New research from scientists at Trinity College Dublin could help explain why babies from multiple species, from mice to humans, are affected by infantile amnesia. The study, published in PLOS Biology, found that microglia, the immune cells of the central nervous system, might modulate this form of forgetfulness. The data also suggests that dysfunctional microglia could contribute to “altered memory trajectories” in neurodevelopment disorders, according to the team. Their new paper is titled “Microglial activity during postnatal development is required for infantile amnesia in mice.”
As infants grow, they absorb large quantities of information that help them make sense of their world. However, episodic and contextual memories from early development are lost, for example, memories of a first birthday party in the case of a human child. This feature is observed specifically in altricial mammals, which are those born helpless, immature, and highly dependent on parents for survival. Precocial mammals, in contrast, are relatively mature and self-sufficient very shortly after birth.
To understand how this occurs, the scientists used pharmacological and receptor-specific tools to inhibit microglia activity in the brains of young mice and then assessed how well they could remember a fearful experience. They also analyzed microglia markers in two memory-related brain areas in the mouse brains, namely, the dentate gyrus of the hippocampus and the amygdala. They used glowing tags to identify engram cells, whose activities are associated with memory formation.
When microglial activity was suppressed, as evidenced by less activity in the hippocampus and amygdala, the mice in the study retained better memories of their fearful experiences. They also observed that the engram cells in the mice were more active, offering a functional explanation for enhanced memory recall. The findings build on previous work that found that mice born to mothers with activated immune systems do not have infantile amnesia. But when they modulated microglial activity during an early postnatal window soon after birth, they were able to restore the normal state of infantile amnesia in the young mice.
From the scientists’ perspective, these results point to common mechanisms that may exist between infantile amnesia and other forms of forgetting. “Infantile amnesia is possibly the most ubiquitous form of memory loss in the human population. Most of us remember nothing from our early years of life, despite having so many novel experiences during these formative years,” said Tomás Ryan, PhD, a neuroscientist at Trinity College Dublin and one of the co-authors on the study. “But what if those memories are still present in the brain? Increasingly, the memory field views forgetting as a ‘feature’ of the brain rather than a ‘bug’. It seems that the brain is filing away the neuronal units that store memory, the engrams, for later use.”
Furthermore, “the biology of infantile amnesia may give us insight into how forgetting happens in the brain in general,” Ryan noted. And “being able to manipulate infantile amnesia opens doors into new ways of imagining how learning, and forgetting, might work during the early years of life.”
