PhD Programme
PhD opportunities exist in our internationally-recognised research programmes in the areas of Cardiovascular & Respiratory Physiology, Cellular & Molecular Neuroscience and Membrane & Ion Transport.
Applications to undertake a PhD in Physiology are welcome at any time. Candidates can be of any nationality and must have attained an above-average degree (minimum of four years study) in biomedical science or closely related subject.
Full scholarships to undertake a PhD in Physiology are available through two sources:
- Department of Physiology PhD Scholarships (from 1 January 2012 $25,000 stipend plus tuition fees for three years). These are awarded on a competitive basis through two advertised rounds held in April and September. Candidates with excellent academic qualifications will be considered at any time.
- University of Otago Scholarships (from 1 January 2012 $25,000 stipend plus tuition fees for three years). These scholarships are available all year round to candidates with an excellent undergraduate degree.
In all cases, applicants must first apply to the Department of Physiology using the following procedure. Send the required documents by email to Tracey Fleet, Departmental Administrator, physiology@otago.ac.nz by the 9th of April 2012. Only complete applications will be accepted:
- Name and country of citizenship;
- CV;
- Certified copy of your academic transcript (must show marks/grades and, if applicable, an explanation of the content);
- Evidence of English language proficiency (this must be a certified copy of a certificate from either TOEFL or IELTS).;
- The names of two referees;
- An indication of research interest(s) and staff member(s) with whom you are interested in studying – see list of PhD Projects available for 2012 below;
- Statement describing why you wish to study for a PhD in Physiology at the University of Otago.
If the staff member(s) with whom you are interested in studying would like to advance your application to the next stage, you will be contacted by them in order to prepare further documentation which must be submitted by the 2nd of May 2012. If you are unsuccessful, you will be contacted within two weeks of receipt of your application.
For further information about studying for a PhD at Otago, please visit the following pages: http://www.otago.ac.nz/study/phd/ and http://www.otago.ac.nz/international - please do not fill in any application forms at this stage.
PhD Projects available for 2012/2013
Cardiovascular & Respiratory Physiology
The following projects are available in the Cardiovascular & Respiratory Physiology group:
Cellular & Molecular Neuroscience
The following projects are available in the Cellular & Molecular Neuroscience group:
Membrane & Ion Transport
The following projects are available in the Membrane & Ion Transport group:
Associate Professor Pat Cragg
Pat Cragg
Head of Department
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4797334
Fax: +64 3 479 7323
Email: pat.cragg@otago.ac.nz
Show Cragg Lab page.
Associate Professor Colin Brown
Colin Brown
Associate Professor
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4797354
Fax: +64 3 479 7323
Email: colin.brown@otago.ac.nz
Show Brown Lab page.
Associate Professor Phil Sheard
Phil Sheard
Associate Professor
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4797045
Fax: +64 3 479 7323
Email: phil.sheard@otago.ac.nz
Show Sheard Lab page.
Dr Ruth Empson
Ruth Empson
Senior Lecturer
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4797464
Fax: +64 3 479 7323
Email: ruth.empson@otago.ac.nz
Show Empson Lab page.
Associate Professor Fiona McDonald
Fiona McDonald
Associate Professor
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4797329
Fax: +64 3 479 7323
Email: fiona.mcdonald@otago.ac.nz
Show McDonald Lab page.
Associate Professor Grant Butt
Grant Butt
Associate Professor
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4797319
Fax: +64 3 479 7323
Email: grant.butt@otago.ac.nz
Show Butt Lab page.
Dr Ruth Empson
Ruth Empson
Senior Lecturer
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4797464
Fax: +64 3 479 7323
Email: ruth.empson@otago.ac.nz
Show Empson Lab page.
Dr Peter Jones
Peter Jones
Lecturer
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4703548
Fax: +64 3 479 7323
Email: pete.jones@otago.ac.nz
Show Jones Lab page.
Dr Ruth Empson
Ruth Empson
Senior Lecturer
Department of Physiology
School of Medical Science
University of Otago
PO Box 913
Dunedin
New Zealand
Phone: 4797464
Fax: +64 3 479 7323
Email: ruth.empson@otago.ac.nz
Show Empson Lab page.
Adrenergic modulation of the diabetic heart
Dr Regis Lamberts & Dr Daryl Schwenke & Associate Professor Pat Cragg
Determine the adrenergic regulation of cardiac function and coronary circulation in the healthy and diabetic heart. In vivo surgical techniques and measurements, isolated cardiovascular preparations and protein analysis will be used. If you are interested and you apply please provide me with YOUR motivation why this is important research!
Show Lamberts Lab page.
Show Schwenke Lab page.
Show Cragg Lab page.
Central modulation of cardiac Sympathetic Nerve Activity following acute MI
Dr Daryl Schwenke & Associate Professor Colin Brown
The majority of people that suffer an acute myocardial infarction (MI) die within the first few hours following the MI. This high early morbidity has been strongly linked with a sustained over-stimulation of the nerves that control heart function; specifically sympathetic nerve activity (SNA). Unfortunately, even if you survive the initial heart attack, this over-stimulated SNA to the heart facilitates progressive damage of the heart tissue, such that the long-term survival prognosis is bleak. Currently, the mechanisms that govern the increase in SNA following acute MI remains to be fully elucidated, although both peripheral and central modulation have been implicated via the cardio-cardiac reflex.
Research Question and Objectives: Advanced electrophysiological techniques will be used, in vivo, to address the fundamental objectives of this line of research, which are i) to broaden our knowledge concerning the central neural mechanisms that modulate cardiac SNA, with specific emphasis on the role of the paraventricular nucleus, and ii) identify the pathways that are interrupted following acute MI which provoke a sustained increase in SNA and iii) identify potential therapeutic strategies to prevent the adverse increase in SNA following acute MI.
Show Schwenke Lab page.
Show Brown Lab page.
Investigation of changes in the neuromuscular system in old age
Associate Professor Phil Sheard
We are investigating changes to neuromuscular structure and function in old age with a view to improving our knowledge of the physiological causes of age-related skeletal muscle weakness. A wide range of specific projects are available investigating age-related changes among lower motoneurons, glial cells of the spinal cord, neuromuscular junctions, and skeletal muscles. Research techniques include electrophysiology, immunohistochemistry and light microscopy.
Show Sheard Lab page.
Studies of seizures and seizure prevention following stroke and brain injury in vitro
Dr Phil Heyward & Professor Brian Hyland
Seizures are common in brain injury and stroke patients, and may initially occur unnoticed. These seizures spread away from the injured or post-hypoxic brain tissue, enlarging the region of neuron loss. Seizures and brain damage can thus both worsen over time. Stopping these seizures may thus be a key early treatment, preventing further damage and loss of function, preserving neurons and improving recovery. In PhD studies in my lab, you will use electrophysiological methods (including whole-cell patch-clamp and field potential recordings, drug microinjection and tissue microdissection) in mouse brain slice preparations to investigate how such seizures spread, and test treatments to prevent them.
Show Heyward Lab page.
Show Hyland Lab page.
Understanding Cerebellar Circuitry
Dr Ruth Empson
The cerebellum integrates sensory and motor information so that we can successfully interact with the world around us. It does this by continually comparing electrical information from other brain regions and then modifies its own output accordingly; the circuitry operates a little like a record and playback device that constantly tests and adjusts its electrical output in real time. Of course our world is highly complex and for the cerebellum to manage the huge diversity of information we experience every day, its circuitry must also be capable of learning our automatic behaviours.
Problems arise if the cerebellum is damaged, as following stroke, during degeneration as in severe movement ataxias, or even by excessive alcohol. The outcome is poor motor control. However, it is becoming increasingly recognized that the cerebellum makes additional contributions since disruptions to the cerebellum accompany autism and schizophrenia.
In this project you will have the opportunity to study the cerebellar circuitry using electrophysiological and imaging techniques together with detection of important proteins (by immunohistochemistry and western blotting). Further details can be obtained by informal discussion with Dr Ruth Empson.
Show Empson Lab page.
Basolateral targeting of the KCa3.1 channel in polarised epithelia
Dr Kirk Hamilton & Dr Steven Condliffe
The KCa3.1 channel plays a critical role in maintaining appropriate gradients for transepithelial ion transport in various epithelia. This is dependent on the correct localisation of KCa3.1 at the basolateral membrane. Increasing evidence indicates that both SNARE and Rab proteins are key components involved in targeting ion channels to precise membrane domains in epithelial cells. This project will investigate the role that specific SNAREs and Rab proteins play in targeting KCa3.1 to the basolateral membrane. This will be approached using a range of protein biochemistry, molecular and cell biology and imaging techniques.
Show Hamilton Lab page.
Show Condliffe Lab page.
COMMD proteins - how do they interact with and regulate protein trafficking machinery?
Associate Professor Fiona McDonald
Signal transduction, cell-cell interactions, ion transport, and the secretion of hormones depend on regulated protein movement through membrane compartments both to and from the cell surface. Defects in protein trafficking result in many human diseases including cystic fibrosis, hypertension, cardiac arrthymias, Alzheimer's disease, and copper toxicosis. Although the basic characteristics of protein transport between membrane compartments in specific vesicles are well established, the details of the regulation of vesicle formation, cargo selection and targeting of each vesicle population to its destination are not well understood. In addition, many cargo and vesicle machinery proteins carry ubiquitin tags believed to act as address labels for correct protein positioning in the cell.
COMMD (COpper Metabolism Murr1 Domain) proteins localise to distinct membrane compartments and/or vesicle populations, interact with trafficking machinery and link to ubiquitin pathway proteins.
This project will use live-cell imaging, and biochemical and physiological assays to uncover the mechanism by which COMMD proteins regulate protein trafficking.
Show McDonald Lab page.
Disruption of the intestinal epithelial barrier in autoimmune diseases
Associate Professor Grant Butt
While many autoimmune diseases appear distinct they share a number of common pathological mechanisms, including a gut-based environmental trigger. Genetic predisposition and a breach in the intestinal epithelial barrier may lead to a heightened immuneresponse towards intestinal bacteria causing inflammation and the characteristics of each disorder. This project will investigate whether there are modifications of the intestinal barrier in diseases such as Inflammatory Bowel Diseases, Type-1 diabetes mellitus and spondylarthropathies.
Show Butt Lab page.
Functional role of SNARE interactions with the Ca2+ signalling machinery
Dr Steven Condliffe & Dr Ruth Empson
The SNAREs are a family of proteins that mediate synaptic vesicle fusion - a process that is critically dependent on the synaptic intracellular calcium concentration. SNAREs interact with several important Ca2+ signalling proteins that may serve both to localise synaptic vesicles to sites of Ca2+ influx and/or to regulate Ca2+ signalling. Recent evidence has shown SNAREs interact with an important Ca2+ transporter protein - the plasma membrane Ca2+-ATPase (PMCA). This project will elucidate the functional role of SNARE interactions for the trafficking and regulation of PMCA using a range of protein biochemistry, molecular and cell biology, cell culture and imaging techniques.
Show Condliffe Lab page.
Show Empson Lab page.
Role of RyR2 in arrhythmia
Dr Peter Jones & Dr Ruth Empson
Cardiac arrhythmias remain the leading cause of death in patients with heart disease. An important trigger for arrhythmias is the inappropriate opening of the cardiac ryanodine receptor (RyR2). However, the mechanism by which these openings occur is not well understood. We have found that mutations within RyR2 and certain arrhythmogenic drugs increase the frequency of RyR2 openings by increasing the sensitivity of RyR2 to intra-store (SR) calcium. These data suggest that alterations in RyR2's SR calcium sensitivity represent a common mechanism underlying arrhythmia. RyR2 is part of a large macromolecular complex with other proteins. Others have shown that loss of these proteins can increase the activity of RyR2 and lead to heart disease. Using protein biochemistry and biophysics coupled with advanced SR calcium imaging in ventricular myocytes from transgenic animals; this project proposes to determine whether the interaction of these RyR2-binding proteins with RyR2 alters the opening of RyR2.
Show Jones Lab page.
Show Empson Lab page.
For further information on research in the Department, see our Research page.
Departmental Postgraduate Handbook for Thesis Students
For further detailed information about life as a thesis students in the Department of Physiology, please download our comprehensive guide.
PhD FAQ
What is the cost of living like in Dunedin? The University of Otago offers a detailed website that gives information about the cost of living in Dunedin. It should be noted that the costs of flatting quoted on the website are for shared accommodation with other flatmates.
How much does a PhD scholarship provide? From January 2012, University of Otago PhD scholarships and our Department PhD scholarships will be $25,000, plus the payment of tuition fees for three years. Sundry fees and insurance (compulsory for international students) is not included.
What are the requirements for a PhD in the Department of Physiology? PhDs are usually completed within 3 years and are 100% thesis based. This means that there are no courses or papers to take and that the majority of the time will be spent conducting research. Postgraduate students are required to present ongoing thesis research as they progress through their degree full details of what is required for a PhD can be found in the Department of Physiology's Postgraduate handbook for Thesis students.
Do I need to pay tuition fees? Tuition fees are paid for by the Department or the University if you receive a PhD scholarship, however, there are other fees that you will still have to pay. These include membership fees for the Otago University Students Association, however, this will give you access to a number of clubs and societies. Membership to the University gym is also included.
Do I require medical insurance if I am an international student? International students in New Zealand are required to be insured against a range of events including medical, personal liability, loss of personal effects etc. Insurance can be purchased overseas, but needs to fulfill certain criteria. Alternatively insurance can be purchased from a provider chosen by the University or other New Zealand insurance companies that meet the criteria required. More information can be found here.
What is life in Dunedin like? Dunedin is a small city of around 120,000 people located on the lower east coast of New Zealand's South Island. Dunedin is in close proximity to pristine beaches and rugged mountains. More information about life in Dunedin can be found on the Department of Physiology website and the University of Otago website.
When should I start my application process? Applicants are encouraged to apply to the Department as soon as possible, so that documentation can be vetted by your prospective supervisor and by the Department?s Research Committee. After approval by the Department, the University's application processing time can be up to four weeks for coursework programmes, and up to three months for programmes that are research only.
Are there English language requirements? Yes, click here for more information.
Do I need to have a minimum grade average to be accepted? Admission into the PhD programme normally requires the completion of a BSc (Hons) at the 2.1 level or a B+ grade average in a MSc or a PGDipSci in the same area of study or a related discipline, as the intended area of research. However to be considered for a PhD scholarship, higher grades are required.
If you still have questions, please contact:
Tracey Fleet
Departmental Administrator
PO Box 913
Dunedin 9054
Email: physiology@otago.ac.nz
Telephone: +64 3 479 7317
Doing a summer research project in Physiology gave me a good idea as to what it's like to actually work within a lab. This allowed me to break down that lecturer-student barrier and get to know people in the Department outside of studies.
