Your first clumsy attempt at crawling. That first sensation of solid food. Perhaps even the very first embrace in your mother’s arms. We might not recall them, but research on rats suggests our brain still has those memories stored away.
A new study from Trinity College Dublin involving immunological models of autism spectrum disorder ( ASD) in mice has revealed the surprising role a mother’s immune system plays in moderating access to memories of life’s earliest experiences in what is referred to as infantile amnesia.
Not only might the findings help us understand – or even access – these precious moments, they go some way in explaining why some people with autism have an uncanny knack for recalling events from ages most of us have long forgotten.
“Infantile amnesia is possibly the most ubiquitous yet underappreciated form of memory loss in humans and mammals,” says Trinity College Dublin neuroscientist Tomás Ryan.
“Despite its widespread relevance, little is known about the biological conditions underpinning this amnesia and its effect on the engram cells that encode each memory. As a society, we assume infant forgetting is an unavoidable fact of life, so we pay little attention to it.”
Our mental autobiography typically commences sometime between our second and third birthday. It’s not that our brains are incapable of perceiving the world before this age. Studies in rats also suggest our brains are fully capable of forming memories, stashing them away in a neurological library in the form of structures called engrams.
Presuming we simply no longer have the key to the vaults holding our earliest experiences, researchers are left to consider the mechanisms at work making those memories inaccessible.
There have been occasional clues. Infantile amnesia has been prevented in rats through the use of pharmaceuticals targeting specific neurotransmitters, as well as the timed use of corticosteroids, strongly implying the tides of biochemistry actively erode the pathways to long term memories.
So Ryan and his team turned their attention to the environmental shifts governed by the mother’s immune system.
Already suspected to influence the emergence of characteristics associated with neurological conditions including ASD and schizophrenia, it was hypothesized maternal immune activation (MIA) might also influence pathways associated with infantile amnesia.
Using young and adult mice conditioned to fear an electrical shock, the researchers compared mice born to mothers in which they’d produced an immune response mid-pregnancy.
Not only did the male offspring of these mothers show signs of social behavior deficits, similar to people with ASD, but there was also evidence of remembering fearful events far longer than their sisters and control mice.
Further testing using transgenic mice carrying a gene that labeled memory neurons revealed critical differences in the structures and sizes of the MIA males’ engrams in an area of the hippocampus called the dentate gyrus, already well understood to be critical in memory formation.
Key to the process seems to be a small immune protein called cytokine IL-17a. Male mice born to mothers engineered without this protein still experienced infantile amnesia when the same immune responses were provoked during pregnancy.
Just why mammalian brains developed a ‘forget switch’ for their earliest moments isn’t clear, though with the mechanisms at work now apparent, researchers are a step closer to understanding why memories remain accessible in some minds and vanish in others.
“Our brains’ early developmental trajectories seem to affect what we remember or forget as we move through infancy,” says neuroscientist Sarah Power, study lead author who is now at the Max Planck Institute for Human Development in Germany.
“We now hope to investigate in more detail how development affects the storage and retrieval of early childhood memories, which could have a number of important knock-on impacts from both an educational and a medical perspective.”
This research was published in Science Advances.