“…But they would contribute only a small fraction to the total information stored in cortical cell assemblies. As discussed in more detail by Miller (1991Miller ( , 1993 and Kuroda (1991), this idea is compatible with many experimental and clinical observations (e.g., Kimble, 1963;Gaffan, 1974Gaffan, , 1977O'Keefe and Nadel, 1978;Olton et al, 1979Olton et al, , 1980Hirsh, 1980;Winocur, 1980;Weiskrantz, 1982;Mishkin et al, 1984;Rawlins, 1985;Aggleton et al, 1986;Squire, 1986Squire, , 1987Loechner and Weisz, 1987;Parkinson et al, 1988;Squire et al, 1988;George et al, 1989;Ridley et al, 1989;Sutherland and Rudy, 1989;Sutherland and McDonald, 1990), but also related to other theoretical models for the hippocampus (e.g., Marr 1971 ;Wickelgren, 1979Wickelgren, , 1992McNaughton, 1988;Miller 1989Miller , 1993. For example, anterograde amnesia, which is typically induced by hippocampal lesions in humans, is a loss of the ability to store new information that is typically complex and multimodal and thus might require the recruitment of "chunking" subassemblies in cortical association areas.…”