Several previous studies have indicated that the consolidation of the memory trace may be temporally defined in terms of the degree to which post-learning electroeonvulsive shock (ECS) results in a retrograde retention deficit for the previously initiated behavior (DuNcAN, 1949; HERIOT and COT,S,~AN, 1962). Several hypotheses have been generated regarding the effect of ECS in relation to memory formation. One of these is the suggestion that those agents or events which result in an experimentally induced retrograde amnesia exert their effects through an alteration in the activity and/or concentration of central nervous system nucleic acids (Ess~AN, 1965). This suggestion has found some indirect support in a study by MIEAILOVICg et al. (1958) in which it was reported that a single ECS in cats resulted in a 20--25~ reduction in brain ribonucleic acid (I~NA). Although this observation does not necessarily explain the relationship between ECS and retrograde amnesia, or between nucleic acids and memory, it is consistent with earlier work which has shown that an intracellular loss of RNA followed insulin-induced convulsions (HYDg~, 1944) and electrical stimulation of spinal ganglion cells (HYping, 1943). More recently, CmTRV, et al. (1964) have shown that localized decrements in neural RNA followed metrazol-induced convulsions in rats. The relationship between nucleic acids and memory has more recently been emphasized by experimental work and hypotheses from HYDgN's laboratory; in this respect it has been proposed that ribonucleic acid may provide for a molecular basis of memory formation. This hypothesis has not been directly tested, and it has been one purpose of the present investigation to explore one aspect of that hypothesis. It would appear that any agent or event capable of increasing the neural stores of RNA should, as a consequence, lead to an attenuation of the amnesic effect produced by post-learning ECS. One agent which has been shown to increase neural