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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 excellent degree (minimum of four years' study) in biomedical science or a closely-related subject.

Applicants must apply to the Department of Physiology as follows:

  1. Refer to the available projects listed below and contact the supervisor(s) whose project(s) interest you the most. In your email, include the following: 
    • Your name and country of citizenship
    • Your CV
    • Certified academic transcript (and, if applicable, an explanation of the content)
    • Certified evidence of English language proficiency (eg IELTS or TOEFL results)
    • The names of two referees
  2. If your application is to be considered, the supervisor will contact you to discuss the next steps, and our Departmental Administrator will check that your documents are complete.

For further information on research in the Department, see our Research section.

Projects available

Opportunities for PhD study in the Department of Physiology for 2019-2020.

Dr Andrew Bahn

Disturbance of the ‘Cellular uric acid homeostasis’ as the driver for diabetes mellitus, hypertension and cancer
My group is interested in how uric acid controls major intracellular metabolic signalling pathways (mTOR, AMPK) in order to understand the onset of diabetes mellitus, hypertension and cancer. Uric acid transporters and especially GLUT9 are emerging as major players for ‘cellular uric acid homeostasis’ in many tissues controlling cellular redox and energy homeostasis and ultimately cell fate and survival.
Students who are interested in the topic and keen to meet a challenge to perform state of the art research are encouraged to apply.

Professor Ruth Empson

3 Projects:
Therapeutic approaches for the treatment of cerebellar ataxias and tremors
Cerebellar ataxias and tremor are devastating movement disorders that often begin early in life and for which there is no cure. We are using a variety of preclinical models and approaches to find new treatments focused towards targets such as the metabotropic glutamate receptors and the membrane chloride transporter protein KCC2.

Optogenetic voltage reporting to understand cerebellar learning
Cerebellar Purkinje neurons, the main output neuron of the cerebellar cortex, undergo a variety of forms of synaptic plasticity that are thought to underlie aspects of motor learning. Using a genetically encoded voltage indicator expressed exclusively in Purkinje neurons we are probing how Purkinje neuron electrical behaviour changes during various forms of motor learning.

Optogenetic voltage reporting to probe cerebellar to motor cortex connections
The cerebellum and the motor cortex are known to communicate during motor behaviour for the refinement of movement. In this project we propose to use a combination of electrophysiology and optical voltage reporting from the motor cortex to probe how error correction signals from the cerebellum drive motor cortex activity and plasticity during motor behaviour.

Dr Jeff Erickson

Novel approaches for treating cardiovascular disease
Cardiovascular disease is the primary cause of death throughout most of the world, and existing therapeutic options are unsuitable for a large percentage of patients. Our group is exploring new targets in the heart and vessels to develop the next generation of cardiovascular treatments. Recent work from our group shows has identified a potential target: calcium/calmodulin dependent kinase II (CaMKII), a key protein mediator of cardiac and vascular dyfunction. We are seeking motivated students with an interest in cardiovascular physiology to join our team and examine the connection between CaMKII and cardiovascular disease. Projects in our group utilize state-of-the-art techniques and reagents, as well as genetic mouse models not available elsewhere in the world. Candidates with a wide range of interests, including molecular and protein biochemistry, fluorescent imaging, and physiological techniques (ex. echocardiography, force development measurements in isolated fibers, etc.) are encouraged to apply.

Dr Martin Fronius

Shear stress sensing in arteries
The Fronius lab is investigating how ion channels are sensing shear stress and how this affects the function of blood vessels and blood pressure regulation. Focus of the research is to understand the interaction of the epithelial Na+ channel (ENaC) with the extracellular matrix and how this mediates vessel function. The lab uses a variety of methods including electrophysiology, pressure myography, expression analyses and atomic force microscopy.

For any inquiry and/or more detailed information please contact Martin by e-mail (martin.fronius@otago.ac.nz)

Dr Kirk Hamilton & Assoc Prof Fiona McDonald

The role of the Exocyst complex in trafficking ion channels in polarised epithelia
Proper trafficking of ion channels in epithelia is key to epithelial cell function. The Exocyst is a series of proteins that act as a complex and aids in tethering post-Golgi secretory vesicles for delivery of ion channels to the plasma membrane. The role of the Exocyst complex in trafficking ion channels still emerging. In this project, we will investigate the role of the Exocyst complex in the targeting of two epithelial ion channels to the appropriate membarne. This will be approached using a range of protein biochemistry, molecular biology, electrophysiological and imaging techniques. The implication of these results is to define novel trafficking partners of K+ and Na+ channels that may be used therapeutically in diseases.

Dr Karl Iremonger

Imaging the rhythms of stress hormone secretion
Corticosteroid stress hormones are released throughout the day in hourly pulses with a peak in secretion prior to the onset of the active period (early morning for humans, early evening for rodents). This secretion pattern is controlled by corticotropin-releasing hormone (CRH) neurons in the brain and corticotroph cells in the pituitary. This PhD project will use calcium imaging in CRH neurons and corticotroph cells both in vitro and in vivo to understand how these daily rhythms of stress hormone secretion are generated.

Dr Peter Jones

Understanding and controlling cardiac arrhythmias
Cardiac arrhythmias remain the leading cause of death in patients with heart disease. An important trigger for arrhythmias is the inappropriate control of calcium within the cells of the heart. We study a protein (RyR2) responsible for regulating the release of calcium within the heart. Our overall aim is to better understand RyR2 and use this knowledge to develop new strategies for treating arrhythmia. We use a host of techniques including molecular biology and biochemistry through to single cell and whole heart calcium imaging in animal models. We are also now moving more of our work into living cardiac tissue from heart disease patients (see heart.otago.ac.nz). Various projects are available utilising a variety of techniques to study the function, dysfunction and pharmacological control of RyR2. Candidates with interests in cardiac muscle physiology and protein biochemistry are encouraged to apply. Several possible projects are available and will utilise a variety of techniques to study the function, dysfunction and pharmacological control of RyR2.

Assoc Prof Rajesh Katare

Understanding the role of lymphatic endothelial cell dysfunction in mediating diabetic heart disease
Diabetes, affects endothelial cells function leading to a condition called diabetic microangiopathy. Majority of the focus is on understanding diabetes-induced changes in arterial or venous endothelial cells. However, very little is known about the role of lymphatic vascular endothelial cell dysfunction in diabetes-induced heart disease, despite their important role in maintaining body-fluid homeostasis, immune cell trafficking and lipid transport. Of interest, all these are dysregulated in the diabetic heart. This project will study the structural and functional changes and molecular alteration in the lymphatic vessels of the diabetic heart. Structural changes and molecular alteration will be first characterized in the human heart tissue. This will be followed by understanding these changes along with molecular alteration with the progression of diabetes using type 2 diabetic mouse model. The animal model will also be used to understand the role of lymphatic vessels dysregulation in mediating diabetic heart disease. 
Please contact A/P Rajesh Katare (rajesh.katare@otago.ac.nz) to discuss the project in detail.

Dr Regis Lamberts & Dr Carol Bussey

Circadian rhythm of heart rate regulation in diabetes
Resting heart rate is the strongest predictor of mortality in patients with cardiac disease. Incompetence in heart rate regulation is an undervalued feature of the diabetic heart with major cardiovascular consequences. Heart rate fluctuates in a circadian manner, and people with diabetes tend to have disturbed circadian profiles of heart rate. However, the underlying mechanisms of the circadian rhythm in heart rate have been debated. The fluctuations can occur either because control of the heart by central nerves (autonomic) or the pacemaker cells within the heart varies their activity (intrinsic). Therefore, the aim of this PhD is to measure whether changes in autonomic control and/or intrinsic regulation is responsible for the disturbed circadian rhythm of heart rate in diabetes. We will address this question using recordings of autonomic nerve activity and isolated heart studies in a type 2 diabetic animal model.

Assoc Prof Fiona McDonald

Epithelial sodium channel as a target in breast cancer
Breast cancer is a major health problem comprising 28% of cancers that affect New Zealand women. Our new data shows that epithelial sodium channel, ENaC, expression in patients' tumours correlates with breast cancer prognosis. ENaC is located in the plasma membrane, and its large extracellular domain senses physical changes in the extracellular environment, while intracellular ENaC domains interact with the cytoskeleton. These connections allow ENaC to contribute to cell shape and rigidity, thus influencing cell migration and differentiation. Changes in mechano-sensing pathways and cell shape are tightly linked to the ability of cancer cells to undergo epithelial-mesenchymal transition (EMT), migrate and metastasise. This project will involve you assessing ENaC’s role in breast cancer cell EMT, migration, and proliferation, and determining physical characteristics of breast cancer cells with changes in ENaC expression by atomic force microscopy. Characterisation of the mechanisms by which ENaC promotes tumour generation will provide a previously unknown target for breast cancer therapy.

Assoc Prof Daryl Schwenke

3 Projects:

Central modulation of cardiac Sympathetic Nerve Activity following acute MI.
The majority of people that suffer a heart attack (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, ii) identify the relative role of the cardio-cardiac reflex (e.g. vagal and sympathetic) for modulating the central integration of SNA following acute MI and iii) identify potential therapeutic targets (within the CNS) to prevent the adverse increase in SNA following acute MI.

Modulation of the pulmonary vasculature in health and disease.
The pulmonary microcirculation is tightly modulated by the autonomic nervous system, the pulmonary vessel endothelium and the vascular smooth muscle. All components act synergistically to selectively perfuse well-ventilated alveoli and, thus, optimize ventilation-perfusion matching. During hostile challenges to the pulmonary microcirculation, such as chronic hypoxia, each of these components can potentially undergo adverse functional changes, which ultimately culminates in the onset and development of pulmonary arterial hypertension. This research essentially aims to investigate the various mechanisms that modulate pulmonary vascular tone, with the ultimate goal of further understanding the pathomechanisms that contribute to the development of pulmonary hypertension. Experiments will be designed to assess the relative role of the autonomic nervous system, endothelium and smooth muscle in modulating pulmonary vascular tone in specific animal models susceptible to pulmonary hypertension, such as obesity, age-related and hypoxia sensitive subjects.

Changes in cerebral blood flow trigger an increase in sympathetic nerve activity – implications following acute myocardial infarction
Heart function is controlled by the sympathetic nervous system. Following a heart attack (myocardial infarction: MI), cardiac sympathetic nerve activity (cSNA) becomes dangerously elevated, triggering irregular heartbeats (arrhythmias) that often prove fatal. In those who survive the initial MI, the sympathetic hyper-excitation is irreversible and facilitates permanent structural and functional damage of the heart. cSNA is ultimately driven by the brain and we have recently shown that the hypothalamic paraventricular nucleus (PVN) appears to facilitate this increase in SNA following MI. However, the trigger that activates these oxytocin neurons following MI remains to be determined. Neuronal activity is modulated by cerebral blood flow (CBF). CBF is impaired in chronic heart failure, which is thought to cause the sustained increase in cSNA. Hence, a sudden decrease in CBF following an MI may trigger PVN activation providing the drive for the increase in cSNA.
Research Question and Objectives
The overall aim of this study is to test the hypothesis that decreased CBF activates PVN neurons to increase cSNA following acute MI. Specifically, i) advanced Synchrotron Radiation microangiography (Hyogo, Japan) will be utilized to image the changes in cerebral blood flow associated with acute MI, ii) changes in CBF will be correlated with PVN activation (immunohistochemistry) and cSNA (electrophysiology).

Assoc Prof Phil Sheard

2 Projects:

Investigation of the structural and functional consequences of advancing age on skeletal muscles, motor nerves, and neuromuscular junctions. The main emphasis on the work is the investigation of the cellular mechanisms by which advancing age results in loss of skeletal muscle mass.

Investigation of the impact of age and exercise on the neuromuscular consequences of anticancer drug treatment. The main emphasis of the work is to investigate the cellular mechanisms by which anticancer drug treatment results in loss of muscle mass, and the effects that age and exercise status might have on those mechanisms.