Dr Peter (Pete) Noakes

Position

Associate Professor | Affiliate Senior Research Fellow

Qualifications and Awards

The Paxinos-Watson Prize - Australian Neuroscience Society ... awarded 2005

Affiliations

To be listed here shortly ...

Associations

Society for Neuroscience (USA)
Australian Neuroscience Society
Australian Physiological Society
Queelsland Brain Institute, University fo Queensland

Contact Details

Location Room 422, Sir William MacGregor Building (64), St Lucia Campus
Mail Queensland Brain Institute; School of Biomedical Sciences,
The University of Queensland,
BNE, QUEENSLAND 4072
Telephone +61 3365 1640
Facsimile +61 3365 1766
Email p.noakes@uq.edu.au

Biography

Dr Peter Noakes is an A/Professor and affiliated senior research fellow with the Queensland Brain Institute conducting research at the School of Biomedical Sciences University of Queensland. Peter’s research centres around the neuromuscular system and neural control with particular emphasis on the mechanisms that regulate motor neuron number and its synaptic connections, in both health and disease.

Research Interests

Trans-synaptic signalling at neuromuscular and motor neuron synapses
The control of motor neuron numbers during normal development and ageing
The cell and molecular mechansims that trigger the death of motor neurons in motor neuron diesase
The role of the innate immune system in the progression of neuromotor diseases, such as motor neuron disease and Huntington's disease.

Selected Publications

Defective neuromuscular synaptogenesis in agrin-deficient mutant mice.
Cell 85: 525-535.
Gautam, M., Noakes, P.G., Moscoso, L., Rupp, F., Schellar, R.H., Merlie, J.P., and Sanes, J.R. (1996)

Failure of postsynaptic specialisation to develop at neuromuscular junctions of rapsyn-deficient mice.
Nature 377: 232-236.
Gautam, M., Noakes, P.G., Mudd, J., Nichool, M., Chu, G.C., Sanes, J.R., and Merlie, J.P. (1995)

The renal glomerulus of mice lacking s-laminin/laminin beta 2: nephrosis desite molecular compensation by laminin beta 1.
Nature Genet. 10: 400-406.
Noakes, P.G., Miner, J.H., Gautam, M., Cunningham, J.M., Sanes, J.R., and Merlie, J.P. (1995)

Aberrant differentiation of neuromuscular junctions in mice lacking s-laminin/laminin beta 2.
Nature 374: 258-262.
Noakes, P.G., Gautam, M., Mudd, J., Sanes, J.R., and Merlie, J.P. (1995)

The complement factor C5a contributes to pathology in a rat model of amyotrophic lateral sclerosis
The Journal of Immunology 2008 Vol 181.
Woodruff TM, Contantini KJ, Crane JW, Atkin JD, monk, PN, Taylor SM and Noakes PG
8727-8734

Rapsyn interaction with calpain stabilizes AChR clusters at the neuromuscular junction.
Neuron 2007 Vol 55
Chen F, Qian L, Yang Z-H, Huang Y, Hgo ST, Ruan N-J, Schneider C, Noakes PG, Ding-Y-Q, Mei l, and Lou Z-G.
347-260

The C5a anaphylatoxin receptor CD88 is expressed in presynaptic terminals of hippocampal mossy fibers
Journal of Neuroinflammation 2009 Vol 6
Crane JW, Baiquni GP, Sullivan RKP, Lee JD, Sah P, Taylor SM, Noakes PG, and Woodruff TM.
6-

Targeting of the ETS Factor Gabp-alpha disrupts neuromsucular junction synaptic function
Molecular and Cellular Biology 2007 Vol 27
O'Leary DA, Noakes PG, Lavidis NA, Kola I, Hertzog PJ, and Ristevski S.
3470-3480.

Glycinergic and GABAergic synaptic activity differentially regulate motoneuron survival and skeletal muscle innervation
The Journal of Neuroscience 2005 Vol 25
Banks GB, Kanjhan R, Wiese, S, Kneussel M, Wong LM, O'Sullivan G, Sendtner M, Bellingham MC, Betz H and Noakes PG
1249-1259

Functional analysis of neurotransmission at beta 2 laminin deficient terminals
Journal of Physiology (London) 2003 Vol 546.3
Knight D, Tolley LK, Kim DK, Lavidis NA, and Noakes PG.

Grants

Molecular mechanisms that underlie pre-synaptic development of motor nerve teminals
Grant Body: NHMRC
Grant Period: 2009-2011

How does neuregulin moduate the clustering of agrin induced post-synaptic acetylcholine receptor clustering in muscle
Grant Body: NHMRC
Grant Period: 2009-2011

The role of central and peripheral synaptic activity in the regulation of motoneuron survival during development

The use of conotoxins in the lableing of voltage gated calcium channels
Grant Body: NHMRC
Grant Period: 2009-2011

3D imaging of synaptic molecular complexes at the neuromuscular synapse
Grant Body: NHMRC
Grant Period: 2009-2011

Projects Available

Noakes-lab Research Projects
The Noakes lab has a number of research projects that are suitable for Summer, Advanced Science, Honours, MSc (lab Rotations), and PhD students. 
 
1) NEUROMOTOR: Electrophysiology and imaging based projects – This project   revolves around the neuro-motor system.  Specifically we are interested in determining the roles of glycine and GABA on motor neuron development – which includes motor neuron activity – morphology- and numbers.  
 
We are also interested our neuromotor research into how the neuromotor system adapts with age. Specifically, how do motor neurons and their central and peripheral synapses change in aging mice.   
 
2)  NEUROMUSCULAR: We have a number of projects centred on trans-synaptic signalling in the formation and maintenance of pre-and post synaptic specializations. These include:
 
i) The role of adhesive molecules (the synaptic laminins) in the formation of voltage gate-active zone complexes (pre-synaptic release sites) at neuromuscular synapses. Synaptic laminins bind to the pore forming subunits of specific voltage gated calcium channels; we are looking at the location and function of these channels in mutant mice missing selected laminin isoforms.
 
ii) The roles of agrin and neuregulin in the modulation of post-synaptic specializations during development and during ageing – neuregulin-1 appears to have short and long term actions on agrin’s ability to cluster and maintain high density clusters of acetylcholine receptors within post-synaptic specializations. These actions appear to be independent of neuregulin’s known gene activation pathways.   For these studies, we employ a combination of in vitro bioassays, and in vivo experiments using a variety of transgenic mice.
 
iii) The functional consequences in perturbations to trans-synaptic signalling at neuromuscular synapses.  These projects centre on the electrophysiological analyses of mice missing selected synaptic signalling molecules. It includes imaging of calcium influxes into motor nerve terminals and their capping Schwann cells.  
 
 
3) NEUROIMMUNOLOGY: We have a host of projects investigating the role of specific innate immune molecules in the normal development (e.g. synapses) and in the diseased nervous system. Specifically we are interested in complement molecules C3a, C5a and their receptors during periods of naturally occurring motoneuron cell death, and during adult motoneuron cell death (e.g. Motor Neuron Cell Death/ALS; Spinal Muscular Atrophy). Our previous work has shown that if we block the receptor for C5a – CD88 we can slow down the death of adult motor neurons in animal models exhibiting motor neuron disease. Blocking of CD88 appears to block the proliferation-activation of surrounding glial cells – how this is achieved is not known. Interestingly C5 and it receptors are also present on normal motoneurons but become unregulated during disease – how this contributes to neuronal death is not known.   Finally C5a has a second receptor C5L2 – it too is expressed on neurons and glia – its function in normal neuronal development and during death is also not known.   These projects use in-vitro bioassays (motor neurons, and glial cells) and transgenic animal models motor neuron disease – SOD1 and TDP43 transgenic mice.

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