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What Changes in Our Brains During Sleep?

And How Do These Changes Promote Memory and Learning?

Have you ever tried to sit through a meeting, study for a test or remember items on a grocery list after a sleepless night? If so, you’ll know just how important sleep can be for our mental functioning. Today, we’re going to be homing in on the neurological and molecular changes that take place in our brains during sleep, with a focus on how sleep helps us to learn and form memories. First, we’ll briefly discuss neurons, synapses and neurotransmitters.

Neurons and Synapses

Neurons are nerve cells that transmit information throughout the brain and body. Synapses, on the other hand, are the spaces between neurons. They allow for neurons to communicate with one another through electrical and chemical impulses. We know that synapses play a central role in the processes of learning and memory formation [1].

For example, when you access an important piece of information – such as the colour of your lover’s eyes – this information is transmitted electrically through your synapse and that specific memory is stored in the form of a synaptic connection. The more a synapse gets activated, the more that synaptic connection is strengthened – and this is how memories are formed.

Neurotransmitters

Neurotransmitters can be thought of as chemical messengers that perform a wide variety of functions within our brains and bodies. Importantly, however, neurotransmitters allow for neurons to communicate with one another – this chemical communication takes place within the synapse.  There are many, many different neurotransmitters that are involved in the brain’s sleep-wake cycle. For the purposes of this article, however, we’re going to focus on just two.

The first is called noradrenaline: the ‘awake’ hormone. Noradrenaline is released during the fight-or-flight stress response and it plays an important role in keeping our minds alert and awake. The levels of this chemical decrease during sleep and start to increase when we wake up in the morning [2].

The second is called adenosine: the ‘sleep’ hormone. When we wake up in the morning, our adenosine levels are at their lowest. This chemical accumulates throughout the day, and at night, when its concentration is highest, we start to feel sleepy. As you sleep, the adenosine breaks down gradually until you wake up and the process repeats again [3].

The Synaptic Homeostasis Hypothesis

The synaptic homeostasis hypothesis helps us understand exactly how sleep promotes learning. Despite the complicated terminology employed, the underlying idea of this hypothesis is simple: our brains are busy during the day, so they need to rest during the night [4].

Let’s say you’re at a disco. Your brain is taking in lots of information: the pounding bassline, flashing strobe light and the body odour emanating from the man dancing next to you. With all of this stimulation, fireworks are happening in your synapses as your neurons transmit all of this contextual information between one another, allowing you to make sense of what’s happening around you.

Your synapses are active as they receive all this data; and they’re strengthening at the same time. But what happens when you go home and fall asleep? Your synapses are no longer exposed to all that external stimulation. Incidentally, their activity scales down, or weakens. Why does this happen?

Firstly, weakened synapses give your brain a chance to store and sort through the information that you have absorbed during the day. By scaling down, your synapses stop expending energy on receiving information, so that this energy can instead be used to store and integrate your disco experience alongside your existing memories [5]. 

Secondly, weakening of the synapses gives them a chance to regenerate energy so that they can be active again for whatever you might choose to do during the following day. In other words, according to the synaptic homeostasis hypothesis, our synapses strengthen during the day and then weaken at night, in order to promote consolidation of memories, or learning [6].

Homer1a

What are the molecular processes that underlie the dance that our brain and synapses perform? Exciting research published by Graham Diering and colleagues has made an important discovery that may help us to answer this question [7].

The researchers looked at Homer1a, which is a gene and neuronal protein. This gene makes its presence known (i.e. it is expressed) in our neurons that are very active, and it appears to trigger the synaptic scaling down process. Furthermore, Homer1a is closely linked to the activity of the brain chemicals which we discussed earlier.

For example, when noradrenaline is present, Homer1a is blocked from entering the synapse. On the other hand, high levels of adenosine are linked to Homer1a’s presence in the synapses. During the day, some neurons will be more active than others. The more active they are, the more Homer1a they’re likely to see at night [7].

An Elegant Design

So, what does this all tell us? The ‘awake’ hormone keeps Homer1a out of the synapses, while the ‘sleepy’ hormone cues Homer1a to make itself known. This is convenient, because Homer1a triggers the scaling down process, which is exactly how we want our synapses to be behaving at night, so that they can process and integrate the day’s memories!

1. Kandel, E. R. (2001). The molecular biology of memory storage: a dialogue between genes and synapses. Science294(5544), 1030-1038.

2. Lena, I., Parrot, S., Deschaux, O., Muffat‐Joly, S., Sauvinet, V., Renaud, B. E. E. A., ... & Gottesmann, C. (2005). Variations in extracellular levels of dopamine, noradrenaline, glutamate, and aspartate across the sleep–wake cycle in the medial prefrontal cortex and nucleus accumbens of freely moving rats. Journal of neuroscience research81(6), 891-899.

3. Landolt, H. P. (2008). Sleep homeostasis: a role for adenosine in humans? Biochemical pharmacology75(11), 2070-2079.

4. Tononi, G., & Cirelli, C. (2003). Sleep and synaptic homeostasis: a hypothesis. Brain research bulletin62(2), 143-150.

5. Tononi, G., & Cirelli, C. (2014). Sleep and the price of plasticity: from synaptic and cellular homeostasis to memory consolidation and integration. Neuron81(1), 12-34.

6. Vyazovskiy, V. V., Cirelli, C., Pfister-Genskow, M., Faraguna, U., & Tononi, G. (2008). Molecular and electrophysiological evidence for net synaptic potentiation in wake and depression in sleep. Nature neuroscience11(2), 200-208.

7. Diering, G. H., Nirujogi, R. S., Roth, R. H., Worley, P. F., Pandey, A., & Huganir, R. L. (2017). Homer1a drives homeostatic scaling-down of excitatory synapses during sleep. Science355(6324), 511-515.

About the Author:

Daniel Sher is a clinical psychologist, trained at the University of Cape Town and registered with the South African Health Professions Council. His professional interests include neuropsychoanalysis, intersubjective and object-relational approaches; and psychotherapy for people with sexual dysfunctions and Type 1 diabetes.

 

 

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