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Glutamate, Spikes, and White Matter Disease

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If you have a question about this talk, please contact Hannah Critchlow.

For the brain to work properly fast information transmission needs to take place, which is achieved by insulating neuronal axons with myelin. Myelin is made by cells called oligodendrocytes. In multiple sclerosis, cerebral palsy, stroke and spinal injury myelin is damaged, leading to mental and physical disability. Myelin damage can be repaired by so-called oligodendrocyte precursor cells, that can differentiate into new oligodendrocytes and remyelinate the axons, but this process often fails. Recently we have made two discoveries that may contribute significantly to our understanding of both myelination and remyelination. First, both oligodendrocytes and their precursors respond to the neurotransmitter glutamate via AMPA and NMDA receptors and this signalling may regulate myelination. Secondly, there are actually two types of oligodendrocyte precursor cell present both in the developing and the mature brain: one type can fire action potentials and senses its environment by receiving synaptic input, whereas the other type lacks action potentials and synaptic input. Furthermore, simulating the diseases mentioned above leads to a rise of extracellular glutamate concentration generating an inward current in oligodendrocytes and OPCs, in part via NMDA receptors. These results make NMDA receptors on oligodendrocyte lineage cells a therapeutic target in white matter disease.

This talk is part of the Cambridge Neuroscience Seminar: New Approaches in Neuroscience series.

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