appeared early in the scanning session and was not detectable during recognition memory. Visual recognition memory recruited the right middle frontal gyrus and the superior anterior cingulate cortex for both negative and neutral stimuli. An interaction oc- curred between emotional content and recognition in the lingual gyrus, where greater activation occurred during recognition of negative images compared to recognition of neutral images. Instead of distinct neu- roanatomical systems for emotion augmenting memory, we found that emotionally salient stimuli appeared to enhance processing of early sensory input during vi- sual recognition.  1998 Academic Press INTRODUCTION Evolution has facilitated the development of critical capacities to distinguish salient from nonsalient stimuli. Emotions can be viewed in this evolutionary context as a behavioral repertoire which enables an organism to make appropriate responses to important environmen- tal cues (e.g., Bower 1981; Toobey and Cosmides, 1990). These capacities include better memory for salient stimuli with strong emotional content. As an extreme example of this mechanism, people often report vivid recall for significant events, e.g., where they were and what they were doing when they learned of Kennedy’s assassination (Brown and Kulik, 1977). While debate exists about the accuracy and the extent of so-called ‘‘flashbulb’’ memories (Christianson and Loftus, 1991; Heuer and Reisberg, 1990), evidence for an interaction between emotional content and memory strength is plentiful (McClosky et al., 1988; McDaniel et al., 1995; Neisser, 1982). Neurobiological investigations into emotion suggest potential neuroanatomical substrates by which stimu- lus content may modulate memory. Studies in animals and humans have demonstrated a pivotal role for the amygdaloid complex (AC) in emotional reactions (Adolphs et al., 1995; Davis, 1992; LeDoux, 1986). In fear-motivated learning, the amygdala appears to modu- late acquisition of the learned response (Gallagher and Holland, 1994; McGaugh et al., 1996). Humans with lesions of the amygdala lose the ability to acquire conditioned autonomic responses (Bechara et al., 1995) and the capacity of enhanced recall of emotional mate- rial (Cahill et al., 1995; Sarter and Markowitsch, 1985). Functional neuroimaging studies in humans have iden- tified AC activation in response to affectively loaded visual stimuli (Irwin et al., 1996; Reiman et al., 1997) and to faces with fearful expressions (Breiter et al., 1996; Morris, 1996; Phillips et al., 1997). However, few functional neuroimaging studies have tested the hypoth- 1 This work was previously presented at the XVIIIth International Symposium on Cerebral Blood Flow and Metabolism, Baltimore, June 1997. 2 To whom correspondence should be addressed at the Department of Psychiatry, University of Michigan Medical Center, UH 9D Box 0118, 1500 E. Medical Center Drive, Ann Arbor, MI 48109-0118. Fax: (734) 936-4401. E-mail: sftaylor@umich.edu. NEUROIMAGE 8, 188–197 (1998) ARTICLE NO. NI980356 188 1053-8119/98 $25.00 Copyright  1998 by Academic Press All rights of reproduction in any form reserved.