Professor Stephen Redman, Head of Division
It has been known for a long time that the control of skeletal muscle by spinal nerves occurs through a precise anatomical structure called the neuromuscular junction. Relatively recently, evidence has emerged to suggest that a specialised anatomical structure also exists in tissues controlled by nerves of the autonomic nervous system. At these neuroeffector junctions, the membranes of the nerves are closely associated with those of the effector cells so as to permit the release of neurotransmitter on to a selective subset of receptors whose activation results in the effector response. Such neuroeffector junctions have been described in a number of blood vessels where nerve-mediated contractions result from calcium entry through voltage dependent calcium channels. We have shown that in other arterioles, where contraction occurs through the activation of a different class of receptors and the release in intracellular calcium, neuroeffector junctions can also be found. These studies have provided further evidence that neuroeffector junctions are typical of autonomic synapses irrespective of receptor types and signal transduction pathways activated. Furthermore, the demonstration of an anatomical correlate of the autonomic synapse in mature animals enables future studies on the relationship between anatomy and physiology during development.
The anatomical relationship between the smooth muscle cells in the walls of arteries and veins is critical to the coordination of vasoconstriction and vasodilation. In most arteries, the wall is composed of several layers of smooth muscle cells and the nerves which modulate contractile activity lie at the outer edge of the muscle layer, where they can only directly activate a few cells. In order to produce a coordinated contraction then, there is a requirement for efficient coupling between the smooth muscle cells in the walls. This is achieved through structures called gap junctions which in turn are comprised of molecules called connexins. Using intracellular microelectrodes we have demonstrated that the muscle cells of small arterioles are electrically coupled suggesting the presence of connexins in their walls. Only three of the connexin family of molecules have been described in blood vessels. Surprisingly, our comparative studies using immunohistochemistry and antibodies directed against these three molecules have failed to detect any of them in the muscle layer of resistance arteries, although there was expression in the larger, elastic arteries. Furthermore, there was heterogeneity in the relative appearance of these three connexins in the endothelium of elastic arteries, small muscular and large muscular arteries. These results highlight the fact that heterogeneity in structure may contribute significantly to function. Interestingly, recent studies suggest that increases in connexin expression play an important role in cardiovascular disease, such as hypertension.
Heterogeneity exists in physiological responses between different vascular beds. While we have previously demonstrated that some of this heterogeneity can be attributed to variation in expression of different receptors, some could also result from variation in structure. Future studies will be aimed at determining the extent to which such anatomical variation might contribute to functional diversity.
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The amygdala is a part of the limbic system that is involved in assigning emotional significance to cognitive events. In particular, it is involved in the processing of fear producing stimuli. One simple form of learning the amygdala is involved is fear conditioning. Fear conditioning is the process during which a normally innocuous stimulus such as a flashing light becomes associated with a fear producing stimulus (like an electric shock) so that the innocuous stimulus itself subsequently produces a fear response. It represents a form of learning and involves the storage of "emotional" memories. |
Disorders of the storage or expression of fear responses are thought to underlie such mental disorders as panic attacks, anxiety and post traumatic stress disorder.
A converging body of literature over the last forty years indicates that the amygdala is critically involved in assigning emotional significance or value to events through associative learning. Stimulation of the amygdala can elicit the same constellation of symptoms as fear, and lesions of the amygdala reduce the acquisition and expression of fear. An understanding of the function of this structure is thus essential in the development of rational therapies for a range of related anxiety disorders. The anatomical organisation of the amygdala is now fairly well understood. However, its physiology is just beginning to be elucidated. The main focus of the cellular neurophysiology group is to elucidate the basic electrophysiological properties of cells within the amygdala and study its synaptic connectivity.
It is known that the major inputs to the amygdala use glutamate as the principal transmitter. Glutamatergic synapses can undergo a type of plasticity which has been implicated in the storage of memories. In the amygdala, these synapses are likely to be involved in the acquisition of fear conditioning. The amygdala is broadly divided into three main subnuclei: the lateral, basal and central. Sensory and cortical inputs enter the amygdala at the level of the lateral and basal nuclei. The different subnuclei are extensively interconnected and finally project to the central nucleus. Cells within the central nucleus project to brainstem and hypothalamic nuclei responsible for evoking the physiological responses associated with fear.
One project in our group is involved with examining the properties of cells in the input side of the amygdala. We have shown that cells within the lateral and basal nuclei can be divided into two broad categories: pyramidal cells and interneurones. Pyramidal cells form the major type of cell (93%) and are similar to excitatory cells found throughout the cortex. The remaining cells (7%) are interneurons which are inhibitory and form extensive connections with the excitatory cells in the amygdala. Surprisingly we found that the properties of synaptic inputs onto interneurons were quite different from those onto pyramidal cells. These findings indicate that the modulation of inhibitory pathways may be an important control mechanism within the amygdala.
Another project is studying the output side of the amygdala - the central nucleus. This structure is divided into two main parts the medial and lateral. It has recently been shown that cells in the lateral division are inhibitory and make local circuits which cells in the medial division project out of the amygdala. We have been examining the effects of a class of drugs called benzodiazepines (eg diazepam or valium). These drugs are widely used as anxiolytics and their role in the amygdala is of great interest. These drugs are thought to work by potentiating the actions of the major inhibitory transmitter in the brain gamma amino butyric acid (GABA). We have found that the central nucleus also contains a second type of GABA receptor which is inhibited by benzodiazepines. This finding may have potential therapeutic implications as it might be a potential target for new classes of drugs.
| The first described mechanism is via the retrograde axonal transport of neurotrophic factors such as the Nerve Growth Factor. This transport occurs in vesicles where the neurotrophic factor is in the lumen of the vesicle and its receptor is in the wall. In this way the machinery required for the signal transduction is physically moved from the terminal to the cell body where it can then interact with the signal cascade leading to nuclear responses. |
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There are also different components of this system used by different neuronal populations, for example different isoforms of the enzyme PI3-kinase are used by sympathetic and sensory neurons in the transport of nerve growth factor.
The nerve cell also derives essential information from molecules in the vicinity of its terminal that are not themselves retrogradely transported. These may be bound to the extracellular matrix or be on the surface of target cells. These molecules require long lasting second messenger molecules in order to transduce their signal from the terminal to cell body. One of the GTP-binding proteins, Gz, has proved to be retrogradely transported and looks promising as a signalling molecule in sensory neurons. In collaboration with the Gene Targeting Group we have made mice deficient in this protein and have been determining the functional sequel of this knockout.
The Gz-knockout mouse has a prolonged bleeding time with no apparent disturbance of aggregation times, calcium fluxes or secretion of ATP in platelets. The mutant has a failure to gain weight at the normal rate during the first three postnatal weeks but returns to normal by 2-3 months of life. It has impairment in the development of the sympathetic nervous system such that there are fewer neurons in the sympathetic ganglia. There appears to be a compensatory role for other G-proteins as sympathetic neurones from the knockout mouse grow normally in tissue culture in response to Nerve Growth Factor but fail to grow normally if pertussis toxin, the inhibitor of the G-proteins Gi and Go is included in the medium.
Gz has been shown to be involved in the mu opoid receptor response and we have commenced behavioural studies to investigate this further. There is a change in the response of these animals to morphine analgesia in that they become extremely tolerant to morphine when tested by the licking response on the hot plate.
The group has been collaborating with Dr Hugh Campbell in RSBS who has been isolating the mouse and human gene for the drosophila protein, Small Optic Lobes (sol), with the aim of finding its role in mammalian development. We have generated a polyclonal rabbit antibody to this protein and have shown it to be present in the olfactory bulb of the developing mouse brain.
 Click to enlarge photo | The balance between the proliferation, differentiation and death of cells is normally under tight control in the body, and this balance can be modified during different stages of development. Thus, during embryogenesis there is a greater bias toward proliferation followed by differentiation than in the adult. During certain disease states, however, this balance can be altered, such as in tumour formation. Here the normal controls inhibiting cellular proliferation break down, and cell division continues with less feedback regulation. |
This work has two main focusses. The first is the control of the cytoskeleton and its role in cellular signal transduction. The second is the role of the GTP-binding protein Gi in growth factor stimulation of the cell cycle, particularly in cell division.
The Cytoskeleton
We have found that the actin cytoskeleton plays a profound role in determining the ability of a cell to proliferate, in that inhibition of polymerisation of actin will dramatically reduce the ability of a cell to replicate. This could result from several potential roles of actin, such as in signal transmission from a receptor or in the more basic structural requirements for the actin cytoskeleton to contribute to cell cleavage. We are examining both aspects to try to determine not only what activates the actin cytoskeleton to polymerise, but also to see if these processes may be potential sites of therapeutic modification to reduce cell proliferation. This work has identified a novel form of the PI 3-kinase system that is involved in the Swiss 3T3 cell to stimulate actin polymerisation, and this enzyme acts to stimulate the p70 S6 kinase, which our laboratory has recently shown to be a key regulator of this process.
Further work is directed toward the basis of regulation of this process upstream of PI 3-kinase, at the level of the receptor and the coupling G-proteins or tyrosine kinases, depending on the receptor type being activated. We have proposed a receptor second messenger competition model which we suggest underlies the cellular response to a particular hormone. In this model we propose, for example, that a G-protein coupled receptor may signal to more than one G-protein, and in a particular cell there may be a bias to one G-protein or another depending on numbers of protein molecules and affinities between the receptor and G-protein. The extension of this predicts that if one can manipulate the affinity or number of molecules that can interact with the receptor then the ultimate response of the cell can be changed to that hormone. We are at present examining pharmacological strategies with which we can modify cellular systems in this way, with the intention of re-biasing growth factor-activated systems away from cellular proliferation toward the signal transduction systems that will result in cellular differentiation. Our initial results suggest that this approach is feasible and our initial studies are now being submitted for publication.
Additionally, in collaboration with Hugh Campbell, RSBS, we are studying the role of the Flightless protein in cell regulation. The evidence so far suggests that this protein may also play a role in regulation of the cytoskeleton.
The Gi GTP-binding protein
We have continued our work on the role of the Gi protein in the cell cycle, and the new function that we have ascribed to this protein. We have characterised previously that the Gi alpha-subunit (Gia)translocates into the nucleus of cells destined to divide, and the Gia binds to the chromatin of dividing cells. Our most recent data has come from the combined use of Flow Cytometry (in collaboration with Geoff Osborne) and immunohistochemistry to show that Gia plays an apparent role as a checkpoint protein in mitosis, and that the site of localisation of Gia is at the kinetochores of the paired chromosomes. This work is also submitted for publication. Our continued work in this area is to elucidate the role and mechanism of action of Gia in mitotic control, particularly in relation to cyclin and cylin-dependent protein kinase regulation.
In their quest to understand how the brain works, neuroscientists often try to reduce the complexity of the problem by dividing it into smaller parts. One way in which this is done is to study neurons in distinct regions of the brain, designing experiments that are informed by what is known about the functions of those regions. For example, some scientists study the effect of painkillers on individual neurons in the midbrain, knowing that the midbrain is somehow involved in pain perception. Others study the ability of neurons in the cerebral cortex to integrate the inputs from many other neurons, knowing that one job of the cortex is to integrate sensory information. Although this seems like an obvious research strategy, it is in fact quite remarkable that it succeeds as often as it does. Even a relatively small part of the brain, like the midbrain, contains many millions of neurons. A single neuron is but one cog in a very complex machine. And yet even a single neuron may possess a complex portfolio of properties that reflect the special role of the circuit in which it is embedded.
Research in the Synaptic Biophysics group is guided by this reductionist approach to studying brain function. Single neurons or pairs of neurons from different brain regions are studied, using the known or suspected functions of those regions as a guide to the design of experiments. Our research uses a range of techniques. In some experiments, single neurons are dissociated from subregions of the brain using a combination of enzymes and mechanical agitation. This procedure shears off all contact with other cells, but allows study of the intrinsic electrical properties of the neuron. In other experiments, neurons are studied in thin slices of living tissue taken from the brains of rats. In this case the contacts between many neurons are preserved, enabling the study of the electrical signals that propagate from one neuron to the next.
A project being conducted in the lab by Dr John Bekkers (JCSMR Fellow) is studying how one class of neurons in the cerebral cortex (pyramidal cells) might combine information coming from other neurons. This process, called synaptic integration, involves the summation of many hundreds of electrical signals that a single pyramidal cell receives from its neighbours via synapses. As a result of this summation process, the cell will decide whether or not to pass on a signal, in the form of an action potential, to subsequent neurons in the chain. Most of the synapses on a pyramidal cell are distributed over its dendrites - those long, fine structures that act like antennae for incoming messages. Synaptic integration will therefore depend critically on the properties of the dendrites. Research in the lab is examining how the dendritic properties of cortical pyramidal cells depend on the behaviour and distribution of a class of membrane proteins, called potassium channels, which are known to be important for the electrical properties of all cells. Experiments indicate that at least three kinds of potassium channel are found in the membranes of cortical pyramidal cells. Remarkably, these channel types have distinct patterns of distribution in the dendrites. Future work will explore the functional impact of this nonuniform distribution on synaptic integration.
Another member of the lab, Dr Billy Chieng (C J Martin Postdoctoral Fellow), is examining the response of dissociated neurons from the midbrain of rats to opiates and related substances, which are known to be involved in pain perception. It turns out that one of the targets of such substances is another important class of membrane proteins, called calcium channels. Calcium channels help determine the level of calcium inside cells. Intracellular calcium is in turn critical to a wide range of cellular functions, such as growth, gene expression, and the release of neurotransmitter. Just as there are different kinds of potassium channels, there are also different kinds of calcium channels. We have found that enkephalin (an endogenous opiate) and GABA (an inhibitory neurotransmitter) modulate these different calcium channel subtypes in different ways. Work done in the lab last year by a former PhD student, Chris Reid (now a Postdoctoral Fellow in London), showed that calcium channel subtypes, like potassium channel subtypes, also have a nonuniform distribution on neurons. Thus, a picture seems to be emerging whereby distinct subtypes of both potassium and calcium channels are targeted to different parts of neurons, where they may be selectively modulated by biologically important substances.
A general conclusion from research in the lab is that neurons exhibit a surprising complexity in their functional microarchitecture. Neurons are not simple elements of large brain circuits, but are processors in their own right, with considerable power and flexibility. They can be said to have minds of their own.
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In photoreceptors as in other neurons, neurotransmitter is secreted via the calcium dependent fusion of synaptic vesicles with the plasma membrane. Calcium enters the cell through electrically sensitive pore-forming proteins in the plasma membrane. The relationship between these calcium channels and the proteins catalyzing synaptic vesicle fusion is a tremendously exciting and active area of research in recent years bringing us closer to understanding the molecular basis of neuronal signaling. This year we have worked on identifying and characterizing the calcium channels in photoreceptor synaptic terminals.
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A second ongoing interest in the lab is the study of the “synaptic ribbons” in photoreceptor terminals. In electron micrographs these structures appear as electron dense bars running perpendicular to the active zone and surrounded by a halo of synaptic vesicles. Their appearance is highly suggestive of a role in the delivery of synaptic vesicles to the plasma membrane. Recently electron microscopic analysis of the ribbons combined with electrophysiological measurements of synaptic vesicle fusion showed that the number of vesicles tethered to the ribbons agrees closely with the number of vesicles immediately released upon stimulation. Despite their intriguing structure and probable importance in transmitter release, synaptic ribbons have eluded attempts to characterize them biochemically. This year we were able to generate antibodies that label the synaptic ribbons on retina sections. We are hoping to that these antibodies will enable us to affinity purify the ribbons. We will then be able to identify the ribbon proteins. Ultimately we would like to be able to reconstitute the interaction between the ribbons and synaptic vesicles in vitro. We will then be able to explore the hypotheses that the ribbons actively transport synaptic vesicles to the active zone, and that the interaction is calcium dependent.
| In order to understand the highly complex functions of the brain, we must understand how individual neurons communicate with each other. This communication occurs at specialized synaptic contacts, and the overall aim of our Group is to understand how synaptic strength is regulated, and how synaptic signals are processed by target neurons. The appropriate regulation of synaptic strength is essential for normal development of the nervous system, and for the proper functioning of the adult brain. Modulation of the strength of synapses is thought to be the basis for many essential central processes such as learning and memory. |
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A thorough knowledge of synaptic transmission requires investigation of both the structural and functional aspects of synaptic connections. Over the past several years, our Group has been studying the structure and function of specialized synapses in the central auditory pathways. We have used a brain slice preparation which offers many distinct technical advantages in the investigation of fundamental mechanisms underlying both excitatory and inhibitory synaptic transmission.
Current Projects
Electrophysiological and immunohistochemical studies of quantal synaptic transmission
When a nerve impulse arrives at a synaptic contact, a neurotransmitter chemical is released in quantal amounts from membrane-bound vesicles within the presynaptic terminal. The released neurotransmitter binds to and activates receptor-channels in the membrane of the target neuron. Receptors generating the postsynaptic currents are clustered at individual synapses, primarily through specific interactions with the cytoskeleton of the cell. Regulation of receptor clustering has been proposed as an important mechanism for modulating the amplitude of postsynaptic currents, although direct experimental evidence is lacking. We have investigated this hypothesis by analyzing inhibitory glycinergic synaptic currents and receptor clusters in neurons of the anteroventral cochlear nucleus. Using combined immuno-fluorescence labelling of glycine receptor clusters and electrophysiological recordings of synaptic currents in the same cells, we have obtained the first direct experimental evidence that the amplitude of quantal postsynaptic currents is correlated with receptor cluster area. These results support a model of central synaptic transmission in which synaptic strength may be regulated by the size of the postsynaptic receptor clusters. Our current experiments are aimed at determining which factors influence the size of postsynaptic receptor clusters, and the role of nerve activity and developmental changes in this process.
Electron-microscopic studies of central synapses
The ultrastructural details of synaptic connections between neurones have provided many clues to the function and modification of synaptic transmission in the central nervous system. For example, the vesicle hypothesis, and the concepts of discrete transmitter release sites and receptor clusters owe their origins directly to electron-microscope studies of synaptic contacts. This project is producing 3-dimensional reconstructions of the entire synaptic contact pattern between individual auditory nerve fibers and neurones in the brain. Detailed measurements of ultrastructural features of the synaptic connections, revealed under the electron-microscope (such as the size and shape of synaptic specializations and the clustering of vesicles) are being used to construct models to investigate the nature of diffusion of neurotransmitter within the synaptic cleft, and the activation of postsynaptic receptors.
The molecular mechanisms of transmitter release
Some synaptic terminal types in the auditory system are the largest in the brain, enabling direct access via a microelectrode. This provides the opportunity to study the molecular mechanisms of transmitter release. In this project, molecules which affect transmitter release are injected directly into the nerve terminal. The results of these experiments will provide insight into the molecular events underlying the mobilisation of synaptic vesicles, and the molecular processes leading to transmitter release. This study is being carried out in collaboration with Professor PR Dunkley and other members of the Medical Biochemistry Discipline, University of Newcastle.
Modulation of Synaptic Transmission
The all or none firing of action potentials by a central neuron is determined by the integration of synaptic inputs and the intrinsic membrane properties of the postsynaptic cell. Both of these factors may be markedly influenced by the presence of neuroactive chemicals, such as serotonin, noradrenaline, acetylcholine, adenosine or neuropeptides. These neuromodulators bind to receptors which can directly gate ion channels, or modulate ion channels via G proteins and various signal transduction pathways. We seek to understand how synaptic transmission in the central nervous system is modulated by these neurochemicals. The results of our experiments will provide valuable insight into the effect of neuromodulators on both the presynaptic release of neurotransmitter and their action on the postsynaptic neuron.
Central Respiratory Pattern Generation
Breathing movements are regulated by a central respiratory pattern generator, consisting of a synaptic network of neurons located in the lower brainstem. The rhythmic output of this network is conveyed to various motor neurone pools controlling respiratory muscles. Rhythm generation occurs through a complex interaction between phasic synaptic inputs and voltage-dependent ionic currents of brainstem neurones. Disturbances of respiratory control may underlie clinical syndromes, such as obstructive sleep apnoea or sudden infant death syndrome. The process of respiratory rhythm generation and motor output, and their neuromodulation, are being studied in vitro, using reduced preparations and characterization of ionic currents and synaptic inputs.
The same experimental techniques are being used to study synaptic transmission between excitatory interneurones and motoneurones. Paired recordings between these two types of neurones are used to evoke synaptic potentials in the motoneurone and biocytin in both pre-and post-synaptic neurones is used to reconstruct the morphology of the synapses. The receptor mix and plasticity are being investigated at these synapses.
Visual processing begins in the retina, embodied in three neural layers lining the back of the eyeball. The first layer is the photoreceptors, the intervening layer the bipolar cells, and the last layer the ganglion cells that send their axons to the brain via the optic nerve. Research in this laboratory focuses on two areas - the connections from the photoreceptors to the bipolar cells, and the neural mechanisms underlying motion processing in a specific class of ganglion cells.
The synapses or connections between photoreceptors and bipolar cells are significant for two reasons. First, since these connections comprise the first synaptic relay in the visual system, they place a fundamental limit on the detectability of stimuli. Any extraneous noise introduced at this stage cannot be removed at later stages. Second, the mechanism of synaptic transmission at these connections is significantly different from that used in the rest of the brain. Photoreceptors release the neural transmitter, glutamate, in a continuous stream, interrupted only to signal detection of light. In contrast synapses in the rest of the brain release transmitter in very brief bursts lasting only one thousandth of a second. A collaboration between this laboratory and Synaptic Biochemistry (see this annual report) is combining electrophysiological, molecular biological, immunohistochemical and biochemical techniques to study how calcium ions mediate synaptic transfer. We have found that the photoreceptors express a novel class of voltage-activated calcium channels, and we are studying how these channels interact with other proteins involved with transmitter release. Amy Berntson, a PhD student in the laboratory, is recording light-evoked synaptic responses from bipolar cells of mouse retina as a way of monitoring the output of glutamate from the photoreceptors. It is anticipated that by comparing the specific molecular machinery of this synapse with what is known for other brain synapses we can gain new insights into factors governing transmitter release.
A further collaboration, with Dr Robert Duvoisin of the Dyson Vision Research Institute at Cornell Medical School in New York, involves the application of transgenic techniques to study photoreceptor-to-bipolar cell synaptic transmission. Dr Duvoisin has produced a transgenic mouse deficient in a glutamate autoreceptor. This receptor is normally present in the synaptic terminals of photoreceptors, and in this location enables the glutamate released from the photoreceptor to feed back and modulate its own release. Such feedback control is common throughout biological systems, but its role in this case is enigmatic. A physiological analysis of the receptor-deficient transgenic mouse is helping to clarify this question. Dr Duvoisin will be a Visiting Fellow in the School for two months early in 1999 during which time we will develop viral based transfection procedures to study specific classes of neurons within the mammalian retina. Motion detection is fundamental for any visual system and in many vertebrate retinas there are specific classes of ganglion cells which are tuned to respond to stimuli moving in particular directions. These direction selective ganglion cells will respond, for example, to a bar of light moving in a preferred direction, and remain quiescent for the same bar moving in the opposite direction. The main thrust of this work is to find the locus of the underlying synaptic interaction. Is direction tuning due to synaptic integration within the dendrites of the ganglion cells, or is it a property of the preceding neural circuitry which is simply registered and reported by the ganglion cells? Three other researchers are collaborating on this project: Professor Bill Levick, a former faculty member of the School and now a Visiting Fellow, and Dr Shigang He and Dr David Vaney at the Vision, Touch and Hearing Research Centre in the University of Queensland. Dr He is an NHMRC funded Senior Research Officer.
School Technical Manager:
RJ Ayling, ECC
Divisional Administrator:
E McNaughton
Assistant to School Technical Manager:
P Blower, BA Hons (Syd)
Administrative Assistant: - Until August
L Hardy (part-time)
Senior Technical Officers:
DG Geary (until November); B Keys
Technical Officers:
E Milinski (until July); G Whalley
Autonomic Synapse Group
Senior Fellow and Leader:
CE Hill, BSc, PhD (Melb)
Postdoctoral Fellow
K Francki, BSc(Hons) (AdeL); PhD (Uni WA)
Technical Officers:
J Ellis (until June); H Hickey (from July)
Temporary Assistant:
J Phillips BVSc(Hons) (Syd) (from November to January)
Cellular Neurophysiology Group
Leader, Sylvia & Charles Viertel Fellow
P Sah BSc, MBBS (NSW), PhD (ANU)
Postdoctoral Fellow:
N Mahanty BE (Chch), PhD (ANU); Magrie, T BSc, PhD (Newcastle) (from June until September)
Developmental Neurobiology Group
Professor and Leader:
IA Hendry, BSc(Med), MB BS (Syd), PhD (Camb)
Postdoctoral Fellow:
S Bartlett, BSc, (Qld InsTTech), BPharm (Qld), PhD (Qld)
Visiting Fellow:
D Megirian, MS (Rochester), PhD (Rochester) (from December)
Research Assistant:
K Heydon
Laboratory Technician:
B Fazackerley (until September)
Membrane Physiology and Biophysics Group - until August
Professor and Leader:
PW Gage, MB ChB (NZ), PhD (ANU), DSc (NSW), FAA
Research Fellow:
B Birnir, BS (Wash), PhD (UCLA)
Postdoctoral Fellow:
AKM Hammarström, BSc(Hons), PhD (Monash)
Research Assistants:
J Curmi, (B Optom)(UNSW); A Everitt, BSc
Muscle Research Group - until August
Professor and Leader:
AF Dulhunty, BSc (Syd), PhD, DSc (NSW)
Visiting Fellows:
D Laver, BSc(Hons), PhD (UNSW), (ARC); J Hart, BSc( Hons), PhD (Monash); E Gallant, BA (Ohio), PhD (Indiana) (from January)
Senior Technical Officer:
S Pace, BSc (UTS)
Technical Officer:
SM Curtis, BSc, PLTC (half-time)
Laboratory Technician:
J Stivala
Synaptic Transmission Group
Professor and Leader:
SJ Redman, ME (NSW), PhD, DSc (Monash), FAA
University Fellow and Emeritus Professor:
DR Curtis, AC, MB BS (Melb), PhD, FRACP, FAA, FRS
Visiting Fellows:
J Clements, BSc (Monash) PhD (ANU) (until December); S Ilschner, MD, PhD (Erlangen)
Wellcome Ttrust Senior Research Fellow:
G Stuart, QEII Fellow, BSc (Monash), PhD (ANU)
Postdoctoral Fellow:
S Williams, BSc(Hons), PhD (Uni College, Wales) (from February)
Technical Officers:
GR Rodda PTC
Synaptic Biochemistry Group
Research Fellow and Leader:
C Morgans, BSc(Hons) (Michigan); PhD (Stanford)
Postdoctoral Fellow:
G De Plater BSc(Hons), PhD (ANU)
Molecular Signalling Group
Fellow and Leader:
MF Crouch, BSc, PhD (Adel)
Postdoctoral Fellow:
LA Berven, BSc(Minnesota), MSc (British Columbia), PhD (Uni Syd) (part-time)
Synaptic Biophysics Group
Research Fellow and Leader:
JM Bekkers, BSc (Hons) (Griffith), MSc (Manchester), PhD (Cambridge)
CJ Martin Fellow:
C Chieng, BPharm (Sydney), PhD (Sydney) (from February)
Synaptic Structure and Function Group
Senior Fellow and Leader:
B Walmsley, BE, PhD (Monash), DSc
QEII Fellow :
M Bellingham, BVSc(Hons) (USyd), PhD (ANU)
Postdoctoral Fellow:
S Oleskevich, BSc(Hons), PhD (Montreal)
Research Officer:
MJ Nicol, BSc(Hons) (ANU), PhD (ANU)
Visual Neurosciences Group
Fellow and Leader:
R Taylor BSc(Hons) (NSW), PhD (ANU)
Visiting Fellows:
D Vaney BSc(Hons) (Canterbury); PhD (ANU); P Anderton BOp, BSc, PhD (NSW), MSc (Melb) (from June to November)
Technical Officer:
E van de Pol, BRTC (from March)
Molecular Neuroscience Facility
Technical Officer:
T Sutherland, B ApP SC (Charles Sturt Uni) (from October)