Freud's trauma theory Sigmund Freud is famous for his theories of
psychosexual development which suggest that people's personality traits stem from their
libido (sexual appetite) which develops from early childhood experiences. Freudian theory, including his explanation for childhood amnesia, has been criticized for extensive use of
anecdotal evidence rather than
scientific research, and his observations that allow for multiple interpretations. Research has found that later memories in childhood have more propositional and emotional content than earlier memories and are rated as more meaningful and vivid. It has been suggested that differences in the emotions experienced by infants and adults may be a cause of childhood amnesia. Some studies have found that emotional experiences are connected with faster retrieval times, leading to the belief that emotional events have heightened accessibility in our memories. Specifically, the
dentate gyrus, a section of the hippocampus, has been observed to primarily develop in the postnatal stages of development. It is theorized that this part of the hippocampus plays a large role in the ability to form and retrieve memories. The ability to store and recall memories gradually increases along with the postnatal development of the dentate gyrus. The
physiological approach appears to support findings of memory loss in relation to amnesiacs and others who have experienced damage to the hippocampus. They cannot efficiently store or recall memories from past events, but still exhibit perceptual and cognitive skills and can still learn new information. While the neurological explanation does account for blanks in very young children's memories, it does not give a full explanation for childhood amnesia because it does not account for the years after the age of four. Nor does it explain why children do not show childhood amnesia. This discovery that three-year-olds can retrieve memories from earlier in their life implies that all necessary neurological structures are in place to recall episodic information over the short-term, but evidently not over the long-term into adulthood. The finding that all
altricial species experience profound forgetting of episodic information formed during infancy suggests that human-centric explanations of infantile amnesia are inherently incomplete. A comprehensive understanding of infantile amnesia will require a neurobiological explanation of why infants forget. There are reasons to believe that different associations within the cerebral hemisphere have an effect on remembering events from a very early period in a person's life.
Mixed-handedness and bilateral
saccadic eye movements (as opposed to vertical or pursuit eye movements) have been associated with an earlier offset of childhood amnesia, leading to the conclusion that interactions between the two hemispheres correlate with increased memory for early childhood events.
Neurobiology Research into the neural substrates of infantile amnesia using animal models has found that the major inhibitory neurotransmitter gamma-amino butyric acid (GABA) may be involved in the regulation of retrieval of infantile memories in adults. GABA activity is known to be higher in early childhood development than it is in adulthood, both in humans and other animals. Researchers have hypothesized that increased GABA activity in development has an effect on memory retrieval later in life. Past studies have shown that GABA aids in the forgetting of fear memories in infancy and that it may be a general mechanism for regulating infant memory retrieval.
Benzodiazepines, a class of psychiatric medication which increase GABA expression, have been found to produce anterograde amnesia, or a failure to encode memories after taking the medication. Subjects taking benzodiazepines are found to perform worse on learning and memory tasks compared to drug-naïve subjects. Previously, it was assumed that neurogenesis, or the continued production of neurons, ended after development. Recent findings have shown that there are high levels of neurogenesis in the hippocampus in early childhood which taper out into adulthood, although neurogenesis continues to persist slowly. As the hippocampus is known to be vital to memory processes, there are obvious implications for childhood amnesia. Animal research has shown that the age of high neurogenesis is in the developmental period when persistent memories are least likely to be formed. It has been proposed that hippocampal neurogenesis degrades existing memories. This may be due to increased competition between the new and existing neurons, followed by the replacement of synapses in preexisting memory circuits. This theory has been supported in mouse models in which increasing neurogenesis levels also increased forgetting. Additionally, decreasing neurogenesis after new memory formation resulted in decreased forgetting. In addition, memories are consolidated via transferral from the hippocampus to the cortex. This transferral occurs preferably during periods of elevated excitability in the hippocampus i.e. during ripple oscillations. Ripple oscillations represent increased hippocampo-cortical communication. This increase in experience-associated activity does not occur up to a certain age suggesting that this might be a mechanism for infantile amnesia. By stimulating neurons used in 'forgotten' fear conditioning in infant mice, Guskjolen et al. found retrieval of the fear response was possible by optogenetic reactivation of the neuronal ensembles that encoded the memory drive. This retrieval lasted for up to three months, suggesting the infantile amnesia was underlaid by a biological failure to access, rather than encode, said memories. In addition, memories are consolidated via transferral from the
hippocampus to the
cortex. This transferral occurs preferably during periods of elevated activity in the hippocampus. This increase in experience-associated activity does not occur up to a certain age, suggesting that this inability to transfer information might be a mechanism for infantile amnesia. This acknowledged link of the past to the present and the concept of continuous-time and therefore a continuous self is also helped by memory talk with adults. If children lack language, they are unable to describe memories from infancy because they do not have the words and knowledge to explain them. Adults and children can often remember memories from around three or four years of age which is during a time of rapid language development. Before language develops, children often only hold preverbal memories and may use symbols to represent them. Therefore, once language develops, one can actively describe their memories with words. The context that one is in when they encode or retrieve memories is different for adults and infants because language is not present during infancy. This has implications for gender and cultural differences. Autobiographical memory begins to emerge as parents engage in memory talk with their children and encourage them to think about why a certain event happened. Memory talk allows children to develop memory systems in order to categorize generic versus unique events. An important aspect of this theory considers the difference between parents who discuss memories at length with their children in an elaborative style, and those who do not. Children of parents who discuss memories with them in an elaborative style report a greater number of memories than children who do not discuss their memories. Memories are described in greater detail. This has implications for cultural differences. == See also ==