Abstract
I n recent years, there has been a surge of interest in research on emotional memory [7-10]. Much of this work has involved the use of classical fear-conditioning procedures, in which a relatively neutral stimulus, such as a tone or flashing light, is associatively paired with a noxious event, typically painful electric shocks delivered to the skin. After one or at most a few pairings of the neutral and the noxious stimulis, the neutral stimulus acquires aversive properties and elicits defensive or protective responses when presented alone. The fear-conditioning literature is relevant to the Focus article by Lenz and colleagues in three respects. First, something like fear conditioning is presumably going on in the patients described, in whom thalamic stimulation elicits affective responses and pain sensations, but only if the patient previously had previous experience of pain with a strong affective component. Somehow, the affective and painful experiences come to be associated, such that the recurrence of the pain sensation causes a revival of the affective reaction as well. We have a fairly good understanding about how all this comes about in the case of fear conditioning, but it is not altogether clear how it might arise in these patients. An interesting difference between fear conditioning and the learning that the patients undergo involves the role of the painful stimulus. In fear conditioning, the painful stimulus is what gives the neutral stimulus meaning. But for the patients, it is the painful stimulus that acquires conditioned meaning, if the proposed hypothesis is correct. Second, studies of fear conditioning have revealed the basic components of a neural system involved in the formation of emotional memory. This system crucially involves circuits into and within the amygdala [7,8,10]. Whether the amygdala and its connections might be involved in the affective learning that the
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