cerebroventricularly after training. Dose-response curves with PREG, PREGS, and DHEA, showed PREGS to be most potent, with significant ME occurring at 3.5 x 10-15 moles/mouse (5).

Test substances were administered after training so that they could not affect acquisition. Retention was tested 1 wk later so that retention of test performance would not be directly affected by their administration. Lack of differences in escape latencies between vehicle controls and mice receiving test substance indicated that ME in mice receiving the steroids was not attributable to proactive motor facilitatory effects of the steroids. Because the substances tested could not directly affect performance during either training or testing, the changes in retention test performance are interpreted as being the result of changes in memory processing occurring shortly after training.

Substances administered intracerebroventricularly penetrate to several brain regions. Prior to attempting to define mechanisms of action of PREGS, it was necessary to determine whether or not regional differences exist in sensitivity to its action so as to help identify the neural circuitry most importantly involved. Memory-active substances (enhancing or inhibitory) generally have produced differing effects when injected into structures of the forebrain limbic system, e.g., mammillary bodies, septum, amygdala, and hippocampus (see 9,10). The latter regions, which are implicated variously in learning as exemplified by retention of FAAT, differ in structure and in distribution of neurotransmitter and neuromodulator systems. Tests of retention of FAAT were made in mice after post-training injection of PREGS into the aforementioned structures. In addition, injections were made into the caudate nucleus, a part of the basal ganglia, as a "control" region, in the sense that it is not considered to play a specific role in retention of learning of conditioned fear responses.

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