Honours research opportunities


For an Honours year in the discipline of Anatomy & Histology, you need to:

  1. Have a Sci-WAM of at least 65*
  2. Pre-enrol via Sydney Student
  3. Organise a project with a lab head and get written confirmation (email)
  4. Confirm your intention to do Honours with the Honours Coordinator (in person)
  5. Be aware of our Summer Scholarship program

Summer scholarships are primarily awarded according to SciWAM. To be eligible, you must be committed to Honours in Anatomy & Histology. Application forms for Scholarships are at the end of this flyer or are available from Dr. Paul Austin; Room E513.

*If you do not meet the criteria but are still interested in Honours, see Dr. Paul Austin to discuss options.

Our Honours Program in Brief:

  • Thesis (~20,000 words; November submission).
  • Seminar (~20 minutes; November). You will present your year's work.
  • Weekly Honours meetings (attend meetings, 1-2 hour/week during semester). At these meetings, each student will present seminars during the year, outlining for example, the project aims and their early results. These presentations will be to the other Honours students and the Honours Coordinators (Dr Paul Austin and Prof Frank Lovicu).
  • Research proposal (3-page proposal at the beginning of Honours)

When choosing a laboratory to undertake Honours, make sure that: you get on with the Supervisor, the lab is filled with happy and likeable people and has recent publications, and most importantly you are interested in the project.


Dr Paul Austin

Effects of alcohol on the expressions and regulation of glutamate transporter GLAST (EAAT1)
A/Prof. Vladimir BALCAR

Gene expression during development of the sea urchin nervous system
Prof. Maria BYRNE, Dr. Demian Koop

The microvasculature: degeneration, inflammation and Alzheimer's disease
Dr. Karen CULLEN

Dr Joanna DIONG
Dr Martin HÉROUX

Dr Katie Dixon

Dr. Denise DONLON


A/Prof Ulrike GRÜNERT

Dr. Flavia DI PIETRO

Chemotherapy-induced neurotoxicities
The motivational and cognitive effects of high fat-high sugar diets

A/Prof. Kevin KEAY (Head of Discipline)

Dr Sean LAL
Prof. Cris dos Remedios
Dr. Amy Li

Prof Frank LOVICU

Monoaminergic Dynamics in chronic pain and stress
Dr David MOR

Changes in the uterus during ovarian hyperstimulation
Prof. Chris MURPHY

Skin-derived neuroprecursor cells – cell therapy and disease modeling projects
Brain Network Responses to Physical and Cognitive Exercise
Associate Professor Michael VALENZUELA
Dr Kathryn Broadhouse


Dr Paul AUSTIN Rm E511. 9351 5061. paustin@anatomy.usyd.edu.au

It is increasingly clear that inflammatory mediators such as pro-inflammatory cytokines from activated glia and immune cells can act on both peripheral and central neurons to alter their functioning. Moreover they have been linked with neuropsychiatric and neurodegenerative diseases. My laboratory is focused on investigating the interaction of inflammatory mediators and behaviour in chronic disease states. Using peripheral inflammatory insults such as nerve injury or lipopolysaccharide in experimental rodents, we investigate fine-grained changes in behaviours, such as foraging, investigation, decision-making and risk-assessment in order to identify deficits in cognition or motivation. We are also investigating changes in immune activation in human chronic pain patients who have depression and anxiety. The laboratory uses a variety of neuroanatomical, immunohistochemical and cytometric approaches to probe the underlying immune mechanisms of these behavioural changes.



A/Prof Vladimir BALCAR Rm S419. 9351 2837. vibar@anatomy.usyd.edu.au

Effects of alcohol on the expressions and regulation of glutamate transporter GLAST (EAAT1)



Prof. Maria BYRNE. Rm S600. 9351 5166. mbyrne@anatomy.usyd.edu.au
Dr Demian KOOP demian.koop@sydney.edu.au

Gene expression during development of the sea urchin nervous system
Sea urchins are a leading model for understanding the genetic networks that regulate animal development. Our lab uses Australian sea urchin species to investigate the evolution of development. We have extensive an extensive annotated developmental transcriptome for this model species which allows us to address a number of questions linking spatial (using in situ hybridization) and temporal gene expression profiles. This allows us to establish which parts of the genetic blueprint for development have been conserved between sea urchins and vertebrates, and will provide insights into the vertebrate ancestor. We investigate aspects of development including axial patterning – such as Anterior-Posterior and Left-Right, genes involved in skeleton formation and genes involved in the development of the central nervous system. The role of key signaling pathways in skeletogenesis and neurogenesis will be also determined by analyzing the effects of pharmacological treatments on development of sea urchin embryos.



Dr Karen CULLEN. Rm S464. 9351 2696. kcullen@anatomy.usyd.edu.au

The microvasculature: degeneration, inflammation and Alzheimer’s disease

Our laboratory is focused on pathology of the cerebral microvasculature. The brain has an extremely dense and very complex microvasculature. Health of this vascular network is essential for normal brain function. Several neurological conditions are marked by pathology of these tiny vessels, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and head injury. Our work investigates the anatomy of the normal and diseased microvasculature, as well as the relationship of damaged vessels to neurodegeneration. Several projects are offered in our laboratory. For instance, the key lesion in the AD is the breakdown of the cerebral microvasculature. Projects in AD involve the mapping of capillary damage and the sequence of inflammatory events from fresh microhaemorrhage to scar formation. In PD, we find breakdown of the microvessels in the terminal fields of the substantia nigra neurons, the cells that die in this movement disorder. Our PD project aims to map vascular anomalies in the striatum in human brain tissue. The techniques used in the lab include tissue processing, immunohistochemistry, brightfield and fluorescence microscopy. We use multidimensional analysis to examine the complex vascular network in human brain tissue. These projects would suit high achieving motivated students with some background in neuroanatomy and good literature research and writing skills.



Dr Joanna DIONG. joanna.diong@sydney.edu.au
Dr Martin HÉROUX. m.heroux@neura.edu.au

Our research aims to understand what makes human movement normal, and why it is impaired in clinical conditions. We focus on understanding the mechanisms of normal human movement, impaired movement in people with stroke or other clinical conditions, motor control during daily activities, mechanisms of human perception, and muscle and nerve neurophysiology. We use transducers to measure force and angle (i.e. the study of kinematics and kinetics), and electromyography to measure muscle activity. We use scientific computing for biological and transducer signal analysis, and we are passionate about research reproducibility and good science. Students in our laboratory are exposed to a variety of experimental research techniques. Projects could include laboratory research on mechanisms of human movement, literature review and surveys in good research practice, or a combination of both.

Available projects for Honours or postgraduate research:

  • Quantifying the effect of unwanted muscle activity on passive joint range of motion after stroke
  • Quantifying the ability to detect unwanted muscle activity during passive joint range of motion
  • Variability in force production and motor control during functional tasks
  • Assessing criteria for reproducible research in key scientific journals



Dr Katie DIXON. Rm. S228. 9351 4633. katie.dixon@sydney.edu.au

Skin cancer is highly prevalent in Australia, with two in three people being diagnosed by the age of 70. While non-melanoma skin cancers are more common, melanoma is responsible for the majority of deaths related to skin cancer. Projects in this laboratory involve the investigation of the molecular mechanisms of ultraviolet radiation-induced skin carcinogenesis, as well as inhibition of the growth and metastasis of melanoma. We are particularly interested in cell signaling pathways in cancer, with an emphasis on identification and targeting of tumour suppressor genes. Techniques include but are not limited to cell culture, immunohistochemistry, western blotting, RT-PCR, siRNA, in vivo studies and simulation of ultraviolet radiation.



Dr Denise DONLON. Rm W601. 9351 4529. ddonlon@anatomy.usyd.edu.au
Dr. Sarah Croker scroker@anatomy.usyd.edu.au




Dr Claire GOLDSBURY. Brain and Mind Centre. 02 9351 0878. claire.goldsbury@sydney.edu.au

Using autopsied human brain tissue, this lab investigates the cellular pathology of Alzheimer’s disease. We are interested in the progression of pathology through the brain and the interaction between glial cells and neurons during this process. The honours project will involve gaining experience in tissue labelling and imaging techniques such as confocal microscopy and image analysis.




A/Prof Ulrike GRÜNERT. Save Sight Institute. 9382 7641. ulrike.grunert@sydney.edu.au

The retina is a thin piece of nervous tissue that lines the back of the eye. It contains five major classes of neurones, which are organised in nuclear and synaptic layers. The project involves the analysis of post-mortem human retinas (obtained from donor eyes with consent from the Lions NSW Eye Bank) and post-mortem monkey retinas. High-resolution light microscopy, in conjunction with immunohistochemical methods will be used for identifying different cell types and their synaptic connectivity. Accurate knowledge of nerve cell populations and their density can allow more accurate prediction of functional properties of normal visual performance, can give a rational basis for understanding the effects of disease and degeneration, and can form a standard of normal anatomical state against which the effects of dis- ease can be measured.

Skills and knowledge you will acquire:
We are looking for an enthusiastic young scientist to learn neuroanatomical methods including cryostat and Vibratome sectioning of retinas, intracellular injections, double and triple immunofluorescence, high resolution light microscopy (deconvolution and confocal) and image analysis.




Prof. Luke HENDERSON Rm. S420. 93517063. lukeh@anatomy.usyd.edu.au
Dr. Flavia DI PIETRO Rm. S518. 9351 6878. flavia.dipietro@sydney.edu.au

Chronic, i.e. persistent, pain is a growing problem worldwide; it affects 20% of the population and costs western societies about as much as diabetes and cancer combined. Pain can have a huge impact on someone’s well-being and function. Despite being such a common and important issue to address, there is so much we do not understand about pain.
Why are so many of us interested in the role of the brain? Injuries do not always cause pain and, conversely, we know that people can experience pain in the absence of injury to their tissues. Given this disconnect, it seems there is something more to pain than simply what is happening in the painful body part. For this reason, among others, much of pain research is now directed at the human central nervous system, particularly the brain.
In our lab we use different types of brain imaging in humans, for example magnetic resonance imaging (MRI), functional MRI, MR spectroscopy, and electroencephalography (EEG), to investigate the structure, function and chemistry of the brain in the pain state. This is the sort of work that leads to an increased understanding of basic pathophysiology, and holds potential to improve the treatments that patients receive.



Dr Ian JOHNSTON School of Psychology, A19. i.johnston@sydney.edu.au

Chemotherapy-induced neurotoxicities
As treatments for cancer become more advanced, the rate and length of survival amongst cancer patients has increased. However, adjuvant chemotherapy is associated with negative side effects, including chemotherapy-induced cognitive impairments (CICI) and chemotherapy-induced peripheral neuropathies (CIPN). CIPN is a significant dose-limiting side effect of some commonly used chemotherapy drugs, affecting up to 70% of patients during treatment. Up to 40% of patients continue to experience symptoms for 6 months or longer, but often persisting 10 years after chemotherapy. Up to 70% of cancer survivors self-report problems with their memory and concentration after chemotherapy, with 17-50% of survivors having significant cognitive impairment on formal cognitive testing up to 10 years after chemotherapy. Survivors report that the impact of these symptoms on daily function is the most troublesome survivorship issue they face. There is no effective treatment for these symptoms.

We have developed animal models of these neurotoxicities, and have used these to assess novel therapies. Your project will be to assess whether these therapies are effective at reducing the behavioural expression of CICI or CIPN, and how these treatments improve underlying pathologies.
The motivational and cognitive effects of high fat-high sugar diets
There are strong correlations between obesity, a high fat-high sugar (HFHS) diet, and low self-control. It is commonly assumed that obesity is due to low self-control: Obese individuals tend to choose HFHS foods and therefore become obese. However, recent work in my lab has shown this is a bidirectional effect. Eating and exercising affects executive function: Diets high in sugars and fats reduces executive function in rats and people, and exercise increases executive function.

This is a new focus for my laboratory, and we are actively exploring the neurobiology of the effect of diet or exercise on executive function, and its relationship to obesity and dieting. So far we have demonstrated that, after randomising rats to groups that either receive standard rat chow or to those that have 2-hr daily access to high-fat, high-sugar (HFHS) drinks (e.g., sweetened condensed milk) or a western cafeteria diet (e.g., cakes, biscuits, pies, etc), the HFHS diet condition show increased impulsivity compared to the control diet rats. I would like to see this work expanded in several directions: How does food affect the neurobiological mechanisms of executive function? What are the major histological or genetic changes? Does diet affect other executive control tasks? How might we reverse or prevent this effect? How does this relate to obesity and consumption of obesogenic foods?



A/Prof Kevin KEAY. Rm S502. 9351 4132. keay@anatomy.usyd.edu.au

Following injury and some surgical procedures, a number of individuals are left with persistent pain that has been attributed to the pathophysiological consequences of nerve damage (neuropathy). In these individuals, pain persists despite well-established post-operative or post-injury clinical management procedures and the use of conventional analgesic treatments. The pain in these individuals persists long after healing of the injury or the surgical site, and is given the diagnostic label of a chronic neuropathic pain state. People with chronic pain states typically present clinically with a range of co-morbid physiological, behavioral, affective and cognitive changes. More often than not it is these co-morbid changes referred collectively to as “disabilities”, that are the significant and debilitating consequences of the chronic neuropathic pain state.

There are three puzzling observations arising from the clinical literature on chronic neuropathic pain: firstly despite similar injuries or surgical procedures, not all people develop chronic neuropathic pain; secondly, the degree of neuropathic pain a patient describes does not correlate with the severity of the disabilities demonstrated and thirdly there are a population of people with the diagnostic sensory criteria of neuropathic pain that have no disabilities at all.

In a rat model of chronic neuropathic pain, we showed that several measures of sensory hypersensitivity (indicators of neuropathic pain) do not correlate with the degree of disability and further that there are rats with sensory hypersensitivity with no disabilities at all.

The rat model recapitulates the clinical picture with remarkable accuracy and we are currently using this to study the following major question: What is the role of early life stress on resilience and vulnerability to developing chronic neuropathic pain? We have asked this question because there is evidence that, early-life stress can modify the resilience or vulnerability of an individual to stress, threat or pain in later life through a number of epi-genomic and non-genomic mechanisms. The model of early life stress we are currently using is early post-natal inflammation. We are determining the central, peripheral and complex behavioural consequences of this early life stress (ELS) on the development of neuropathic pain.



Dr Sean LAL. Room S468. 9351 3209. sean.lal@sydney.edu.au
Associate supervisors: Prof. Cris dos Remedios and Dr. Amy Li

Our translational research focuses on the human heart. We aim to investigate the molecular basis of cardiomyopathies, cellular changes in ageing, and intrinsic mechanisms of cardiac regeneration. We uniquely draw on tissue from The Sydney Heart Bank (SHB), which comprises of over 20,000 cryopreserved human cardiac samples from our collaborations with St Vincent's Hospital and Royal Prince Alfred Hospital. Over the years, we have developed an extensive tissue database and international research network with the common goal to further our understanding of human heart failure. Techniques include tissue microarray profiling, immunohistochemistry, immunofluorescence, RT-PCR, Western blots, cell culture and functional phosphorylation studies.



Prof Frank LOVICU. Rm S252. 9351 5170. frank.lovicu@sydney.edu.au

Research in our laboratory is directed at identifying the mechanisms that regulate cell behaviour involved in eye lens development, growth and pathology. Using a range of techniques (including tissue culture, immunolabelling, qRT-PCR, chromatography, Western blotting, light and confocal microscopy, in vitro biological assays and transgenic mouse strategies), we investigate the expression, effects and function of different growth factors and their receptors, as well as the regulation of their intracellular signalling in cells.
To date, we have shown that growth factors such as fibroblast growth factor (FGF) are important regulators of lens epithelial cell proliferation, migration and differentiation and are important for the normal development and maintenance of the lens. We have also shown that other growth factors, such as members of the transforming growth factor family (TGF-ß), can regulate lens cells to transdifferentiate into myofibroblasts through the process of epithelial to mesenchymal transition (EMT) that leads to cataract (loss of lens transparency), similar to that found in humans, resulting in blindness. Regulation of the different growth factors and their respective signalling pathways has led us to identify key molecules and mechanisms that alter lens cell behaviour, in turn preventing or blocking cataract formation.
Students that undertake Honours projects in our laboratory can expect to be exposed to a wide array of techniques, encompassing cellular, developmental and/or molecular biology, and can carry out a project in one or a combination of the following areas:
Normal Lens Biology
  • Investigate the role of growth factors (FGF, IGF, EGF) and their signalling pathways in regulating lens cell proliferation and fibre differentiation using lens epithelial explants and/or transgenic mouse models.

  • Study factors (BMPs) that maintain the normal lens epithelial phenotypic characteristics including cell-cell and cell-matrix adhesion and communication.

  • Use transgenic mice and/or in vitro assays to determine the role of cell proteins (proteoglycans, Spreds1/2) thought to be involved in regulation of growth factor bioavailability and signalling.

  • Use tissue culture to identify the molecules in the ocular fluid that are important for lens cell differentiation and how this contributes to lens transparency.


Lens Pathology (Cataract)

  • Use transgenic mouse models to understand how TGFß induces and regulates cataract formation.

  • Use lens explant cultures to determine how TGFß disrupts normal lens signalling pathways and induces an epithelial-mesenchymal transition, characteristic of cataract.

  • Use lens explant cultures to identify putative inhibitors of TGFß-signalling as a means of preventing cataract.


Many of the growth factor signalling pathways we study in lens cells that lead to fibrosis and cataract, also mirror the signalling processes in human cancer. To test this, we also offer a project involved with the comparative analysis of cancer cells to identify common regulatory mechanisms to those found in lens pathology, and use this in potentially block cancer progression.



Dr David MOR david.mor@sydney.edu.au

Stress, either physical or psychological, has direct effect on the cognitive processes that regulate behavioural selection. A mild stress can enhance cognitive function, behavioural flexibility and motivation. More severe or prolonged stress can alter the neural circuits regulating behaviour, leading to disruption in their function beyond the duration of the stress. This can lead to symptoms such as: reduced behavioural flexibility, or the ability to select and change behaviour to match changes in the environment; reduced motivation to engage in rewarding tasks; increased impulsivity and reduced attention. These symptoms characterise many stress-related pathologies such as depression and anxiety disorders. There are also links between stress and exacerbations in behavioural and attention pathologies found in attention deficits, compulsive behaviours and loss of behavioural inhibition.

The neural circuitry regulating these processes includes forebrain structures such as the prefrontal cortex and striatum. This circuitry is highly regulated by monoamine projections such as dopamine, serotonin and noradrenaline from selected brainstem nuclei. Monoamine input into the prefrontal cortex and striatum is crucial for healthy cognitive and affective functioning and is one of the major mechanisms through which stress can alter behaviour, both the improving effect of mild stress and the detrimental effect of severe and/or prolonged stress.

My lab focuses on the way that the prefrontal cortex and striatum regulate behavioural selection, attention and motivation in the healthy state and how exposure to stress changes monoamine input into and activity in this circuitry. Projects offered in this lab will use animal models of acute and/or chronic stress in order to better understand how stress alters behavioural selection and motivation. The animal work will be followed by molecular work, using techniques such as HPLC, immunohistochemistry and gene and protein expression techniques, attempting to link the molecular differences found following chronic stress with the altered behaviour.



Prof. Chris MURPHY. Rm N364. 9351 4128. histology@medsci.usyd.edu.au
Dr. Laura LINDSAY. Rm N364. 9351 2508. laural@anatomy.usyd.edu.au
Dr. Sam DOWLAND. Rm N364. 9351 2491. sdowland@anatomy.usyd.edu.a

The work in this lab is centered around reproductive biology and medicine and in particular the biology of the uterus, uterine receptivity for blastocyst implantation and hormonal influences on the uterus. We are interested in how it is that the uterus manages to tightly regulate those times during the reproductive cycle when it will allow the blastocyst to attach but to prevent attachment and the beginning of a pregnancy at other times. We are particularly interested in uterine epithelial cells and the molecular interactions that occur between the surface of these cells and the implanting blastocyst. A variety of methods are available including light & electron microscopy, immunohistochemistry, Western blotting and PCR. The work uses both animal and human tissues and involves basic cell biological research. We also have a number of in vitro models of implantation. The laboratory also has extensive contacts with The School of Biological Sciences and the Australian Centre for Microscopy and Microanalysis (ACMM) which involves a major project on the evolution of viviparity (live birth) and the development of the placenta. This work involves study on mammals and lizards in particular but also other animals to understand the biology of different types of placentas. We would accept students interested in mammalian reproduction and/or students interested in working on an aspect of the evolution of live birth and placentation. An honours place in conjunction with the ACMM could also be arranged. We are particularly interested in accepting Honours students who may be interested in progressing to a PhD and have laboratory-funded top-up scholarships available for such students.

Changes in the uterus during ovarian hyperstimulation
Controlled ovarian hyperstimulation (COH) is part of the in vitro fertilisation (IVF) protocol to harvest multiple eggs from a woman. It has been known for many years that the drugs used in COH leads to a decrease in uterine receptivity, however there is currently no known mechanism of how this occurs. We use a rat ovarian hyperstimulation model (OH) to investigate changes in the rat uterus during OH pregnancy, especially at the time of blastocyst implantation. We use several molecular and histochemical techniques to investigate changes in protein localisation and expression, such as immunofluorescence microscopy, western blotting and ELISAs. We also use a range of microscopy techniques such as light microscopy, transmission electron microscopy and scanning electron microscopy. The ultimate aim of this project is to identify factors or proteins associated with the decreased uterine receptivity in women undergoing ovarian hyperstimulation. A more detailed understanding of these factors may increase the pregnancy rate in IVF procedures.



Canine dementia - a new translational model for Alzheimer's disease research
Dr Thomas Duncan Brain and mind Centre. 9351 0893. thomas.duncan@sydney.edu.au
Prof Michael VALENZUELA Brain and mind Centre. 9114 4136. michael.valenzuela@sydney.edu.au

This project is a valuable opportunity to be part of a collaborative environment, working with leading academics in the field of Alzheimer’s disease research. At the Regenerative Neuroscience Group we aim to develop a stem cell therapy for Alzheimer’s. Towards this goal, we have pioneered the classification and diagnosis of canine dementia - a naturally occurring neurodegenerative disease in older dogs clinically analogous to Alzheimer’s disease in humans. Comparatively little is known about the pathology and neurobiology of this disease in dogs. We have now established an internationally unique Canine Brain Bank to study this disease. This Honours project offers the opportunity to acquire skills in histology and microscopy and to contribute to cutting edge neuropathology research. There is great potential to reveal new pathogenic mechanisms of Alzheimer’s disease and further research into canine dementia as a relevant model for human Alzheimer’s disease research.