If memory can be defined as “a past that becomes a part of me”, can forgetting be defined as “a past that is no longer a part of me”?
Smokers who have abstained for years may not consciously be able to recall the sensation brought forth by smoking, but can suddenly feel craving upon seeing a smoking-related cue – often a cigarette brand logo – and relapse into smoking again. Tobacco companies know this only too well.
This illustrates a past that may have been forgotten but is not gone. It’s consistent with what’s known as the cue-dependent theory of forgetting, which states difficulty in recollection when the stimuli present during memory encoding are absent. Upon presentation of such stimuli, recollection becomes easy.
When a memory exists but cannot be recalled, such forgetting represents a retrieval failure. When a memory cannot be recovered in any way it represents a storage failure.
I have experienced such storage failure repeatedly throughout my education. Information I have studied before an exam is usually remembered during the exam.
As soon as the exam finishes, the information seems to immediately fade, mostly fading beyond recovery. It’s always made me feel like a faker.
This type of forgetting is consistent with what’s known as the trace decay theory of forgetting. It states that without rehearsal, memory will gradually decay over time, to disappear for ever.
Unfortunately, both psychological theories outlined above are very limited in terms of explaining forgetting.
Cue-dependent theory is criticised because memories can generalise over time, their elements becoming less specific. Trace decay theory fails to explain different fading speeds of different memories.
Neuroscience comes to the rescue at this point. What happens to the brain when something is forgotten? Although there are not many studies, some insight on the neural basis of forgetting has been provided by infantile amnesia research.
Infantile amnesia commonly refers to the general inability to remember experiences that happened early in life, before three to five years of age. This is a pervasive phenomenon displayed by all humans.
Importantly, infantile amnesia is not due to an inability to form episodic memories before that age. Children younger than three years have been shown to be able to encode specific episodic memories and even remember them for two years.
Instead, these memories do not persist into later childhood and adulthood, indicating children forget at a more rapid rate than adults.
Amazingly, infantile amnesia is ubiquitous. It is believed to occur in all altricial species (species that, like us, require parental care after birth), and has been observed even in worms, goldfish, chickens and rats. These species require care-givers to survive into adulthood.
This is in contrast to precocial species (species that don’t require parental care) such as guinea pigs, that do not require care-giving to survive.
In 1962, Byron A Campbell and his wife Enid Campbell showed that juvenile rats forget considerably faster than adult rats. They trained rats of various ages to avoid the black chamber of a black–white shuttle box.
This memory retrieval was measured by the latency to enter the black chamber when placed in the white chamber. When tested immediately after training, rats of all ages were equally able to express avoidance of the black chamber.
But when testing occurred later, infant rats showed nearly complete forgetting after seven days, whereas adult rats showed nearly perfect avoidance of the black chamber even after 42 days.
This finding has since been replicated with different learning paradigms and different species, including humans.
Since that time, infantile amnesia has been placed in a “too hard basket” and has not been studied, although most psychologists believed that it was a very important clue to how our memory works.
Reducing GABA allowed juvenile rats to retrieve a forgotten fear memory. In the mammalian brain, GABA is the king of inhibitory communication. Removing this inhibition removed whatever was blocking the fear memory from being retrieved.
Freud was right: infantile amnesia involves repression of aversive memories that can recover later in life!
But this recovery of memory in rats was only possible ten days after the memory was made, and reducing GABA had no effects after 60 days. So sometime between ten to 60 days in these rats, roughly equivalent to a period of between eight months to five years for us, forgetting turned from being a retrieval failure to storage failure.
In the latest follow-up to this study, my colleagues and I reported this year that a brain region called the amygdala, a very primitive part of the brain responsible for emotion, expressed traces of fear memory that was forgotten by the juvenile rat.
That trace was in the form of increased activation of a chemical called mitogen-activated protein kinase (MAPK) in the neurons, an important kinase (an enzyme involved in the transfer of energy within cells) necessary for gene activation and transcription.
Perhaps this is part of the “engram” (a presumed means by which memory traces are stored as biochemical changes in the brain, allowing retrieval of forgotten memories) scientists have been hunting for decades.
Understanding infantile amnesia may provide a key to unlock the secrets of forgetting that some happy individuals appear to possess. After all, people who develop a post-traumatic stress disorder following a traumatic event suffer from lack of forgetting.
And there are still so many other questions. Is memory erasure possible? What about reconstruction of memories? Will Jason Bourne ever completely recover from his amnesia caused by physical trauma?
Author: Jee Hyun Kim, The Florey Institute of Neuroscience and Mental Health
This article was originally published on The Conversation.
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