Plasticity of neurone to glial signalling in the cerebellum

Lead Research Organisation: Babraham Institute
Department Name: UNLISTED

Abstract

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Technical Summary

The brain is composed of billions of neurones, which conduct electrical signals, and are connected by specialized junctions known as synapses. At the synapse, an incoming electrical signal causes the release of a chemical neurotransmitter, which crosses the synapse and binds to receptor proteins, thereby initiating an electrical impulse in the postsynaptic cell. An important property of synapses is that the strength of synaptic transmission can be modified, depending on the frequency with which electrical excitation occurs. This principle is known as 'synaptic plasticity' and is thought to be the cellular basis of learning and memory. A second class of brain cells known as astrocytes provide support to the neurones, and are electrically non-excitable. In recent years it has been discovered that astrocytes also express receptor molecules similar to those found at neuronal synapses, and that astrocytes can respond to release of neurotransmitter by initiating biochemical signalling pathways in particular, by accumulating calcium ions. In this way, astrocytes and neurones can communicate information with one another. We have been investigating neurone to astrocyte signalling in a region of the brain called the cerebellum. We discovered that the strength of neurone to astrocyte signalling could also be changed by the frequency of activity at the synapse: astrocytes also express plasticity. Interestingly, plasticity at the astrocyte differed from that of the adjacent neurone. The aim of this project is to investigate the plasticity of neurone to astrocyte signalling in more detail. The biochemical mechanism by which astrocyte signalling is altered will be explored, and the impact of the plasticity on the strength and timing of synaptic transmission will be determined. We will then investigate another type of synapse, to see if the plasticity we have observed is a general mechanism for modifying cell to cell communication in the brain.

Planned Impact

unavailable

Publications

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