The process of memory consolidation, initially formulated as a period of perseverative neural activity following learning within which the memory trace was still vulnerable to disruptive influences,l has received considerable attention within the past several years. A variety of agents or events have been shown to possess properties capable of disrupting the consolidation process, to the extent that, when they are presented in close temporal proximity with a training or learning experience, a resulting subsequent retention deficit for this experience is manifested. The consolidation period, usually defined within the limits of the posttraining interval within which disruption occurs, has been considered as lasting only seconds or even, perhaps, hours. While there is evidence for a temporal gradient for such retrograde amnesia, i.e., a decreased amnesic effect as a function of increased training-disruptive interval between stimuli, differences in the definition of such a temporal gradient and in the duration of the consolidation period appear dependent on species, age, training experience and the parameters therof, the nature and intensity of the disruptive conditions, and the measures utilized to assess both retention and amnesia. All these obvious variables, in addition to others that are perhaps not so obvious, appear to have as a common denominator of the retention-amnesia behavioral result, a series of molecular events associated with cellular or multicellular processes operative in the fixation, storage, and retrieval of information, as well as with the disruption of the memory consolidation process; the latter seems to imply that, with consolidation not completed, storage and retrieval are precluded. One macromolecular unit that appears to fit some of the requirements of consolidation and storage is ribonucleic acid (RNA), which has found favor in several memory schemata,* serving as a possible molecular component of a memory input and storage signal system. One would thus expect that behavioral differences could account for differences in molecular structure components,3 synthesi~,~ and con-centration6 in regional sites within the central nervous system that are presumably responsive either to input modifications characterizing behavioral differences or to changes in stimulation.6 Disruption of memory fixation would thereby also involve either identical or related molecular changes. With regard *This paper was presented at a meeting