Pretraining and Reminder Treatments
The effects of pretraining have been studied rather extensively with a wide range of amnesic treatments, which have included direct electrical stimulation of the cortex, hypothermia, electroconvulsive shock (ECS), intrahippocampal injections of AP5 (an NMDA antagonist), and more recently protein synthesis inhibition (e.g., Gold, Bueno, and McGaugh, 1973; Jensen and Riccio, 1970; Lewis, Miller, and Misanin, 1968; Nader, Schafe, and Le Doux, 2000; Roesler et al., 1998; Sara and David-Remacle, 1974). However, studies involving pretraining are limited with regard to amnesia produced by brain lesions, and the experiments that have been conducted have led to inconsistent findings (for a review, see Olton and Markowska, 1989).
In addition, numerous studies have shown that presenting a reminder treatment prior to testing (e.g., brief exposure to the conditional stimulus or the apparatus) can lead to the reactivation of a presumably inaccessible memory (e.g., Riccio and Richardson, 1984; Spear, 1973). The effects of reminder treatments have been examined in experiments involving hippocampal lesions (e.g., Land, Bunsey, and Riccio, 2000); however, our study is the only one to examine the effect of reminder treatments on perirhinal/entorhinal-lesioned rats (Hanson, Bunsey, and Riccio, 2002).
Our study (Hanson, Bunsey, and Riccio, 2002) found that pretraining rats on the Bunsey digging task did not protect them from amnesia induced by a perirhinal/entorhinal lesion, and, as expected, fornix-lesioned rats did not differ from controls (the hippocampal formation presumably is not needed for simple odor discriminations, so fornix and controls should remember fine). However, the reminder treatment findings are interesting in that they show an improvement in performance for animals that are not impaired (i.e., fornix and control rats) as well as those exhibiting severe memory impairments (i.e., PRER-lesioned rats). All rats performed better after receiving a reminder treatment, even rats that had severe memory impairments on the previous trial (before the reminder treatment). Alternative explanations, like new learning or motor impairments, are controlled for with the reminder treatment paradigm, so it appears that the improvement is due to the reminder treatment and not other, less interesting, factors. It is quite remarkable that severely impaired rats with brain lesions are able to recall previously learned information after a simple reminder treatment.
Other questions for future research:
Are pretraining manipulations more effective at reducing amnesia when the amnesia-producing agents are less destructive (e.g., neurotoxic rather than electrolytic or aspiration lesions, or even drug injections)? Or when more (or less) time lapses between pretraining and the amnesic insult?
Do smaller lesions preserve the effects of pretraining manipulations?
What effects do pretraining and reminder treatments have on amnesia for a spatial task (e.g., the Sand Maze or Morris Water Maze)? Or a nonspatial task that is relational, or nonrelational?