Neuroscience

Introduction

Understanding the human brain is one of our greatest scientific challenges. In the Division of Neuroscience, we study the fundamental molecular and cellular mechanisms underlying brain processes involved in vision, hearing, movement, cardiovascular control, emotion and memory.

The brain is made up of billions of neurons which transmit information to each other via specialized junctions called synapses. An individual neuron may receive synaptic information from hundreds or thousands of other neurons. The strength of the signal transmitted at each synapse may be modified during development of the brain and in processes such as learning and memory formation. Alterations in synaptic strength and connectivity may also underlie many neurological disorders. A major focus of research in the Division is to understand the molecular and cellular processes which regulate the strength of synaptic connections and how individual neurons process this information. Over the past year, a number of significant advances have been made by individual groups, such as the discovery of how neurons in the retina interpret moving objects, and how synaptic signals and nerve impulses interact within individual neurons in the brain. Because of the multidisciplinary nature of neuroscience research, many of the research projects carried out within the Division of Neuroscience have continued to benefit from cross-discipline collaborations established with scientists in the JCSMR and other national and international institutions.

Bruce Walmsley
Division Head

Essays

Cellular Neurophysiology Group
Dr Pankaj Sah

Minds as we know them not only think but also feel. Reason and emotion are two aspects of brain function which have often been thought to be separate, despite there being little doubt that emotion can disrupt reasoning. It has become clear that reason and emotion are two aspects of the same phenomenon and go hand in hand as parts of mental function. Experiments in the last few years established that the amygdala, which is a small collections of neurons in the medial temporal lobe, plays a key role in emotions, particularly fear. Fear is a very old emotion which is particularly important to animal and human existence. It is a normal response to threatening events and is a common part of life. Disorders of processing of fear are thought to underlie such mental disorders as panic attacks, anxiety and post traumatic stress disorder. The development of rational and directed therapies for these disorders requires an understanding of the function of the amygdala. Much is known about the anatomy of the amygdala and its connections with the rest of the brain. However, the physiology of this structure is not well understood.

In the Cellular Neurophysiology group we are studying the neurophysiology of the amygdala. The questions we are addressing are: What kinds of cells are present in the amygdala? What are the neurotransmitters which are present? What are kinds of synaptic plasticity present in the amygdala which might contribute to the storage of emotional memories? What is the mechanism of action of compounds which are known to affect the processing of emotional information?

The lateral and basolateral nuclei of the amygdala receive information from a variety of cortical and sensory areas. This information is processed locally, then transmitted to the central nucleus which is one of the main output stations of the amygdala. Projections from the central nucleus to the hypothalamus and brain stem are responsible for controlling the changes in heartrate and sweating which accompany emotional responses. We are doing experiments on both the input side and output side of the amygdala using acutely prepared brain slices maintained in vitro.

In experiments on the lateral amygdala we have shown that there are many different types of neurons in this structure than was previously suspected. These cells have different types of firing properties which are controlled by different types of currents in these cells. We are now beginning to address questions relating to how these cells are connected to each other and what the nature of synaptic inputs to these cells are. We have found that the inhibitory interneurons in the lateral amygdala receive excitatory inputs which activate very different glutamate receptors from inputs which go to the pyramidal cells. These inputs to interneurons show a novel form of plasticity.

In experiments on the central amygdala we have found that these cells express a new type of GABA receptor. GABA receptors are the major inhibitory receptors in the mammalian brain. Drugs which are used in the treatment of anxiety disorders, such as diazepam (valium) work by modulating the function of GABA receptors. The new type of GABA receptor we have found reacts differently to diazepam than GABA receptors in most other parts of the brain. We are now investigating if this receptor may be a new target for the development of drugs aimed at alleviating anxiety disorders.

Autonomic Synapse Group
Dr Caryl Hill

The efficient functioning of organs within the body relies on an adequate supply of nutrients and removal of waste products via the blood. The control of blood flow to organs of the body and the maintenance of blood pressure in turn relies on a balance between factors which make blood vessels reduce their diameter (constriction) and those that make them increase their diameter (dilation). These various factors differ in different parts of the body and also under disease conditions. For example, in hypertension, which is a major risk factor for stroke and heart attack, the factors which cause constriction outweigh those that cause relaxation and blood pressure is increased. Our work is concerned with understanding the mechanisms underlying this balance of vasoconstriction and vasodilation and determining what factors perturb this balance in disease states.

The walls of blood vessels are made up of two types of cells, an inner layer of endothelial cells which line the vessels and are in contact with the blood, and several outer layers of muscle cells which surround the endothelial cells. Contractions and relaxations of these muscle cells are responsible for changes in diameter of the blood vessels which in turn affect blood pressure. We have been interested in the question of whether changes in the structure of blood vessels may underlie changes in function. Of particular interest are structures called gap junctions which are channels which form between adjacent cells in the walls of blood vessels. These gap junctions enable the transfer of both electrical and chemical information between the cells and are therefore important for the coordination of contractions in blood vessels. We wish to determine whether the number and form of these gap junctions are responsible for changes in blood pressure in health and disease.

Nicole Rummery, PhD student with Caryl Hill

Our recent studies have shown that there are significant differences in the number and structure of gap junctions in different blood vessels. We have also shown that these changes are correlated with changes in the mechanisms associated with relaxation of the same vessels. In addition, we have found that differences in the incidence and structure of gap junctions can also be found between blood vessels in normal animals and in animals which have a genetic defect that causes them to develop high blood pressure. These changes are not present before the development of the high blood pressure but coincide with the increases in blood pressure of these animals. The results suggest that there are important structural changes in blood vessels which correlate with significant changes in blood vessel function and blood pressure. Our future experiments will be aimed at determining whether there is a causal relationship between these anatomical changes and the changes in function which accompany the hypertensive state.

Developmental Neurobiology Group
Professor Ian Hendry

Nerve cells are dependent on information they receive from the cell they are to make contact with in order to survive and mature. As they are extremely long, sometimes over a meter in length from the cell body along the axon to the terminal, there is a major problem for signal transduction for molecules acting on receptors at the nerve terminal that need to convey the survival signal to the cell body. Survival of neurons during development of the nervous system is dependent upon both soluble and insoluble trophic factors signalling from the nerve terminal to the cell body. Understanding the processes that control the flow of information from the nerve terminal to the cell body is essential if we are to understand neuronal development and apply this understanding to nerve regeneration.

Soluble neurotrophic factors such as NGF promote the survival of sympathetic and sensory neuronal populations by binding to receptors present on the nerve terminal, and the complex internalised and transported to the cell body. This transport occurs in multivesicular bodies where 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. Our current research aims to examine this targeting to try to find a way to increase the availability of neurotrophins during regeneration.

Other molecules that are not transported but generate second messengers in the nerve terminal may influence neurotrophin endocytosis or transport. We have been investigating the mechanisms of control of the retrograde axonal transport of 125I-NGF, 125I-NT-3 , 125I-NT-4/5 125I-BDNF to determine the additional factors that may regulate this pathway of signal transduction and thus be able to act in synergy with the neurotrophins. These molecular mechanisms have been investigated by identifying potential signalling molecules using specific pharmacological inhibitors. Our studies suggest that retrograde axonal transport of these proteins relies on the dynein motor protein in vivo and that a wortmannin-sensitive isoform of PI3-kinase or PI4-kinase has an important function in the intracellular transport of neurotrophic factors. The activators of protein kinase C when applied at the nerve terminal block retrograde axonal transport of the neurotrophins and this blockade is reversed by the inhibitors of the calcium independent isoforms of protein kinase C. The results of this study will suggest alternate ways to enhance neuronal regeneration by perturbing the second messenger cascades promoting axonal transport.

Molecules that are not themselves retrogradely transported may generate stable second messenger molecules at the nerve terminal, which are stable enough to survive the long time for transport to the cell body. We have examined the downstream signalling pathways looking at molecules that are associated with retrogradely transported NGF. We found that molecules that could be activated at the nerve terminal will move along the axon together with NGF and that blockage of their activation will prevent this association. The recruitment of associated second messengers to the signalling organelle requires their activation at the nerve terminal and not at the cell body. Thus activation of other signalling pathways may regulate the mix of proteins retrogradely transported to the cell body and thus alter the final signal delivered.

In a further attempt to describe such messengers we examined the role of the GTP-binding proteins as potential stable second messengers and demonstrated the retrograde transport of Gi and Gz. In order to study the function of Gz in more detail, in collaboration with the Gene Targeting Group, we have made mice deficient in this protein. The animals had a prolonged bleeding time and fail to thrive over the first 3 weeks of age. Behavioural tests on the Gz-alpha deficient mouse showed no abnormalities in the rotarod, maze, righting reflex and cortical placing reaction.

Heterotrimeric G-proteins couple to m and opioid receptors. Two of these G-proteins, Gz and Gi, have been shown to be involved in m-mediated supraspinal analgesia. We therefore tested the Gza deficient animals for morphine induced spinal analgesia using the tail flick test and supraspinal analgesia using the hot plate test. Gz deficient mice develop tolerance to morphine more rapidly and to a greater extent than control mice. In these mice receptor binding assays show a small decrease in the affinity of tolerant animals but the increased tolerance in the Gza deficient is not due to receptor down regulation as the maximum binding and receptor affinity do not differ between control and Gza deficient mice. Thus it appears that the alteration in tolerance observed in these experiments is due to a perturbation of G-protein coupled second messenger cascades. Thus Gz may normally play a role in the prevention of the development of opioid tolerance and the presence of Gza delays the development of morphine tolerance. Conversely, preliminary data suggests that during naloxone precipitated withdrawal the Gza deficient animals respond as if they were naive rather than more tolerant than the wild type. These results provide insights as to the mechanisms of morphine tolerance and dependence and may lead to new approaches to the control of morphine addiction.

Molecular Signalling
Dr Michael Crouch

Growth Factor Receptor Synergy: Our experiments have been directed toward a better understanding of the cellular processes underlying hormonal synergy, whereby stimulation with two or more growth factors induces a cellular response that is greater than the sum of their individual effects. This work has described a new mechanism of hormonal synergy, whereby co-activation of a cell with one growth factor will induce the subcellular accumulation of other growth factor receptors. Such receptor clustering was found to occur in discrete F-actin-containing structures, particularly the actin arc of migrating cells. The receptors accumulated with downstream signalling proteins, and this appears to be an important determinant of the synergistic cellular stimulation by these growth factors.

Synaptic Biophysics Group
Dr John Bekkers

A small child, playing happily, suddenly freezes and gazes vacantly into space. A young woman staggers then falls to the ground, back arched and limbs writhing. These are some of the outward signs of epilepsy, that frightening disease in which the sufferer, for brief periods, literally loses his mind. In its most debilitating form, a firestorm of uncontrolled electrical activity can sweep across the brain, obliterating all thought and action. Epilepsy can wreak terrible havoc. Not only does it limit activities that many of us take for granted, like driving a car, but also when unchecked it can cause long-term damage to the brain.

Many drugs and surgical interventions are now available for the treatment of epilepsy, greatly improving the quality of life of patients. However, these treatments tend to be crude. Without answers to some of the most basic questions about epilepsy - how does it start? how does it stop? who gets it and why? - the prospect of finding better treatments remains dim. Basic research being done in the Synaptic Biophysics Group is laying the groundwork for answering these and other questions about epilepsy, leading to the possibility of improved treatments.

In simple terms, the brain is like a complicated see-saw. In normal operation it maintains a delicate balance between two opposing forces, excitation and inhibition. Too much inhibition leads to depression; too much excitation leads to epilepsy. In physiological terms, hyperexcitability can arise when there is an imbalance in the different kinds of neurotransmitter, which are chemicals used by brain cells (neurons) to communicate with each other. Or it can arise when neurons have errors in the proteins that act concertedly to generate the nerve impulse, that electrical signal that is the 'computer bit' of our brains. Research done in the Group over the past year has concentrated on one of these proteins, the potassium channel.

The potassium channel works to dampen down the activity of neurons - that is, it contributes to the inhibition side of the see-saw. Using rat brains for our experiments, we have been identifying the different kinds of potassium channels that are found in neurons in the cerebral cortex. We have found at least three kinds of potassium channels with different properties and distributions, each producing a characteristic form of inhibition. In future work we hope to discover which of these channels goes wrong in epilepsy. This may lead to new, specific treatments for epilepsy that are targeted to just those channels that are faulty.

The Synaptic Structure and Function Group
Dr Bruce Walmsley

The auditory system processes sound information extremely rapidly. As a consequence, synaptic connections between nerve cells in those parts of the brain which process auditory signals contain some of the fastest and most powerful synaptic connections in the brain. In the Synaptic Structure and Function group, we study the fundamental mechanisms underlying the generation of synaptic signals and the processing of these signals in neurons of the auditory brainstem. Over the past year, we have also begun to study differences between normal auditory synapses and those which develop in animals congenitally deaf from birth. The results of these experiments will be extremely valuable in our understanding of human congenital deafness and the role of synaptic activity in shaping and modifying synaptic strength at central synapses, during development.

Our experiments involve studies of the structure of synapses using electron-microscopy and fluorescent labelling of receptors in the target cell, and functional studies using electrical recording from individual neurons in living slices of the auditory brainstem. In addition, due to their large size, we are able to visualize individual synaptic terminals and obtain direct recordings from them. This allows us to perform molecular studies of the fundamental (quantal) nature of neurotransmitter release from these terminals.

Over the past year, we have investigated the role of the two major inhibitory neurotransmitters in the brainstem cochlear nucleus, GABA and glycine. We discovered a new role for GABA, which acts on presynaptic receptors to inhibit the release of glycine from nerve terminals containing both GABA and glycine.

We have completed an electron microscope study of the large excitatory synapses in the cochlear nucleus. Our results demonstrate that there are many hundreds of neurotransmitter release sites in a single auditory nerve terminal, and that there is a very large range in the number of synaptic vesicles containing neurotransmitter at each release site. The three dimensional structure revealed in this study will provide the basis for a functional model of transmitter release and diffusion.

We also completed a study on the role of protein phosphorylation in regulating transmitter release from excitatory auditory synapses. Our results show that the state of phosphorylation of proteins in the presynaptic terminal may dramatically influence transmitter release during single nerve impulses and during trains of impulses generated in the auditory nerve.

We have investigated the differences between auditory synapses in the brainstem cochlear nucleus of normal hearing and congenitally deaf mice. Our results reveal that the lack of auditory input during development of the deaf mice results in a dramatic alteration in neurotransmitter release. We are currrently investigating the involvement of the inhibitory neurotransmitters GABA and glycine in normal and congenitally deaf mice.

Synaptic Integration Laboratory Group
Dr Greg Stuart

The brain is made up of billions of neurons connected to each other to form specific neuronal networks. The working hypothesis is that when we think, move and feel what is happening is that particular sets of neurons become activated. Most neurons receive thousands of inputs from other neurons and are connected to thousands of other neurons. This divergence and convergence of information gives our brains extraordinary computational power. Individual neurons, however, do more than simply add up the different inputs they receive. Rather, single neurons shape and integrate the synaptic inputs they receive in complex ways.

The main focus of my group is to understand how individual neurons integrate synaptic inputs. To do this we place a slice of living brain tissue under a high-power light microscope, allowing individual neurons and their processes (dendrites and axon) to be visualised. Electrical recordings using the patch-clamp technique are then made from neurons under visual control.

A nerve impulse, or action potential, is the main output single used by neurons to communicate with other neurons and to interface the brain with our bodies. To influence action potential initiation synaptic inputs must spread from their site of generation in the dendrites to the soma and finally the axon – the site of action potential initiation in neurons. As they spread within the dendritic tree synaptic inputs become attenuated and filtered just as electrical signals do as they propagate down cables. Recently, we discovered that the expression of a high density of a particular channel (called Ih) in the dendrites can overcome the way dendrites filter synaptic inputs. This influences the way synaptic inputs summate prior to action potential initiation. We also found that action potentials interact with synaptic inputs in two interesting ways. Following an action potential synaptic inputs near the cell body, or soma, were found to be substantially reduced. In the dendrites, however, we found that synaptic inputs can increase the size of action potentials propagating back into the dendritic tree. This latter finding is likely to be important for the way our brains lay down memories. Finally, we found that the "backpropagation" of action potentials into dendrites is also increased during particular patterns of action potentials firing. This result has implications for our understanding of the way that information is coded by the pattern of action potential output. Together, these findings further advance our understanding of the way that single neurons integrate synaptic inputs. In doing so they show what a complex and powerful processing unit the single neuron is.

Visual Neurosciences
Dr Rowland Taylor

Our brains consist of hundreds of millions of neurons all connected together in a vast and complex network. This network is not a single entity, but can be seen as a large number of inter-connected subsystems each having different functions. This separation of processing is obvious from our everyday experience - when we close our eyes, thus shutting off input to the visual system, we can still hear perfectly well. This trivial observation underscores an underlying organizing principal. Our brains are parallel processors. The larger subsystems, visual or auditory for example, can be further broken down into component subsystems. As neuroscientists, we are seeking to understand how the brain works, and to do this, we must first understand how the component sub-systems of neurons perform their calculations.

An ideal system to study should satisfy a number of requirements. It should be easy to isolate and readily accessible to experimental manipulations. We need to know what computation the individual neurons within the system are doing. It would also be desirable to have detailed information about the elements within the neural circuit, and how they are connected together. The direction-selective ganglion cells in the retina of the eye satisfy all these requirements, and a major focus for the group this year was to understand the synaptic basis for direction-selectivity. Direction-selective neurons in the eye perform one elementary computation – they tell the brain which direction the image on the retina is moving. We were able to make a major advance this year, supported in part by the National Health and Medical Research Council, by showing that the non-linear synaptic interactions which generate direction selectivity occur within the dendrites of the ganglion cell (Taylor et. al., 2000, Science, 289; 2347).

Another area of research concerns night vision. We are exquisitely sensitive to light stimuli, to the extent that we can see flashes of light during which only 3 to 5 photons are captured by the retina. Thus our eyes can reliably detect single photons and pass this information to our brains where they are perceived. How is this possible? At these very low light levels we use our rod-photoreceptors to capture single photons. The rods amplify the single photon events via a biochemical cascade, producing a signal of about one thousandth of a volt for each photon. This signal is passed to the second order neurons, the so-called rod-bipolar cells. Single-photon signals have not yet been observed in mammalian rod-bipolar cells and a major effort has been directed towards investigating the physiological properties of these cells (Berntson & Taylor, 2000, J. Physiol. 524; 879). Studying the very weak neural signals generated by single photon events will give us insight into a fundamental problem that neural systems must overcome. Anyone who has used a two-way radio will be familiar with the problem of background noise when the signal becomes weak. Turning up the volume doesn't help, the noise just becomes louder and the signal no more distinct. Neural systems are similar in that they are inherently noisy. For very weak single photon signals the background "neural noise" becomes a limiting factor. Fortunately neural systems are far more complex than a radio and are able to extract weak signals from the background noise. Future work is aimed at measuring single photon signals in rod-bipolar cells, and discovering how these cells are able to amplify the signal and suppress the noise.

Synaptic Transmission
Professor Stephen Redman

Spinal Motoneurones and Interneurones

Prof Steve Redman with Hannah Evans . photo pb

Motoneurones are neurones in the brain stem and spinal cord whose axons make contact with our skeletal muscles. When these neurones generate electrical impulses, the muscles they innervate contract. The generation of impulses in motoneurones is determined by the strengths of the excitatory and inhibitory synaptic inputs they receive from spinal interneurones and sensory nerves, and by the excitability of their membrane.

Steve Redman with Hannah Evans, a summer vacation scholar from Otago, NZ.

The membrane properties of motoneurone dendrites have long been a mystery because of their inaccessibility to conventional recording techniques. A recent innovation which uses differential interference microscopy at infra-red wavelengths has allowed motoneurone dendrites to be imaged in vitro. Recording electrodes can be placed directly on the dendrites, and transmission between the soma and the dendrites can be measured directly. We (with David Thurbon) have recently shown that the action potentials are generated near where the axon leaves the soma and that they spread backwards into the dendrites where they rapidly attenuate. The sodium current needed to maintain the action potential in the dendrites is not present with sufficient density. The low density of sodium current in the dendrites also appears to make it ineffective in boosting synaptic potentials as they spread towards the soma. This is in contrast to pyramidal cells in the cortex, where the action potential back-propagates into the distal dendrites, and boosting of synaptic potentials by sodium current can occur in dendrites.

Many kinds of spinal interneurones make synaptic contact with motoneurones. The properties of these synaptic connections are generally not well understood. It is now possible to breed mice in which interneurones with defined genetic lineages can be made to contain a fluorescent protein. Each type of interneurone defined in this manner can be associated with specific roles in controlling movement. These fluorescing interneurones can be visualised in thin slices of spinal cord. The synaptic connections formed by these interneurones with motoneurones can be investigated by stimulating the interneurones and recording from motoneurones. This approach will allow us to understand the way in which interneurones with different functional roles in movement control motoneurone excitability.

Staff - Division of Neuroscience

Senior Fellow and Head:
B Walmsley BE, PhD (Monash) DSc (NSW)
School Technical Manager: (until June)
RJ Ayling ECC (until June)
School Technical Support Officer: (from June)
Russell Taylor (from June)
Divisional Administrators:
E McNaughton (part-time);
A Summerfield (part-time from November)
Assistant to School Technical Manager:
P Blower BA(Hons) (until June)
Senior Technical Officer:
B Keys (until June)
Technical Officers:
G Whalley; R Cappuccio; C Symons (until June)

Autonomic Synapse Group
Senior Fellow and Leader:
CE Hill BSc, PhD (Melb)
Postdoctoral Fellows:
K Francki BSc(Hons) (Adel.) PhD (Uni WA) (until July);
S Sandow BSc(Hons) (La Trobe) PhD (ANU)
Temporary Assistant:
K Kelleher BSc(Hons) (UNIWA) (July-September)
Technical Officer
H Hickey

Cellular Neurophysiology Group
Leader, Sylvia & Charles Viertel Fellow:
P Sah BSc, MBBS (NSW) PhD
Postdctoral Fellows:
ESL Faber BSc(Hons) (Edinburgh) PhD (Bristol);
JM Power BSc(Hons) (Ill.) PhD (Northwestern);
M Lopez de Armentia BSc(Hons) PhD(Universidad Miguel Hernandez) (from December )

Developmental Neurobiology Group
Professor and Leader:
IA Hendry BSc(Med), MB BS (Syd) PhD (Camb)
Postdoctoral Fellows:
N Ozsarac BSc (NSW), PhD (NSW)
Visiting Fellows:
S Bartlett BSc (Qld Inst.Tech), BPharm (Qld) PhD (Qld) (to December);
D Megirian MS, PhD (Rochester)
Temporary Assistant:
K Kelleher (BSc(Hons)(IUNIWA) (March-November)
Laboratory Technician:
J Holgate

Synaptic Transmission Group
Professor and Leader:
SJ Redman ME (NSW) PhD, DSc (Monash) FAA
University Fellow and Emeritus Professor:
DRCurtis AC, MB BS (Melb) PhD, FRACP, FAA, FRS
Postdoctoral Rellow:
C Raymond BSc(Hons) (Otago) PhD (Otago)(until March)
Visiting Fellow:
Professor R. Grantyn MD, PhD (Leipzig) DSc (Munich) (from September)
Research Assistant (Part-time):
D Webb BSc (NTU) MSc(Prelim) (Syd)
Technical Officer:
GR Rodda PTC

Synaptic Integration Laboratory
Wellcome Trust Senior Research Fellow:
G Stuart QEII Fellow, BSc (Monash) PhD
Postdoctoral Fellows:
S Williams BSc(Hons) PhD (Uni College Wales) (until October);
A Gulledge BSc(Hons)(Uni California) PhD(Uni Texas ) (from June)

Synaptic Biochemistry Group
Research Fellow and Leader:
C Morgans BSc(Hons) (Michigan) PhD (Stanford)

Molecular Signalling Group
Fellow and Leader:
MF Crouch BSc, PhD (Adel) (until December)
Postdoctoral Fellow:
LA Berven BSc (Minnesota) MSc (British Columbia) PhD (Uni Syd) (part-time)

Synaptic Biophysics Group
Research Fellow and Leader:
JM Bekkers BSc (Griffith) MSc (Manchester) PhD (Cambridge)

Synaptic Structure and Function Group
Senior Fellow and Leader:
B Walmsley BE, PhD (Monash) DSc (NSW)
Research Fellow
S Oleskevich BSc(Hons) PhD (Montreal) (from August)
Postdoctoral Fellow:
S Oleskevich BSc(Hons) PhD (Montreal) (until August)
Research Officer:
M Nicol BSc(Hons) (Wollongong) PhD

Visual Neuroscience
Fellow and Leader:
R Taylor BSc(Hons) (NSW) PhD
Visiting Fellows:
WR Levick, MSc, MB BS (Syd), FOSA, FAA, FRS
D Vaney BSc(Hons) (Canterbury) PhD
Technical Officer:
E van der Pol BRTC (until May)

Molecular Neuroscience Facility
P Gaughlin BSc(Hons) (from January to July)