![]() ![]() A hypothesis implicating the hippocampus rests on findings, also from animal studies, and on the fact that infants exhibit high levels of hippocampal neurogenesis (together with an inability to form lasting memories). One candidate is the hippocampus, because of its role in memory, especially declarative memory in animal research. Neuroscientific interpretations as to why infants may not recall events later in life have arisen in recent years based on evidence that the neural circuitry of the brain has not become full functional. Another interpretation holds that the sort of memory under consideration is a retrieval problem. Perhaps this not surprising given that, for example, objects may appear much larger and offer different affordances than is the case for adults. And it does seem strange that adults have only a few recollections of early childhood despite the fact that they engage in very active forms of learning. ![]() One is that the memory loss is due to a storage problem such that early experiences do not become functionally transformed into long-term memories. Broadly speaking, there are two theoretical interpretations about infantile amnesia. Since 1996, there has been much speculation about its particular function. ![]() Her own programme of research on infant memory has made important contributions to challenging this simplistic portrayal of infantile amnesia. In a seminal paper published in 1996, Carolyn Rovee-Collier rightly stressed that it is not only based on anecdotal evidence, but that it was “… an effort to explain a phenomenon that does exist.” (p. It was Sigmund Freud (1856-1939) who put forward the idea that infant amnesia amounts to a suppression of any early traumatic events of experiences. They also indicate that learning over an extended period of time induces a more persistent memory, which then relates to the number of cells that reside in the hippocampus.The more rapid forgetting of memories during infancy than later in development. ![]() Together, these data indicate that learning, and not mere exposure to training, enhances the survival of cells that are generated 1 wk before training. The strength of that memory correlated with the number of new cells remaining in the hippocampus. Consequently, animals trained with spaced trials performed as well as those trained with massed, but remembered the location better two weeks later. In the second experiment, the time between blocks of trials was increased. Moreover, performance during acquisition correlated with the number of cells remaining in the dentate gyrus after training. Rather, animals that learned well retained more cells than animals that did not learn or learned poorly. In the first experiment, animals trained with spaced trials in the Morris water maze outperformed animals trained with massed trials, but there was not a direct effect of trial spacing on cell survival. Because the cells are generated over time and because learning enhances their survival, we hypothesized that training with spaced trials would rescue more new neurons from death than the same number of massed trials. This phenomenon, known as the spacing effect, was explored with respect to its effect on learning and neurogenesis in the adult dentate gyrus of the hippocampal formation. Information that is spaced over time is better remembered than the same amount of information massed together. ![]()
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