Although early experiences are important for personal development and future life, as adults we recall nothing or very little of those early formative events, such as making first steps or learning first words. In fact, when adults are asked about their first memories they usually don’t recall events before the age of 2-3, with only fragmented recollection of events that happened between the age of 3 and 7. This phenomenon is often called childhood or infantile amnesia. It represents an inability of both children and adults to recall episodic memories (i.e., memories for particular events or stimuli that occur in a particular context) from infancy and early childhood, before the age 2-4.
Sigmund Freud was the first researcher to develop the theory of infantile amnesia, as he had observed that his patients rarely had been able to recall memories of events that took place during the first years of life. He believed that childhood memories are being repressed and thus forgotten. Still, modern theories focus on cognitive and social development as an important predictor of childhood amnesia. One possible explanation of childhood amnesia is the lack of neurological development, i.e., the development of brain parts that are in charge of storage and retrieval of episodic memories. For instance, some researchers believe that the development and functioning of the prefrontal cortex (cortex area at the front of the brain) is crucial for the creation of contextualized memories. Moreover, the prefrontal cortex and hippocampus are assumed to be crucial for the development of autobiographical memories. Importantly, these two brain structures develop around the age of 3 or 4.
The lack of neurological maturation, i.e., maturation of brain structures required for creation, storage, and recall of memories during infancy and early childhood might explain the phenomenon of childhood amnesia. According to this explanation, childhood amnesia occurs not due to the loss of memories over time (the forgetting explanation), as Freud had suggested, but rather due to the lack of storing of these memories in the first place. The lack of stored memories, according to this theory, is due to brain immaturity.
Some evidence has suggested that amnesia for events taking place in early childhood (before the age of 2) could be at least partly explained by difficulties with verbally recalling memories that were encoded before language acquisition. In line with this is the fact that the majority of words (the vocabulary) are acquired between the age of 2 years and 6 months and 4 years and 6 months. This is the time period that the earliest memories can be recalled.
Childhood amnesia seems not to be an exclusively human phenomenon. Indeed, some researchers have observed something like infantile amnesia in animals (for instance, rodents). The discovery of amnesia in animals has pointed to the possibility of investigating the underlying mechanisms of childhood amnesia, such as neurological events, by using animal models. The animal studies have addressed the importance of some parts of brain and their development in relation to the childhood amnesia. For instance, they have indicated that high rate of neurogenesis in hippocampus as observed in infancy might explain the accelerated forgetting of contextual fear memories. It seems that integrating of new neurons into the existing circuit might destabilize and weaken the existing memories.
Some researchers believe that it is unclear whether childhood amnesia occurs due to the failure of memory retrieval or failure of their storage. Forgetting might be described as a linear function of the time passing since the event. Since there is a long time span between the early events and recall in adulthood, it might be assumed that early events are simply forgotten. Still, some researchers disagree. This is because they have found that subjects recall far less memories for events occurring between the age of 6 and 7 as would be expected by simply extrapolating the forgetting curve. Thus, forgetting could not completely explain the phenomenon of childhood amnesia. This is why a neurogenic hypothesis of childhood amnesia has been developed.
According to its inventors, a neurogenic hypothesis explains childhood amnesia through the continuous adding of new neurons (neurogenesis) in the hippocampus, as already mentioned above. According to this hypothesis, high levels of postnatal neurogenesis (which occurs in both humans and some animals) in the hippocampus prevents the creation of long-lasting memories. This hypothesis has been experimentally tested in animal models (mouse and rat). The findings emerging from these models have proposed that high levels of neurogenesis jeopardize the formation of long-term memories, possibly by replacement of synapses in pre-existing memory circuits. In addition, the same findings indicate that the decline in hippocampal neurogenesis corresponds with the emerging ability to form stabile memories.
Thus, according to these animal studies, the theory of neurogenesis appears to be a logical explanation for childhood amnesia.
Although the early theory regarding the forgetting or repressing of memories might look like a good explanation of childhood amnesia, more recent findings demonstrate that something else is happening in our brain that contributes to this phenomenon. Whether this is the lack of development in some brain parts, or the continuous synthesis of new neurons, or both, remains to be further investigated. Childhood amnesia cannot be explained by simple forgetting.
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