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Spatiotemporal properties of Ca2+ signalling pathways in cerebellar astrocytes

Reference	BBS/E/B/0000L135
Principal Investigator / Supervisor	Dr Tomas Bellamy
Co-Investigators / Co-Supervisors
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	323,545
Status	Completed
Type	Institute Project
Start date	01/11/2004
End date	31/10/2009
Duration	60 months

Abstract

The brain is composed of two major classes of cells: neurones, which communicate through electrical and synaptic signals (synapses are specialised junctions at which nerve cells communicate with other cells), and glial cells, which cannot transmit electrical signals, but provide nutritional support to the neurones. As a result of these properties, for many years glial cells were thought to be passive, and not involved in the main role of the brain: processing information. More recently, however, it has been discovered that glia are capable of communicating through biochemical pathways, particularly accumulation of calcium ions (Ca2+). The role of glial Ca2+ signalling in brain function is poorly understood, but is implicated in processes such as development of proper brain architecture, and the formation of memory. Dysfunction of glial Ca2+ signalling would therefore lead to onset of disease. The aim of this research is to investigate how glial cells respond to activity in the neuronal network, and, reciprocally, what effect glial Ca2+ signalling has on neuronal excitability. Using cells from the cerebellum, a region of the brain involved in fine motor coordination and learning (such as playing the violin), we will investigate the size and timing of the glial Ca2+ signals that result during stimulation of nearby neurones. We also aim to determine which biochemical pathways control glial Ca2+ signalling, and what effect the artificial triggering of Ca2+ signalling in glia has on neuronal activity. In this way, the aim is to better understand the role and importance of glial cell Ca2+ signalling in the operation of the brain, and how the signalling may go wrong during disease.

Summary

unavailable

Committee	Closed Committee - Biochemistry & Cell Biology (BCB)
Research Topics	Neuroscience and Behaviour
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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