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(A) A novel confocal approach for enhanced spatio-temporal localisation of Ca2+ transients with current recordings in neurones

Reference	JE412589
Principal Investigator / Supervisor	Professor Michael Ashford
Co-Investigators / Co-Supervisors	Dr Andrew Irving
Institution	University of Aberdeen
Department	Biomedical Sciences
Funding type	Research
Value (£)	127,971
Status	Completed
Type	Research Grant
Start date	12/01/2000
End date	12/07/2000
Duration	6 months

Abstract

We propose to examine some of the fundamental aspects of [Ca2+] i signalling in neurones and supporting cells using state-of-the-art, high definition confocal imaging, for fast Ca2+ i transient detection in combination with single channel and whole-cell recordings. The main features we intend to investigate are the role(s) Ca2+ i transients play in hippocampal neurone function, with respect to both slow events, i.e. hormone (leptin and insulin) signalling and fast transients, through mGlu receptor signalling in dendrites, underlying synaptic plasticity. Overall neuronal Ca2+ i handling will be examined with respect to the actions of a novel anti-hyperalgesic agent, gabapentin, and through the use of caged forms of the putative intracellular signalling molecules, sphingolipids and cycle ADPribose. Dynamic changes in [Ca2+] i associated with physiological electric fields are purported to control epithelial cell division and motility, and this concept will be explored using lens and corneal epithelial cells. Understanding synaptic vesicle dynamics is vital to our knowledge of overall synaptic function. Accordingly, the contribution of elevated Ca2+ i to synaptic vesicle re-cycling will be determined. Finally, neurodegenerative diseases are significantly correlated with oxidative stress and Ca2+ i overload, which lead to an as yet ill-defined cascade of intracellular events and eventual cell death. We intend to examine the role(s) of a novel ion channel, which is responsible for Ca2+ i overload in certain cells and its putative connection to free-radical induced mitochondrial dysfunction.

Summary

unavailable

Committee	Closed Committee - Biochemistry & Cell Biology (BCB)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	Joint Equipment Initiative 1999 (JE4) [1999]
Funding Scheme	X – not Funded via a specific Funding Scheme

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