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Nerve cell survival is dependent on both growth-promoting factors and factors released by neurotransmission, which can promote recovery in neurodegenerative conditions by overriding cell death pathways. The molecule responsible for activating death pathways in the nervous system is called p75. This project will investigate how p75 results in cell death, how synaptic signals can prevent the activation of the p75 death pathway and whether blocking p75 function can limit neurodegeneration.
Synaptic Inhibition And The Control Of Excitability In The Rodent Piriform Cortex
Funder
National Health and Medical Research Council
Funding Amount
$459,738.00
Summary
We are studying the properties of neurons (nerve cells) and brain circuits that enable mammals to recognise and remember odours. Our experiments will focus on neurons in the odour-processing region of the cerebral cortex of mice. This work will answer fundamental questions about how the brain interprets sensory inputs in order to build a coherent picture of the external world. Our findings will also provide a deeper understanding of the causes of epilepsy, leading to improved treatments.
PROBABILITY OF QUANTAL SECRETION AT NEUROMUSCULAR SYNAPSES
Funder
National Health and Medical Research Council
Funding Amount
$334,232.00
Summary
The classical preparation for the study of synaptic transmission is the amphibian neuromuscular junction, for which there is the largest body of experimental data. This synapse was instrumental in the discovery that transmitters are released in packets or quanta, that this occurs at specialized release sites in the nerve terminal, and that receptor molecules on the muscles cells are strategically placed to receive the transmitter. Our work on this synapse has shown that each of these release sit ....The classical preparation for the study of synaptic transmission is the amphibian neuromuscular junction, for which there is the largest body of experimental data. This synapse was instrumental in the discovery that transmitters are released in packets or quanta, that this occurs at specialized release sites in the nerve terminal, and that receptor molecules on the muscles cells are strategically placed to receive the transmitter. Our work on this synapse has shown that each of these release sites have different probabilities for the secretion of a quantum and that this probability is correlated with the width of the release site. More recently we have shown that, whilst the size of a quantum does not vary between adjacent release sites, the area over which the quantum is released does vary between sites. The probability of quantal secretion is proportional to this area, as is the number of vesicles present at the release site. In this project we intend to relate this probability of secretion to the proteins that regulate the release of a quantum and in particular how these proteins interact to determine the time course of increase in probability at a release site after the passage of an impulse. The affects of trains of impulses on this probability are also to be delineated, in particular how the calcium which enters the terminal during these trains determines a long-term enhancement in probability after the train has ceased. This research will provide a molecular description of secretion from motor-nerve terminals.Read moreRead less
Structure-function Studies Of Ion Permeation And Selectivity In Recombinant Glycine Receptor Channels
Funder
National Health and Medical Research Council
Funding Amount
$331,300.00
Summary
Ligand-gated ion channels (LGICs) are members of a superfamily of receptor channels, with very significant structural and functional similarities, which play a major role in fast synaptic neurotransmission within the brain and spinal cord, and underlying the complex behaviour of the nervous system, but when dysfunctional can result in major neurological problems. Glycine is one of the two most important inhibitory neurotransmitters in the central nervous system. Impaired glycine-mediated neurotr ....Ligand-gated ion channels (LGICs) are members of a superfamily of receptor channels, with very significant structural and functional similarities, which play a major role in fast synaptic neurotransmission within the brain and spinal cord, and underlying the complex behaviour of the nervous system, but when dysfunctional can result in major neurological problems. Glycine is one of the two most important inhibitory neurotransmitters in the central nervous system. Impaired glycine-mediated neurotransmission underlies a range of inherited neurological diseases and already, it has been shown that the human disorder, familial Startle disease (hyperekplexia) occurs because of point mutations that have impaired the permeation and activation of the glycine receptor (GlyR). Similarly, certain epilepsies are now known to be caused by mutations in, or close to, the channel region in the excitatory acetylcholine receptors (AChRs), which affect channel activation and ion permeation. However, because of their very significant structural and functional similarities, information obtained in one member of the LGIC family of receptors has strong potential application to the other members and the GlyR with its simpler structure has certain advantages for investigation. The first aim of this project is to investigate how the molecular biological structure of these ion channels controls permeation, how it affects how different ions are selectively allowed to move through it and how it affects channel activation. A second related aim is to learn more about the process of desensitization of GlyR receptors, whereby a sustained presence of a high concentration of agonist can cause a reduction in receptor response. A third aim is to specifically investigate the mechanisms underlying the mode of molecular disruption resulting from two new Startle disease mutations, which, in addition to their own inherent clinical value, can also give general information about receptor function.Read moreRead less
Regulation Of P75 Death Signalling: How Neurotransmitter- And Neurotrophic- Signals Determine Cell Survival
Funder
National Health and Medical Research Council
Funding Amount
$292,216.00
Summary
Nerve cell survival is dependent on trophic support in the form of growth factors and synaptic input, both of which promote recovery after nerve injury. The survival pathways activated by growth factors are generally well characterised, whereas survival signals activated by synaptic activity are largely unexplored. This proposal aims to discover how synaptic activity prevents nerve cell death by looking at how synaptic activity inhibits the processes active in dying nerve cells.
Development And Refinement Of Neural Connections In The Adult Brain In Health And Disease
Funder
National Health and Medical Research Council
Funding Amount
$8,061,596.00
Summary
Our group will use innovative approaches such as advanced imaging and cell-sorting and development of animal models to determine how new neurons are generated, how they travel to different parts of the brain and how they integrate into the existing brain circuitry. These discoveries will point to new ways in which to treat brain damage both during ageing and during pathology. Since team members have previously been involved in progressing molecular discovery to clinical trials, we are also in a ....Our group will use innovative approaches such as advanced imaging and cell-sorting and development of animal models to determine how new neurons are generated, how they travel to different parts of the brain and how they integrate into the existing brain circuitry. These discoveries will point to new ways in which to treat brain damage both during ageing and during pathology. Since team members have previously been involved in progressing molecular discovery to clinical trials, we are also in a good position to exploit these discoveries in partnership with the biopharmaceutical industry.Read moreRead less