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An investigation of neuronal properties synaptic function and plasticity in the brains of PrP-null and other PrP-mutant mice

Reference	BS205537
Principal Investigator / Supervisor	Dr Nikki Macleod
Co-Investigators / Co-Supervisors	Professor Jean Manson
Institution	University of Edinburgh
Department	Biomedical Sciences
Funding type	Research
Value (£)	129,229
Status	Completed
Type	Research Grant
Start date	01/08/1996
End date	01/08/1999
Duration	36 months

Abstract

It has been proposed that PrP protein is required for normal synaptic transmission following the observation that LTP is weakened in PrP-null mice. In our inbred strain of PrP-null mice, stimulus protocols which induce LTP in wild type mice induce only short lasting potentiation in PrP-null mice. We propose to define the role of PrP in synaptic transmission by investigating synaptic function in brain slices from areas susceptible to activity-dependent changes in synaptic strength. We will focus on the interactions of amino acid-mediated excitatory and inhibitory transmission in the hippocampal fields CA1 and CA3 which show NMDA-dependent and independent forms of synaptic plasticity. Complementary anatomical methods will be used to study the role of PrP in normal neuronal morphology, including intracellular dye- filling and immunocytochemistry.

Summary

unavailable

Committee	Closed Committee - Agri-food (AF)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	Biology of Spongiform Encephalopathies - Phase 2 (BS2) [1993]
Funding Scheme	X – not Funded via a specific Funding Scheme

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