from the AC. However, based on anatomical considerations alone (cf. Krettek & Price, 1978), other brain sites including neocortex and thalamic nuclei may also receive a memory-modulatory influence via innervation from the AC. Further research is necessary to examine the range of brain structures that may receive a modulatory influence from the AC, as well as the interactions among these sites.
Although the hypothesis that the AC is a critical component of a memory modulatory system is strongly supported by considerable experimental evidence, some findings are consistent with an alternative hypothesis that the AC is a critical structure mediating local changes in plasticity underlying learned behavior. This latter view is primarily supported by studies examining the role of the AC in fear-motivated learning (e.g. Davis, 1986; LeDoux et al., 1988), as well as findings indicating that the AC may play a selective role in the storage of second-order stimulus-reward associations ( Everitt, Cador, & Robbins, 1989; Gaffan & Harrison, 1987; McDonald & White, 1993).
In studies of fear-motivated learning and second-order conditioning, AC damage severely impairs task acquisition. These findings stand in contrast to our suggestion that one characteristic of a modulatory memory system is that it is not critically necessary for learning to occur. However, although the "modulatory" and '"essential circuit" views of the role of the AC in memory may not appear compatible, we have no a priori reason to believe that they are mutually exclusive for all tasks. The hypothesis that the AC plays a modulatory role in memory does not necessarily exclude an additional storage role in memory for some learning tasks. However, it is important to reiterate that the time-dependent nature of AC involvement in memory storage has not been extensively studied in tasks in which amygdala damage impairs acquisition.
Finally, consideration of the anatomical relationships among various AC nuclei and their target structures may be important in distinguishing possible storage and modulation mnemonic functions of the AC. Thus, functional manipulations of discrete AC nuclei may prove useful in determining whether these two hypothesized roles of the AC in memory are mediated by a differential involvement of separate AC nuclei.
Research supported by NRSA 1 F32 NS08973-01 from NINDS (MP), National Science Foundation grant BNS-90006175 and University of California Presidents Fellowship (CLW), NIA Institutional NRSA AG00096 (LC), and U.S. Public Health Service grant MH12526 from National Institute for Mental Health (NIMH) and National Institute on Drug Abuse (NIDA) (JLM).