I is for…Infantile Amnesia

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Image credit: Cristina-Monica Moldoveanu

 

 

The newborn brain is still undergoing extensive organisation and development, as well as having masses of new information to make sense of. Even though babies are born with the vast majority of their lifetime’s neurons, there are two parts of the brain in which neurons continue to form well into adulthood. One of those is the hippocampus, a prominent area in laying down and retrieving memories, especially memories for places and events. This process of neuron growth, or neurogenesis, is most prolific in infancy, slowing down with ageing.

 

Some research has suggested that neurogenesis might be related to forgetting information because the existing connections between cells, which are important for preserving memories, may have to be reorganised to accommodate new cells. Freshly-made neurons have to compete with existing ones for in- and out-going connections, and these may replace old connections or alter the balance of existing ones. These adjustments might disrupt the process of storing information and possibly even lead to memories being lost – which would imply that the high rate of neurogenesis in infancy may explain why infantile amnesia occurs.

 

A recent study by a team of researchers in Toronto supports this idea, as they found that manipulating neurogenesis affected the memory prowess of mice and rodents.

 

Similarly to humans, the researchers observed that neurogenesis occurred less in older than younger mice, and that the connections between neurons were less likely to be reorganised as the mice got older. They also showed that baby mice were more forgetful – when trained to expect an electric shock in a specific situation, baby mice froze in anticipation the day after training, whereas adult mice continued to freeze for up to a month, despite all mice reacting equally to the shocks during training. It seemed that baby mice had formed a memory for the shock, but were showing forgetting of the training, comparable to that of infantile amnesia.

 

To test whether neurogenesis was more directly responsible for this effect, the team then manipulated the rate of hippocampal neurogenesis occurring in adult mice. Getting mice to run voluntarily has been shown to increase neurogenesis, and when these researchers checked their own work, it had also encouraged reorganisation of cells in the hippocampus. Adult mice with access to a running wheel after training had reduced fear memory of an electric shock, whereas access to a locked wheel had no effect on memory, suggesting that the act of running, rather than a change in the mice’s habitat, had affected the mice’s memory.

 

The Dementia drug, Memantine, which also increases neurogenesis, had the same effect on forgetting as running. The researchers later checked that no other metabolic processes caused by the running had affected the ability to form a memory, and this was confirmed. What’s more, running had no effect on the mice’s conditioned recognition of an unpleasant taste, a form of memory which does not rely on the hippocampus. Ergo, increasing neurogenesis in the hippocampus had affected memories formed in the hippocampus only.

 

Conversely, the researchers posed that preventing neurogenesis in baby mice should prevent forgetting. Using gene editing, the researchers suppressed neurogenesis in a group of infant mice, and trained them to expect an electric shock as before. One day after training, the mice showed a similar freezing reaction to those with natural rates of neurogenesis. After seven days though, the GM mice showed more freezing behaviour – the GM mice had superior memory.

 

Unlike humans and mice, guinea pigs and degus undergo most of their hippocampal neurogenesis before birth, and do not experience infantile amnesia. However, increasing neurogenesis in these species also caused forgetting after memory training. Perhaps then, neurogenesis alone is sufficient to influence memory function.

 

In all these experiments, neurogenesis appeared to be affecting already established memories, rather than the ability to form memories in the first place. This accords well with human research suggesting that very young children do create memories, but these become very difficult, even impossible, to access.

 

Nonetheless, whilst this seems like compelling evidence that infantile amnesia is all down to neurogenesis, some researchers think that this is only part of the story. Though its plausible that disrupting the balance of neural connections could cause some information to be lost, its not totally clear how neurogenesis causes this to happen. Neurogenesis can’t easily explain forgetting in adulthood, as neurogenesis slows with age, so other processes must also be in play to explain adult forgetting. Memory also has several different forms, such as memory for events, facts and procedures, and each are likely to be dealt with differently by the brain, so forgetting may also be different for each type. There is also the question of whether infantile amnesia is simply a by-product of postnatal neurogenesis, or whether this effect has a greater purpose, such as allowing more rapid learning, unhindered by stores of all the new information an infant is unwittingly presented with. For now, then, the effect of neurogenesis on memory remains as murky as forgotten infant memories themselves…

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