Dr Lynette Fernandes (School of Medicine and Pharmacology) A/Prof Alan Everett (Physiology, School of Biomedical Biomolecular & Chemical Science)




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НазваниеDr Lynette Fernandes (School of Medicine and Pharmacology) A/Prof Alan Everett (Physiology, School of Biomedical Biomolecular & Chemical Science)
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Neuroscience Honours Projects – 2009


Rho-kinase modulates presynaptic function in airway cholinergic nerves


Dr Lynette Fernandes (School of Medicine and Pharmacology)
A/Prof Alan Everett (Physiology, School of Biomedical Biomolecular & Chemical Science)


The broad aim of the work is to identify key cellular pathways in airway motoneurons that control acetylcholine release from nerve terminals (boutons) and subsequent airway narrowing. In particular, experiments will investigate the role of Rho-kinase in the mobilization of transmitter-containing vesicles in nerve terminals. The mobilization of these vesicles from a reserve pool within terminals determines the number of vesicles available for releasing transmitter. Understanding what controls how much transmitter is released, and therefore synaptic strength, could lead to dramatically improved outcomes in the pharmacological treatment of asthma.

The understanding of synaptic function and vesicle pool dynamics in combination with recent work on the potential role of the Rho-kinase enzyme in the regulation of cholinergic transmitter release has lead to our working hypothesis.  This enzyme normally promotes the phosphorylation of myosin light change kinase and increases intracellular calcium levels, at least in smooth muscle.  Our own work (Fernandes et al., 2006 Eur J Pharmacol 550, 155-161) has shown that Y-27632 suppresses cholinergic nerve-mediated contractile activity in murine airways and increases acetylcholine release from murine tracheal preparations.  Rho-kinase has been shown to phosphorylate endophilin.  Endophilin, in turn, is involved in clathrin-mediated endocytosis of synaptic vesicles. 

Our working hypothesis is that the Rho-kinase pathway controls the phosphorylation level of endophilin in synaptic boutons of autonomic nerves.  Endophilin is involved in clathrin-mediated endocytosis of synaptic vesicles and thus regulates the number of synaptic vesicles available for recycling and neurotransmitter release.  A change in the activity of Rho kinase will therefore impact on cholinergic nerve-mediated contraction of airway smooth muscle.

Effects of Dexamphetamine in Humans on Prepulse Inhibition of the Startle Reflex, Time Perception and the evoke EEG P300 response


A/Prof Mathew Martin-Iverson, School of Medicine and Pharmacology


Much research has shown relationships between the effects of dexamphetamine and schizophrenia. Both have been associated with decreased prepulse inhibition of the startle reflex (PPI) and with changes in time perception. Schizophrenia has also been associated with alterations in the P300 evoked response potential in the electroencephalographic measurement of cortical potentials. However, the effects of dexamphetamine in these measures in humans is not presently clear. In this project, all three measures will be taken in people who have been given 0.45 mg/kg of dexamphetamine or placebo.


The role of RGS5 in schizophrenia


A/Prof. Mathew Martin-Iverson, A/Prof Ruth Ganss, (WAIMR) 

We recently identified “Regulator of G protein signalling 5” (RGS5) as an important protein which modifies blood vessels in the brain and tumours (1). RGS proteins comprise a family of molecules with a unifying catalytic function but varying tissue distribution. They inactivate G protein-coupled receptors by stimulating the intrinsic guanosine triphosphatase (GTPase) activity of activated Gα subunits and thereby accelerating G-protein inactivation. RGS5 has been found to directly interact with Gαq and Gαi G proteins. Although much is known about the biochemistry of RGS molecules, their receptor specificity and physiological role in vivo is largely unknown. Therefore, we have generated RGS5-deficient mice to study the role of this particular molecule under various pathological conditions and to examine RGS5-mediated signalling pathways. Interestingly, recent literature associates RGS molecules, including RGS5, with severity of schizophrenia. This project will use our knock-out mice to assess a potential link between RGS5 and mental illness, such as schizophrenia. We have measured specific alterations in the prepulse inhibition of the startle reflex (PPI) in patients with schizophrenia (3), where the relationship between the intensity of a startling stimulus and the magnitude of the response is shifted to the right in healthy volunteers but not in patients with schizophrenia. PPI is easily measured in rats (4) and mice (5) and this therefore provides an ideal model for assessing the possibility that RGS5 may play a role in schizophrenia by assessing PPI in RGS5-deficient mice.

 



Schematic representation of the role of RGS molecules in G protein coupled receptor signalling. RGS molecules act as guanosine triphosphatases (GTPase) and negatively regulate G protein signalling. 1) Hamzah, J., Jugold, M., Kiessling, F., Rigby, P., Manzur, M., Marti, H., Rabie, S., Kaden, H.-J., Groene, G.J., Hämmerling, G., Arnold, B. and Ganss, R. (2008) Vessel Normalization in Regulator of G protein 5-deficient Tumors Promotes Immune Destruction, Nature, 453: 410-4.
2) Campbell, D.B., Lange, L.A., Skelly, T., Lieberman, J., Levitt, P., and Sullivan P.F., Association of RGS2 and RGS5 variants with schizophrenia symptom severity (2007). Schizophrenia Res. 101: 67-75.
3) Kedzior KK, Martin-Iverson MT Attention-dependent reduction in prepulse inhibition of the startle reflex in cannabis users and schizophrenia patients--a pilot study. European Journal of Pharmacology 2007; 560: 176-182.
4) Hince DA, Martin-Iverson MT Differences in Prepulse Inhibition (PPI) Between Wistar and Sprague-Dawley Rats Clarified by a New Method of PPI Standardization. Behavioral Neuroscience 2005; 119: 66-77.
5) Stoddart, C.W., Noonan, J & Martin-Iverson, M.T. (in press) Stimulus quality affects expression of the acoustic startle response and prepulse inhibition in mice. Behavioral Neuroscience.

Mapping connections of an efferent control system in the auditory nervous system


Dr Helmy Mulders and Professor Don Robertson (Physiology, School of Anatomy, Physiology and Human Biology)


The auditory nervous system consists of ascending (afferent) components that carry information from the periphery to the higher centres, and descending (or efferent) pathways by which the brain exerts synaptic control over the flow of incoming information. The efferent system is thought to play a number of roles in auditory processing, but its detailed connectivity with afferent subsystems is poorly understood. In this project, we will label selected populations of afferent neurons using retrograde tracers injected into the brainstem of experimental animals and then anatomically map the synaptic connections that the efferent systems make with these labeled neurons by using anterograde tracers injected into the sites of origin of the efferent pathways.


Plasticity in the auditory midbrain after partial unilateral deafness


Dr Helmy Mulders and Professor Don Robertson (Physiology, School of Anatomy, Physiology and Human Biology)


We have now established that after a partial unilateral deafness induced by loud sound exposure, there is a time-dependent rise in the background neuronal firing levels in the contralateral auditory midbrain (the inferior colliculus). This neuronal hyperactivity is of interest because it is a likely neuronal correlate of tinnitus (phantom auditory sensation) that is an increasing problem in today’s society.  We have studied the inferior colliculus contralateral to the sound-exposed ear because the principal projection from cochlea to midbrain is crossed. However, there is a also substantial projection from the damaged ear to the ipsilateral midbrain. This altered ipsilateral input must interact with the intact contralateral projection from the unexposed ear. It is of interest to know whether hyperactivity is observed here as well, or whether the intact contralateral input acts as a brake on plastic alterations.  The project will involve recording single neuron activity in anaesthetized guinea pigs. Students will acquire skills in small animal handling, anaesthesia and surgery, digital data acquisition and analysis and histological verification of recording sites.


Effects of loud sound on gene expression in the cerebellum

Professor Don Robertson and Dr Jenny Rodger 

Loud sound exposure is known to provoke changes in gene expression in central auditory pathways and these changes are of interest for understanding the molecular and cellular basis of phenomena such as hyperacusis and tinnitus. It has recently been reported that human tinnitus patients have elevated neuronal activity in part of the cerebellum, a structure with multisensory roles but not normally associated with auditory processing.  This project will use experimental animals to investigate changes in gene expression in the cerebellum that may be associated with this hyperactivity. Primers for a number of candidate guinea pig genes have already been constructed and qPCR will be used to measure changes in mRNA expression after loud sound exposure.

Note: this project would be suitable for a student with level 3 knowledge of molecular biological techniques (either PHYL3300 orPHYL3340 or GENE3300 together with  SCIE3325).

Binaural effects on responses of auditory midbrain neurons


Professor Don Robertson and Dr Helmy Mulders


In the auditory midbrain of mammals, neurons are known to have a diversity of responses to sound when controlled acoustic stimuli are presented to the ear that supplies the dominant synaptic drive to those neurons. However, there is no good investigation in the literature of how these diverse “monaural” responses patterns may be shaped by two possible factors 1) spontaneous afferent input from the opposite ear converging onto the same neurons and 2)  acoustically-driven input from the opposite ear when sound presented to one ear is loud enough to physically leak across the head. Such information is vital to a proper interpretation of the responses seen in the auditory midbrain, both in normal animals and in animals with various peripheral auditory pathologies. In this project, students will use metal microelectrodes to record the activity of single neurons in the auditory midbrain of anaesthetized animals and will study the effects on response patterns caused by experimental elimination of inputs from the non-dominant ear.

Promoting functional recovery following burn injury


Professor Fiona Wood, AO, School of Surgery and Professor Sarah Dunlop, School of Animal Biology

Burns are amongst the most devastating of medical conditions, assaulting all aspects of the patient from physical to psychological. Each year more than 100,000 Australians suffer a burn injury with 6000 children presenting to emergency departments (http://www.nisu.flinders.edu.au/pubs/injcost/burns.html ). An overarching source of morbidity after burn injury is excessive scarring. The normal process of re-epithelialisation is impaired and overtaken by excessive extracellular matrix production. A critical factor influencing the degree of scarring is time taken to heal. Faster healing leads to better re-epithelialisation with reduced scarring [1]. Typically, human wounds that heal within 14 days have less than 5% chance of developing a hypertrophic scar, whilst those that persist beyond 21 days have a greater than 80% chance. A variety of grafting and reconstructive procedures are currently used to promote rapid wound coverage and better healing thereby minimising suffering and long-term scarring [2]. However, although such treatments significantly improve physical appearance, functional recovery is often poor with either no sensation in the healed skin which can lead to significant inadvertent damage, or neuropathic pain and intense itching.

We have recently shown in a mouse model that a single topical application of a small naturally occurring protein, metallothionein I/II, at the time of injury significantly improves time taken to heal and reduces scarring [3]. However, preliminary behavioural testing suggests that, similar to grafting procedures, functional recovery is minimal with long-term loss of sensory function. Following injury to the peripheral nervous system, it has been shown that task-specific training improves functional outcome [4].  The “use it or lose it” principle has also been established in a number of other injury models [5]. The current project will examine whether “sensory training”, either alone or combined with metallothionein I/II, improves sensory function after burns injury.

References
1. Chai J, Song H, Sheng Z, Chen B, Yang H, Li L. (2003) Repair and reconstruction of massively damaged burn wounds. Burns, 2003. 29(7): p. 726-32.
2. Wood FM, Stoner ML, Fowler BV, Fear MW. (2007). The use of a non-cultured autologous cell suspension and Integra dermal regeneration template to repair full-thickness skin wounds in a porcine model: a one-step process. Burns. 2007 3(6): 693-700.
3. Morellini NM, Giles NL, Rea S, Adcroft KF, Falder S, King CE, Dunlop SA, Beazley LD, West AK, Wood FM, Fear MW. Exogenous Metallothionein-IIA promotes accelerated healing after a burn wound. Wound repair and Regeneration (in press, accepted 3rd June 2008)
4. Angelov DN, Ceynowa M, Guntinas-Lichius O, Streppel M, Irintchev A, Neiss WF, Dunlop SA. (2007). Training diminishes polyneuronal reinnervation of paralyzed facial muscles and promotes full recovery of whisking function. Neurobiology of Disease 26: 229-242.
5. Dunlop SA. (2008). Activity-dependent plasticity: Implications for recovery from spinal cord injury. Trends Neurosci. 31:410-418

Scholars:
Prof Adrian West, School of Medicine, University of Tasmania
Dr Roger Chung, School of Medicine, University of Tasmania
Dr Mark Fear, School of Animal Biology, The University of Western Australia

The role of Neurotrophins, cAMP or ATP agonists on the formation of myelin in central Glia


Dr Giles Plant, Dr Alan Harvey (School of Anatomy, Physiology and Human Biology)

The proposed studies will address the issue of OEG myelination by examining the inherent capacity for OEG to remyelinate axons using defined in vitro co-culture systems, molecular analyses and viral vector technology. This proposal will clarify whether the size or age of the axon is an important factor in triggering myelin formation in OEG. Lastly, extrinsic factors will also be tested to ascertain whether external agents are the trigger for OEG myelin formation. Adult derived SC cultures will be used in parallel control experiments. The findings will have important implications for the future use of OEG not only for spinal cord injury, which has both primary and secondary demyelination events, but also perhaps for promoting remyelination in diseases such as multiple sclerosis. These are important particularly with the ongoing clinical trials in Portugal, Australia and China.

To determine in OEG/neuronal co-cultures whether membrane bound neuregulinâ1-Type III, or factors such as brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3), CPT-cAMP or ATP agonists stimulate compact myelin formation by adult OEG.

Contact: W/Prof Alan Harvey alan.harvey@uwa.edu.au or 08 6488 3294

Carbonyl scavenging agents and their effects in neuronal viability and axonal growth after exposure to Acrolein or carbonyl stress

Dr Giles Plant and Dr Philip Burcham (School of Medicine & Pharmacology).

The broad hypothesis underlying this work is that carbonyl-scavenging compounds that block cell damage by acrolein and related electrophilic carbonyls will protect against spinal neurodegeneration following traumatic spinal cord injury (SCI).  This hypothesis is based on a growing body of literature showing a role for acrolein, a reactive & highly toxic endogenous electrophile, as well as other reactive carbonyls in SCI pathogenesis. A subsidiary hypothesis is that exposure to mixtures of reactive carbonyl compounds, as occurs in the damaged spinal cord, is more toxic to neuronal cells than exposure to individual compounds.  These hypotheses will be tested using a combination of in vitro or in vivo approaches:

Projects:

1. Using  primary neuronal cells comprising dorsal root ganglia from rat embryos or adults, to explore the effect of acrolein and “carbonyl stress” on neuronal viability and axonal growth, and establish whether carbonyl-scavenging agents attenuate any disruption of axon extension.
2. Using a contusion spinal cord injury in the rat (12mm 10g weight drop) to ascertain the effectiveness of 2 pharmacological compounds to block acrolein activity and improve anatomical and behavioural outcomes.

Contact Dr Burcham at Philip.Burcham@uwa.edu.au

The use of anti –angiogenic peptides such as Ang001 and their role in spinal cord injury recovery.


Dr Giles Plant, Dr Dharmarajan (Anatomy, Physiology and Human Biology)

Interest in angiogenesis research remains strong in recent years: many laboratories worldwide are actively involved in the study of several aspects of this field and the literature on angiogenesis increases exponentially.

The growth of new microvessels from resting vessels is the outcome of a fine balance between molecules that are either positive or negative regulators of angiogenesis (the so called "angiogenic switch"). The explosion of clinical research in angiogenesis is a result of the realization that in many diseases characterized by persistent, unregulated angiogenesis, as cancer, atherosclerosis, rheumatoid arthritis, diabetic neuropathy, and wound healing a common underlying pathogenetic aspect is a derangement in angiogenesis.  Suppressors of angiogenesis have potential clinical applications in conditions where abnormal proliferation of blood vessels is related to the disease progression.  Several laboratories report new findings about anti-angiogenesis in chronic inflammation.  Investigating the vasculature targeting strategies for the treatment of chronic inflammatory diseases has considerable clinical implications.   In this study we will explore the role of a novel anti-angiogenic protein, Ang001 in would healing after a spinal cord injury.  These studies will be carried out in collaboration with Professor Dharmarajan who isolated this novel antiangiogenic protein.  Both in vitro and in vivo studies have clearly demonstrated a low does such as 250pg is able to significantly reduce wound healing and new blood vessel formation.

Specifically we will:
(i) Determine the ability of Ang001 administered after 12mm contusion injury (24 hours) to increase axonal sparing/regeneration, tissue sparing and behavioural recovery using BBB open field testing and Catwalk.
(ii) Determine the ability of  Ang001 administered after a complete spinal cord transection

Contact E/Prof Arunasalam Dharmarajan 08 6488 2981 or arunasalam.dharmarajan@uwa.edu.au

Do human bone marrow stromal stem cells promote regeneration after complete spinal cord injuries?

Dr Stuart Hodgetts and Dr Giles Plant (School of Anatomy, Physiology and Human Biology)

True neuronal regeneration in a complete transection model of spinal cord injury (SCI) will be investigated using human bone marrow stromal stem cells (hBMSCs) isolated from human SCI patients. Previous studies using incomplete contusion injuries that leave some motor/sensory pathways intact, make it difficult to determine whether the functional improvements observed are a result of true regeneration of injured tracts or due to behavioural compensation, remyelination of damaged (but intact) axons, or sprouting of spared axons. The findings will have important implications for the future use of hBMSCs in clinically relevant cell based transplantation strategies.

The project will involve animal work including the behavioural analysis of rats subjected to complete SCI using our novel computerized Catwalk Gait analysis system, as well as tissue processing and immunocytochemical analysis to assess the amount of true regeneration following SCI.


Contact:
Dr. Stuart Hodgetts: stuart.hodgetts@uwa.edu.au or 08 6488 8642

Investigating the myelination potential of bone marrow stromal stem cells for application in the treatment of spinal cord injuries

Dr Stuart Hodgetts and Dr Giles Plant (School of Anatomy, Physiology and Human Biology)

The use of human bone marrow stromal stem cells (hBMSCs) to treat acute and chronic (long term) in a contusion model of spinal cord injury (SCI) has shown marked improvements in both functional (behavioral) and anatomical recovery. The student will investigate whether hBMSCs (isolated from human SCI patients) can effect myelination of spared axons directly or whether they promote indirectly an endogenous repair mechanism. Growth promotion and myelinating capability of hBMSCs in vitro will be assessed using contact and non-contact co-culture experiments with embryonic dorsal root ganglia (DRGs).

The project will involve extensive tissue culture and immunocytochemical analysis.

Contact: Dr. Stuart Hodgetts: stuart.hodgetts@uwa.edu.au or 08 6488 8642

Investigating the differentiation and proliferation of cocultured human bone marrow stromal stem cells and neural stem cells for application in the treatment of spinal cord injuries

Dr Stuart Hodgetts and Dr Giles Plant (School of Anatomy, Physiology and Human Biology)

Clinically promising cell based transplantation strategies to treat spinal cord injury (SCI) include human bone marrow stromal stem cells (hBMSCs) and neural stem cells (NSCs). These cell types may be involved in the formation of regenerating axonal pathways and/or tissue sparing/repair. We will investigate the potential combinatorial use of hBMSCs (isolated from human SCI patients) and NSCs by assessing the proliferation and differentiation capabilities of these cell types in vitro using contact and non-contact co-culture experiments. The findings will have important implications for the future use of emerging new combinatorial strategies in clinically relevant cell based transplantation strategies.

The project will involve extensive tissue culture and  immunocytochemical analysis.

Contact:
Dr. Stuart Hodgetts: stuart.hodgetts@uwa.edu.au or 08 6488 8642


Analysis of visual projections in knock-out mice using viral vectors

Dr Jenny Rodger, Prof Alan Harvey

In genetically modified mice lacking one or more ephrin-As, the retinotectal projection displays topographic defects of increasing severity as individual or pairs of genes are removed (Frisen et al., 1998; Feldheim et al., 2000), a result attributed to the absence of ephrin-A guidance cues. We performed the first electrophysiological study of the retinotectal projection in ephrin-A-/- mice and showed that these abnormal retinotectal arborizations are functionally active (Haustead et al., 2008). Together, the anatomical and physiological studies of ephrin-A knockout mice indicate that many points in the SC receive input from multiple retinal locations (Feldheim et al., 2000); however it is unclear whether abnormally located terminations are branches of axons that additionally terminate in an appropriate SC location, or whether appropriate and inappropriate projections arise from distinct RGC populations.
The project will address this question by using a novel methodological approach. We will use viral vectors to label and image isolated RGC axons along the length of the visual pathway. Mice will receive a single 1.0µl injection of adeno-associated viral (AAV) vector encoding green fluorescent protein (AAV-GFP) into nasal or temporal retina. AAV preferentially labels RGCs in adult mice and AAV-GFP can be used as a sensitive anterograde tracer in RGCs (Harvey et al., 2002; Leaver et al., 2006). Pilot studies in our lab have shown that a single injection of diluted, low titre virus into one retinal quadrant results in labeling of a small number of RGCs, allowing us to follow the trajectory of individual GFP-containing axons into central visual target structures in the thalamus and midbrain. Mice will be sacrificed after 30 days, transcardially perfused (4% paraformaldehyde) and the eyes and brain dissected. The retina will be flat mounted and labelled cells visualized by fluorescence microscopy and terminal structure and distribution within the primary visual brain structures examined quantitatively.

Feldheim DA, Kim Y-I, Bergemann AD, Frisen J, Barbacid M, Flanagan JG (2000) Genetic analysis of ephrin-A2 and ephrin-A5 shows their requirement in multiple aspects of retinocollicular mapping. Neuron 25:563-574.
Frisen J, Yates P, McLaughlin T, Friedman G, O'Leary D, Barbacid M (1998) Ephrin-A5 (AL-1/RAGS) is essential for proper retinal axon guidance and topographic mapping in the mammalian visual system. Neuron 20:235-243.
Harvey AR, Kamphuis W, Eggers R, Symons N, Blits B, Niclou S, Boer GJ, Verhaagen J (2002) Intravitreal injection of adeno associated viral vectors results in the  transduction of different types of retinal neurons in neonatal and adult rats: a comparison with lentiviral vectors. Mol Cell Neurosci 21:141-157.
Haustead D, Rowlands J, Werren C, Clutton G, Arrese CA, Sherrard RM, Rodger J (2008) Abnormal visual system function in ephrin-A knockout mice. J Neurosci.,
Leaver SG, Cui Q, Plant GW, Arulpragasam A, Hisheh S, Verhaagen J, Harvey AR (2006) AAV-mediated expression of CNTF promotes long-term survival and regeneration of adult rat retinal ganglion cells. Gene Therapy 13:1328-1341.

Gene expression in developing rat retinal ganglion cells

Professor Alan Harvey, School of Anatomy, Physiology and Human Biology

We will use molecular and cell sorting techniques to study expression of genes in identified cohorts of postnatal rat retinal ganglion cells (RGCs), in vivo and in vitro.  Such molecular profiling will aid in determination of genes important in promoting viability and regeneration of adult RGCs after injury.

Tinnitus, a phantom auditory sensation, is prevalent in the human population and is often associated with hearing loss

Dr Helmy Mulders, Prof Mathew Martin-Iverson, Prof Don Robertson


Tinnitus, a phantom auditory sensation, is prevalent in the human population and is often associated with hearing loss. Tinnitus is thought to be linked to hyperactivity in the central auditory brain pathways. In the auditory laboratory we are working on a guinea pig animal model of hyperactivity in the auditory midbrain in response to traumatic hearing loss. In order to pursue this animal model we need to establish that the guinea pigs are experiencing tinnitus. The proposed project will, in collaboration with Prof. Martin-Iverson from Pharmacology, investigate whether the guinea pigs that show hyperactivity in the brain, also perceive phantom sounds. The project combines predominantly behavioural testing and small animal handling and surgery.

Axon regeneration induced by genetic engineering

Prof Alan R Harvey


Using viral vectors it is possible to introduce growth factor genes into retinal ganglion cells (RGC) and into Schwann cells. We have shown previously that Schwann cells genetically modified to express CNTF can be incorporated into peripheral nerve sheaths and, when grafted onto the injured optic nerve, they promote increased regeneration of adult RGC axons. There are two possible projects. In one project, we will examine whether similar types of engineered PN graft also promote the regeneration of RGC axons when the injury occurs in the optic tract in the brain, at a significant distance from the eye. In the other project, RGCs will be modified using appropriate viral vectors and axonal regeneration after optic tract injury will be assessed. The studies address a critical issue in neural repair - the extent to which the site of axon injury affects the regenerative capability of an injured nerve cell.


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