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Regulation of neuronal signalling through alternate splicing of a sodium channel gene

ReferenceBB/C003926/2
Principal Investigator / Supervisor Professor Richard Baines
Co-Investigators /
Co-Supervisors
Institution The University of Manchester
DepartmentLife Sciences
Funding typeResearch
Value (£) 109,270
StatusCompleted
TypeResearch Grant
Start date 01/06/2007
End date 31/10/2008
Duration17 months

Abstract

To function correctly, developing neurons must acquire a characteristic mix of voltage-gated ion channels to allow appropriate integration of synaptic excitation and action potential firing. Which channels are expressed, together with their subcellular location and density, are likely set as part of a developmental program that is both intrinsic (ie. specific transcription factors) and extrinsic (ie. exposure to synaptic transmission and cell-cell contract) to individual neurons. The mechanisms that govern these fundamental decisions are, however, poorly understood. This study focuses on the role of alternate splicing to produce diversity in signalling properties. The Na+ current, present in Drosophila neurons, is encoded by paralytic and multiple splice variants of this gene have been identified. The question remains as to how each variant contributes to neuronal signalling. This study will identify and characterise the channel properties of the major splice variants for para expressed in the embryonic CNS. The contribution of these variants to neuronal signalling and motor behaviour will also be determined by in vivo expression in the embryonic CNS. The information provided will represent the first detailed examination of how regulated splicing underlies the emergence of appropriate behaviour in a developing organism.

Summary

unavailable
Committee Closed Committee - Animal Sciences (AS)
Research TopicsNeuroscience and Behaviour
Research PriorityX – Research Priority information not available
Research Initiative X - not in an Initiative
Funding SchemeX – not Funded via a specific Funding Scheme
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