Panel: The Science of Memory and Emotion
"How Developing Memory Systems
"How Developing Memory Systems
Jocelyne H. Bachevalier, Ph.D., is Associate Professor in the Department of Neurobiology and Anatomy at the University of Texas Health Science Center in Houston.
An important discovery made in recent years is that memory involves different mechanisms subserved by separate brain circuits. Declarative, or explicit, memory involves structures in the medial temporal lobe, medial diencephalon, and ventral portion of the prefrontal cortex. Procedural, or implicit, memory involves the neostriatum and cerebellum.
This dissociation between memory mechanisms gave us a novel on the development of memory in both animals and humans. Now we could ask, Do these memory systems develop at different times during maturation? If one system has a more protracted development, could this be due to a slow development of brain areas serving those memory processes?
A number of studies of infant monkeys suggests that the answer to both questions is yes. We tested infant monkeys, at different ages, with tasks that measured different forms of memory and compared their performance to that of animals that had received specific lesions of the brain, such as the ventral prefrontal cortex and hippocampal formation. Damage to these two areas in adult monkeys results in severe loss of declarative memory while procedural memory is preserved.
We found that recognition memory (that is, the ability to learn that a new object is rewarded with food on any given trial) improves slowly after birth. The poorer performance of the youngest monkeys on this task was similar to that of adult animals with ventral prefrontal lesions but not those with hippocampal lesions, who performed normally. This suggests that the ventral prefrontal cortex may not be fully functional during the first months of life in monkeys.
The ability to learn new associations between events, furthermore, which is known to be impaired by hippocampal lesions but not ventral prefrontal cortex lesions, is clearly retarded up to the end of the first postnatal year, indicating a protracted maturation of the hippocampal formation. By contrast, on tasks measuring procedural memory, monkeys as young as three months of age could perform as efficiently as adults. These developmental behavioral findings thus indicate that the different types of memory processes found in adult animals are developmentally dissociable and allow us to make inferences on the maturation of the neural structures underlying these processes.
Similar dissociation of memory processes also is found in human children. Procedural memory emerges very early after birth, while associative memory emerges later, around age four or five. The close parallel between the developmental time course of memory processes in infant monkeys and human infants enables us to infer much about brain maturation in human infants.
After we learned that declarative memory processes emerge late in development, we asked what would happen to an animal or human being if this powerful memory system were dysfunctional at birth. The traditional views of brain development held that localized brain injury occurring early in life has little effect on cognitive development. The belief has been that there is sufficient plasticity in the immature neural systems to allow for compensation and, therefore, relatively normal development. Thus, one outcome could be that such an early neural insult may result in little memory loss.
Indeed, at the time we began our experiments, there was no indication of severe global anteretrograde amnesia in children. Nevertheless, we conjectured that such memory deficit could exist in infancy but be masked by other severe changes in behavior because at this early age children have to learn not only about the world, but also how to emotionally and socially react to their environment. As a result, such profound memory loss also would result in poor emotional and social skills. To check this hypothesis, we tested newborn monkeys with damage to the medial temporal lobe several times from birth to adulthood in tasks measuring the development of their learning and memory abilities as well as their emotional reactions and social interactions with normal peers.
As we predicted, and contrary to the traditional views of recovery of functions, we found that infant monkeys with damage to their medial temporal region showed severe and long-lasting memory losses and a host of behavioral abnormalities that were not evident in early infancy but became progressively more debilitating as the animals matured.
We believe that the similarity in the development of cognitive memory functions in infant monkeys and human infants, together with the fact that infant monkeys--as human infants--display complex emotional and social behavior, indicate that infant primates can provide excellent experimental models. We can use these models to assess and understand the errors of central nervous system development that can cause children to become learning-disabled, dyslexic, autistic, schizophrenic, or mentally retarded. If successful, such models may serve as a point of departure for many future studies aimed at searching for the causes of early neuropathology, such as genetic defects, maternal intoxication, anoxia, and toxic agents, as well as a search for possible treatments.
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