Our work on oligodendrocytes covers the development, plasticity and pathology of these cells. Oligodendrocytes myelinate axons, and thus speed action potentials, but in pathological conditions like cerebral palsy, stroke, spinal cord injury and multiple sclerosis oligodendrocytes are killed, leading to mental and physical impairment.
We have shown that neurotransmitter receptors for glutamate and GABA regulate the development of oligodendrocyte precursor cells into myelinating oligodendrocytes (Káradóttir et al., 2005; Lundgaard et al., 2013; Hamilton et al., 2016; Kougioumtzidou et al., 2017). Current work is focused on how the length of the node of Ranvier is set, how it affects conduction speed, and whether it can be changed in situations where neuronal circuitry needs to be plastic to alter behaviour (Arancibia-Carcamo et al., 2017). For pathology, we recently discovered that a damaging rise of calcium concentration in the myelin sheath that occurs in ischaemia is produced by intracellular protons activating TRP channels (Hamilton et al., 2016). Ischaemic pathology also damages the node of Ranvier, and we are characterising the mechanisms by which this occurs.