University of Otago.Department of Physiology.Department of Physiology.

Physiology TV

An overview of Physiology at the University of Otago.

News

13th November, 2017

Otago study could mean hope for infertile couples

Crucial new information about how the brain controls fertility has been unlocked by University of Otago researchers, with their findings just published in prestigious journal Proceedings of the National Academy of Sciences of the United States of America.

13th November, 2017

Phenomenal success for Physiology researchers in latest Marsden funding round

Four 3-year project grants were awarded to Department of Physiology researchers in this year’s Marsden Fund - totalling over $3.8M.

25th October, 2017

Charlotte Steel, BSc (Hons) NEUR student in the Department has gained a Cambridge Rutherford Memorial PhD Scholarship

Our congratulations to Charlotte who is currently completing a BSc (Hons) degree in Neuroscience in the Department of Physiology with supervisor Assoc Prof Phil Sheard.

8th September, 2017

PhD student wins two awards at Queenstown Research Week

Congratulations to Mauro Silva, PhD student in the Department of Physiology. Mauro is supervised by Dr Rebecca Campbell.

8th September, 2017

Triennial Medal awarded to Professor Colin Brown

Congratulations to Colin who as been chosen by the Physiological Society of NZ (PSNZ) to be the recipient of the NZ Triennial Medal.

PhD Programme.

Summer Research Scholarships

The Physiology Department has its own internal application process.

Every year a number of summer research projects are offered in the Department of Physiology. Being selected for one of these projects means 10-weeks of paid, hands-on experience, working in a lab alongside researchers who are at the forefront of their field.

200-level students or above with a PHSL, NEUR or FUHB background are invited to apply, particularly those students who are keen on pursuing 400-level study in these subjects.

Applying for a Project

The Physiology Department has its own application process where students submit preliminary information about which summer research project(s) in the Department that they would like to ubdertake. From these applications, academics will choose which students they would like to invite to do summer research projects in their labs for ten weeks between November/December 2017 and January/February 2018.

How to Apply

Have a look at the list of possible projects available for download and on noticeboards on the ground floor of the Lindo Ferguson Building.

Talk to the academics offering the projects that you are interested in to find out more about the project itself and see if it is suitable for you.

Decide which project(s) you would like to be considered for – you can choose a maximum of three.

Fill in an application form available here or from Karla Sellwood in the Physiology Administration Office and hand it in to Karla by midday, Thursday 10 August 2017.

What Happens Next?

Karla will give a copy of your application form and academic record to the academic(s) that you wish to work with.

The academics will go through their applications and decide which student they would like to offer their summer research project.

All students will be informed whether or not they have been accepted to submit a project for a summer research scholarship in the Physiology Department by Wednesday 16 August 2017.

Selected students work with their academic supervisor to prepare an application for a summer student scholarship. Deadline for application and letter of recommendation from the supervisor to Karla is Wednesday, 23 August 2017. Karla will ensure this is signed by the HoD and will electronically send to the Division of Health Sciences by the due date.

Projects Available

A list of the summer research projects available in the Department of Physiology for 2017/18 is below.

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:

Autonomic innervation of the diabetic heart

Most patients with type 2 diabetes develop some form of heart disease. In our cardiovascular laboratory, we investigate the pathophysiology of the autonomic control of the diabetic heart. This project will aim determine the changes in neuronal autonomic innervation of the diabetic heart. We are looking for an enthusiastic student who after this summer project might also be interested to continue with a BSc (Hons) or BBiomedSc (Hons) project. Please feel free to contact me for additional information. (regis.lamberts@otago.ac.nz)

Dr Regis Lamberts
Show Lamberts Lab page.

Associate Professor Phil Sheard
Show Sheard Lab page.

Characterising ENaC function as shear sensor in endothelial cells

The diameter of blood vessels is regulated by the blood flow (shear force), passing through the lumen of the vessels. This mechanism is dysregulated in cardiovascular diseases (e.g. hypertension, diabetes). We hypothesise that impaired vascular ENaC expression and function leads to the functional changes in the vascular responses. Therefore, the objective of this project is to determine the role of ENaC in endothelial cells that were grown under different shear stress levels by performing expression analysis and electrophysiology. For any inquiry and/or more detailed information please contact Martin by e-mail martin.fronius@otago.ac.nz

Dr Martin Fronius
Show Fronius Lab page.

MicroRNAs in diabetic cardiovascular disease

People with diabetes mellitus are more likely to suffer from cardiovascular disease, which is the leading cause of death in these patients. The pathophysiology behind the development of diabetic heart disease is still not clear. MicroRNAs (short, noncoding RNAs) are recently gaining interest due to their active role in several diseases including cardiovascular diseases. However, the role of microRNAs in pathophysiology of diabetic heart disease is not known. Our laboratory is currently working on several projects to unravel the unknown facts of diabetic heart disease. If you are interested in joining our team, please come to discuss the potential projects with Rajesh. For more details, please visit the following website: http://phsl.otago.ac.nz/peoplelab.php?lab=4

Associate Professor Rajesh Katare
Show Katare Lab page.

Role of RyR2 in cardiac arrhythmia

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 coupled with advanced SR calcium imaging this project proposed to determine whether the interaction of these RyR2-binding proteins with RyR2 alters the opening of RyR2. Email pete.jones@otago.ac.nz for further information.

Dr Peter Jones
Show Jones Lab page.

Central regulation of reproduction

We investigate how the brain controls pregnancy and birth. We currently focus on the mechanisms that alter hypothalamic oxytocin neuron activity to prevent pre-term delivery and that alter vasopressin neuron activity to ensure adequate blood supply to the developing fetus. A range of projects are available around these topics, using electrophysiology or immunohistochemistry. Contact colin.brown@otago.ac.nz for further information

Professor Colin Brown
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Polycystic ovary syndrome and the female brain

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder and the leading cause of anovulatory infertility. Characterised by hyperandrogenism, menstrual dysfunction and polycystic ovaries, PCOS is a broad-spectrum disorder unlikely to stem from a single common origin. Although commonly considered an ovarian disease, the brain is now a prime suspect in both the ontogeny and pathology of PCOS. Projects in my laboratory are aimed at understanding the role of the brain in PCOS by investigating changes in neuronal wiring and function in a pre-clinical model of the syndrome. A summer project following this line of investigation will be available in my laboratory for a suitable candidate. A project may involve transgenic mouse models, animal handling and blood sampling, cryo-sectionning of brain tissue, immunohistochemistry, light and confocal microscopy, and the application of imaging software. Contact rebecca.campbell@otago.ac.nz for further information.

Dr Rebecca Campbell
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Regulation of corticotropin-releasing hormone (CRH) neuron excitability

We are seeking students to join our laboratory within the Otago Centre for Neuroendocrinology (http://www.neuroendocrinology.otago.ac.nz/). Our laboratory focuses on understanding neural circuits which control stress. Corticotropin-releasing hormone (CRH) neurons are activated in response to stress and are responsible for controlling the levels of stress hormones in the body. Research projects in the lab focus on determining how the excitability of CRH neurons is controlled before, during and after stress. For more information, please contact Dr Karl Iremonger karl.iremonger@otago.ac.nz

Dr Karl Iremonger
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Regulation of intercommunication in cortico-limbic brain circuit

Neuropsychiatric and degenerative brain disorders can involve altered connectivity within neural networks underlying perception, cognition and the regulation of emotion. Potential Summer Scholars are invited to apply to work in research on how current and potential treatments for such conditions might make intercommunication within these networks more stable, accurate, and reliable. We use a range of in vitro electrophysiological techniques, to study how the output of neurons interconnecting cortical and limbic regions is regulated, and how it may be disturbed by mechanisms thought to underlie disease. If you are interested in work in this area, please contact Dr Heyward phil.heyward@otago.ac.nz to talk about specific research projects.

Dr Phil Heyward
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The role of brain inflammation in obesity, diabetes and circadian rhythm

We are seeking a summer student to join a multidisciplinary research group at the Centre of Neuroendocrinology. Our group is studying the neuroendocrine regulation of body weight and glucose homeostasis and the link between the circadian clock and metabolism. We are particularly interested in the role of brain inflammation as predisposing factor for the development of obesity and diabetes. Various projects are available that focus on different aspects of brain inflammation, obesity, diabetes and circadian rhythm disorders. Our research combines molecular biological and neuroanatomical techniques with metabolic phenotyping and behavioural analyses. Email alexander.tups@otago.ac.nz for further information.

Dr Alexander Tups
Show Tups Lab page.

Cardiac stem cell function under hyperuricemic conditions

Stem cells are known to be the regenerative backup system of tissues in cases of tissue damage or degeneration and they have been found in almost every organ including the heart. Cardiac stem cells (CSCs) can be found in the myocardium and epicardium of the heart, where they function to regenerate the diseased myocardium. In order to perform at its full potential, stem cells are dependent on their environment, which may be compromised in hyperglycaemia and hyperuricemia in patients with diabetes mellitus. Stem cells are currently in the spot light to become the magic tool for tissue repair for clinicians in many diseases such as neurodegenerative diseases, type 2 diabetes mellitus or heart disease. However, knowledge about the effect of the environment on stem cell function is limited. We are interested in the effects of hyperuricemia (high plasma urate levels) on CSC function to decipher the pathways that affect CSC performance for stem cell therapy. This research project will involve human tissue samples and cell model studies combining different molecular biological and cell culture techniques. Students who are interested in the topic and keen to meet a challenge to perform state of the art research on stem cells are encouraged to apply. Please contact the supervisors for further information: Dr Andrew Bahn and Assoc. Prof Rajesh Katare Department of Physiology School of Biomedical Sciences Telephone: 479 – 7314 (Andrew), 7292 (Rajesh) Email: andrew.bahn@otago.ac.nz; rajesh.katare@otago.ac.nz

Dr Andrew Bahn
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Associate Professor Rajesh Katare
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How are ion channels recycled

‘Retromer’ is a newly recognised protein complex that decides whether transmembrane proteins will be recycled, or sent for destruction. The epithelial sodium channel, ENaC, known for its role in sodium balance and blood pressure homeostatsis associates with Retromer, but we don’t know which Retromer proteins are essential for this interaction. In this project, you will measure Na+ transport through ENaC expressed in an epithelia, using an Ussing chamber system. You will then knockdown a specific Retromer protein using siRNAs, and test the effect of reduced Retromer protein on Na+ transport. Further, you will use western blotting to confirm that protein knockdown is successful. Your results will contribute to our understanding of how ENaC cell surface population is regulated to control whole body Na+ balance, and blood volume and pressure. Email fiona.mcdonald@otago.ac.nz for further information.

Associate Professor Fiona McDonald
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Use of optogenetics in pancreatic β-cells to decipher the role of GLUT9 under hyperuricemic conditions

Hyperuricemia or high serum uric acid (SUA), a condition that is considered to cause gout, is a consequence of an unhealthy diet high in fructose, red meat or alcohol. High SUA is currently in the spotlight and connected to many diseases such as cardiovascular disease, metabolic syndrome, diabetes mellitus or cancer. We have established that elevated SUA contributes to impaired insulin secretion and β-cell death in the pancreas. We are now interested in dissecting the uric acid effects from the glucose effects on pancreatic β-cell function using an optogenetic approach in order to identify the uric acid-driven molecular mechanisms that link hyperuricemia to the development of type 2 diabetes. There are several projects available to evaluate optogenetic approaches in β-cell function using molecular methods and calcium imaging. Email andrew.bahn@otago.ac.nz for further details

Dr Andrew Bahn
Show Bahn Lab page.

Physiology is the stepchild of medicine. That is why Cinderella often turns out the queen.

Martin H. Fischer