We are working out how neuronal synapses are regulated, and how this regulation goes wrong in diseases that affect the brain.
The brain is essential, because it enables us to respond to and interact with our environment. However, it comes at a high price. The human brain accounts for just 2% of the body's mass, yet demands 20% of the body's energy.
Much of this energy is used to power synapses, where neurons connect and communicate with each other. An individual neuron contains many hundreds of synapses, although not all of them will be active and communicating at the same time. Active synapses use more energy than resting synapses, and so neurons need a way to manage these changing energy demands.
Mitochondria are small, specialised structures found in large numbers within nearly all cells of the body, and generate most of the energy used to power cellular activity. They are also mobile, and can move around within cells to where they are most needed. Unsurprisingly, they frequently position themselves at synapses, where they can provide energy to power neuronal communication.
Our recent work has shown that, as well as providing energy to support synaptic activity, mitochondria can also move to synapses and reduce their activity by mopping up (and therefore reducing) a signal that triggers synapses to release chemicals called neurotransmitters.
Our aim is to understand why mitochondria have this dual role in regulating synapses, the molecular mechanisms by which this regulation occurs, and how this regulation changes in neurological and psychiatric disease. Through understanding more about this form of synaptic regulation, we hope to open up new ways of treating these conditions.