Improving memory is a quest that never seems to end. For centuries, humans have attempted to find the right combination of social actions to better retain what we’ve learned. Over the years, some options have shown promise such as fasting and strenuous exercise. While effective, they are not particularly popular. Then there’s the odd concept of intranasal injection of insulin. It goes to show that an idea with promise might not be the best idea.
All these activities, regardless of their attractiveness, have one thing in common. They all stimulate an area of the brain responsible for catalyzing long term memory – the hippocampus. While it is not a storage house for memories – they are stored throughout the brain – this area does seem to be responsible for understanding one’s place in an environment (called spatial memory), and autobiographical events (referred to as episodic memory).
There is another means to improve memory through stimulation of the hippocampus. It’s sleep and in particular rapid eye movement (REM) sleep where dreams typically occur. As our bodies rest, our brains are catching up with our experiences, processing them and placing them into our neural network for use at a later time, a process named memory consolidation.
The involvement of REM sleep in memory consolidation has been suspected for several decades. Yet the actual proof that REM sleep is responsible for memory consolidation had not been proved. Researchers can show deprivation leads to a lack of memory retention, as well as self-confidence and psychological mood, yet the underlying mechanism has yet to be elucidated. As a result, the quest for better memory through sleep has continued to be enigmatic.
But that may now change thanks to researchers from McGill University. A team led by Dr. Sylvain Williams, has recently revealed that REM is indeed causal for memory consolidation in mice. The study, which appears in Science also found a part of the brain that may be the lynchpin to foster murine memories.
The group used mice for the experiments so they could examine and follow hippocampal electrical activity. But the target of the experimental manipulation was a different area of the brain known as the medial septum. Previous research had shown that neurons of this regions are connected to the hippocampus and release the neurotransmitter GABA to generate a particular type of oscillating electrical current – known as theta waves –during REM sleep. The team theorized this wave was responsible for memory consolidation and as such, the medial septum played a causative role.
In order to prove this, however, an intricate type of experiment known as optogenetics was needed. This process involved first changing the genetic nature of the GABA neurons of medial septum neurons such that the activity of these cells would be inhibited, and consequently of GABA release in hippocampus, would be stopped with the flash of a yellow light.
The first experiment involved the use of yellow light to stop GABA release during REM sleep. As expected, the size of the theta waves in the hippocampus was significantly reduced. This in itself was an achievement as it showed the medial septum was indeed responsible for the production of theta waves in the hippocampus. But this wasn’t the ultimate goal.
The next experiment went to the heart of the theory. Mice were exposed to two different objects and then allowed to sleep. Some of the mice were treated with yellow light during REM sleep while others were left as controls. The next day, the mice were returned to the cage but one of the objects had moved.
If the team was correct, the control mice would ignore the unmoved object – having already memorized it. In contrast, the mice treated with yellow light would explore both objects as if they were new. The mice did exactly as expected. The inhibition of medial septum neurons resulted in a lack of memory formation.
The group went on to attempt other experiments to determine which types of experiences were under this similar control. Fear and contextual memory recall experiments revealed the same outcome. However, when a cued recall test was performed, there was no change. This latter result was expected as this type of memory occurs in a different area of the brain.
For the authors, the study proved their theory at least in mice. Yet, there are hints these results may have usefulness in the human context. By stimulating medial septum neurons that release GABA, we may be able to develop a sleep-based route to improve memory. While this may be years away, the promise is quite high thanks to a recent though unrelated study examining the use of theta wave stimulation in epilepsy patients. In this study, not only does the condition improve, but the volunteers also experience an enhancement in memory consolidation.
Original research article:
Boyce R, Glasgow SD, Williams S, Adamantidis A. Causal evidence for the role of REM sleep theta rhythm in contextual memory consolidation.Science. 2016 May 13;352(6287):812-6. doi: 10.1126/science.aad5252.