Lesions, temporal inactivation, electrical stimulation and administration of drugs that antagonize synaptic activity of the striatum lead to significant deficits of memory. Also, it has been shown that interruption of dopaminergic, GABAergic, or cholinergic activity in discrete areas of this structure is sufficient to disrupt cognitive functions. In spite of the known interactions among dopamine, GABA, acetylcholine, and serotonin, there is a notable scarcity of data germane to the participation of striatal serotonin in learning and memory. It was important, therefore, to investigate the possible involvement of serotonin in cognition. In light of the differential distribution of serotonergic elements within the striatum, a prediction was made that focal injections of serotonin into distinctive regions would produce dissimilar effects on memory. Rats were trained in a one-trial step-through inhibitory avoidance task and a retention test was carried out 24 h later. Posttraining injections of serotonin into the dorsal and ventral aspects of the posterior region produced strong amnesia compared to similar injections into the dorsal and ventral aspects of the anterior region. The present findings support the hypothesis that striatal serotonergic activity is involved in memory functions and also provide further evidence of neurochemical heterogeneity within the striatum regarding memory consolidation.

Memory is markedly impaired when normal activity of any of a number of cerebral structures is disturbed after a learning experience. A growing body of evidence indicates, however, that such interference with neuronal function becomes negligible when the learning experience is significantly enhanced. We now report on the effects of enhanced training on retention after temporary inactivation of cerebral nuclei known to be involved in memory, namely the substantia nigra (SN), striatum (STR), and amygdala (AMY). When training was conducted with a relatively low intensity of footshock (1.0 mA), post-training infusion of lidocaine into the SN, STR, or AMY produced a marked memory deficit. Increasing the aversive stimulation to 2.0 mA protected memory from the amnesic effect of intranigral lidocaine, but there was still a deficit after its infusion into the STR and AMY. Administration of lidocaine into each of these nuclei, in the groups that had been trained with 3.0 mA, was completely ineffective in producing alterations in memory consolidation. Simultaneous infusion of lidocaine into STR + SN, AMY + SN, or AMY + STR was also ineffective in altering memory formation when the highest footshock intensity was used for training. To our knowledge, this is the first demonstration that an enhanced learning experience guards against memory deficits after simultaneous temporary interruption of neural activity of brain nuclei heretofore thought to be necessary for memory formation. These findings support the proposition that brain structures involved in memory processing are functionally connected in series during memory consolidation and that, after an enhanced learning experience, these structures become functionally connected in parallel.

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