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Plasticity of neurone to glial signalling in the cerebellum
Reference
BBS/E/B/0000L186
Principal Investigator / Supervisor
Dr Tomas Bellamy
Co-Investigators /
Co-Supervisors
Institution
Babraham Institute
Department
Babraham Institute Department
Funding type
Research
Value (£)
18,426
Status
Completed
Type
Institute Project
Start date
03/07/2006
End date
02/07/2009
Duration
36 months
Abstract
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.
Summary
unavailable
Committee
Closed Committee - Animal Sciences (AS)
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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