John Hubbard Memorial Prize

The John Hubbard Memorial Prize is awarded annually in recognition of excellence in studies towards a PhD.

 Eligibility:

• Applicants must be in their final year of PhD study at a Tertiary Institution in New Zealand or no more than one year should have elapsed since the PhD was conferred
• Supervisors also must be a member of the PSNZ in good standing for 12 months prior to the call for applications, with the ability to pay membership in arrears (i.e. pay membership fee for the previous 12 months)
• Applicants must be members of the PSNZ at the time of presentation

 

 How to Apply:

At the time of abstract submission you will need to indicate whether you want to be considered for the John Hubbard Memorial Prize. Please contact and send an application consisting of the following to A/P Rajesh Katare, secretary of the PSNZ (rajesh.katare@otago.ac.nz) by 19^th July 2019.

1. A summary of the PhD work to-date (no more than 10 pages) placing it in the context of its contribution to the associated research field. Particular care must be placed to outline the PhD components, their logical progression, and the variety/complexity of techniques used. The supervisor(s) should have minimum input into the writing of this summary.
2. An abstract of a substantial component of the PhD to be presented ORALLY in a 20-minute talk at the Society’s Annual Meeting. The abstract should be formatted according to the instructions for authors normally used for the Proceedings of the PSNZ. Again, the supervisor(s) should have minimum input into the writing of the abstract.

3. Curriculum vitae

4. A brief report/reference should be submitted separately by the supervisor(s). It should include:

(i) a fair assessment of thealance of input from student/supervisor/other people into the protocol design, conduct of experiments and scientific interpretation and

(ii) a statement about the degree of input from the supervisor(s) into the writing of the submitted summary.

After Application:

Applications will be assessed by a Committee appointed by PSNZ Council.

• All applicants will be notified of the results of the preliminary screening at least three weeks before the Society’s Annual Meeting
• A short-list will be compiled
• Short-listed applicants will be expected to present a 20-minute talk, followed by 10 minutes for questions, at the Society’s Annual Meeting
• The quality of the presentation and the ability to answers questions will be judged by the above Committee and will contribute to the selection of the winner
• The Winner will be announced at the Society’s Dinner
• The Prize is a Certificate and a cheque for $500
• No award shall be made if none of the applicants merits such recognition

2016 Winner – Christopher Lear

 

 

 

 

 

 

 

 

 

 

 

2014 Winner – Aleisha Moore

Department of Physiology, University of Otago – “Investigating changes in the gonadotropin-releasing hormone neuronal network in a model of polycystic ovarian syndrome”

Investigating changes in the gonadotropin-releasing hormone neuronal network in a model of polycystic ovarian syndrome

Polycystic ovarian syndrome (PCOS) is the most common form of infertility amongst women of reproductive age worldwide. Although the aetiology is unclear, there are a number of features that identify PCOS as a disease of the brain.  Fertility is regulated by a small population of cells in the brain, gonadotropin-releasing hormone (GnRH) neurons. To function appropriately, GnRH neurons require feedback information from circulating steroid hormones produced by the gonads, including estrogen and progesterone. Because GnRH neurons do not express the appropriate steroid hormone receptors, the afferent neuronal network is thought to be responsible for relaying this critical information to GnRH neurons. Women with PCOS are found to exhibit impaired estrogen and progesterone negative feedback, resulting in an increase in GnRH neuron activity that leads to the defining symptoms of hyperandrogenaemia and infertility.

For my PhD, I hypothesised that impaired steroid hormone negative feedback results from alterations within the steroid hormone-sensitive afferent neuronal network. To investigate this, I utilised a mouse model of PCOS generated by prenatal androgen (PNA) treatment.  I first used serial blood sampling techniques to confirm that PNA-treated mice mimic the clinical neuroendocrine phenotype of impaired progesterone negative feedback. Imaging of GnRH neurons revealed increased putative GABAergic inputs in PNA-treated mice, and mapping of steroid hormone receptor expression revealed that PNA mice had 59% fewer progesterone receptor (PR) expressing cells in the arcuate nucleus of the hypothalamus (ARN). To address whether increased GABA innervation of GnRH neurons originates in the ARN, I used a viral-mediated Cre-lox approach to trace the projections of ARN GABA neurons in vivo. Remarkably, projections from ARN GABAergic neurons heavily contacted and even bundled with GnRH neuron dendrites, and the density of fibers apposing GnRH neurons was even greater in PNA-treated mice (56%). Additionally, this ARN GABA population showed significantly less co-localisation with PR in PNA-treated animals compared to controls, indicating that impaired progesterone sensitivity in PCOS may be mediated through ARN GABAergic neurons.

Together, the work from my PhD describes a novel and robust GABAergic circuit originating in the ARN that is disrupted in a model of PCOS and may underpin the neuroendocrine abnormalities of the syndrome. Of clinical relevance, these findings help explain the impact of GABA agonist drugs on menstrual cycle irregularity and interference with oral contraceptives, and could be the basis for understanding clinical therapies of PCOS.

 

Previous Recipients

• 2013 Simon de Croft, Dept of Physiology, University of Otago – Elucidating the properties of arcuate nucleus kisspeptin neurons through electrophysiology
• 2012 June-Chiew Han, Auckland Bioengineering Institute, The University of Auckland – Does the heart really operate at ‘isoefficiency’.
• 2011 Rachel Cheong, Dept of Physiology, University of Otago – Investigating the role of estrogen on the brain’s control of reproduction
• 2010 Isuru Jayasinghe, Dept of Physiology, University of Auckland – Resolving the structural basis of cardiac excitation-coupling
• 2009 Rosemary Brown, Dept of Anatomy and Structural Biology and Dept of Physiology, University of Otago – Mechanism of hyperprolactinaemia-induced infertility
• 2008 Karen Peebles (Co-winner), Department of Physiology, University of Otago – Changes in cerebral vasoactive factors during acute alterations in arterial blood gases in humans.
• 2008 Lindsea Booth (Co-winner), Department of Physiology, University of Auckland – Renal sympathetic nerve actiivity in the preterm fetus.
• 2007 Jenny Clarkson, Department of Physiology, University of Otago – Kisspeptin activation of GnRH neurons at puberty
• 2006 Natalie Harfoot, Department of Physiology, University of Otago – The Expression of Secretory NBC and CFTR in the Ileal Epithelium of the Australian Common Brushtail Possum (Trichosurus vulpecula)
• 2005 Kevin Webb, Department of Physiology, University of Auckland – Membrane Properties of Differentiating Fiber Cells in the Rat Lens
• 2004 Robert S. Kirton, Department of Physiology, University of Auckland – Does Strain Soften the Heart?
• 2004 Adèle J Pope, Department of Physiology, University of Auckland – Ventricular Remodelling as a Mechanism for Heart Failure
• 2002 Gareth B Miles, Department of Physiology, University of Auckland – Differential Expression during Postnatal Development of Voltage-Activated Calcium Channels in Functionally Distinct Motoneurons Controlling Airway and Extraocular Muscles
• 2000 Bridget L Leonard, Department of Physiology, University of Auckland – Sympathetic Neural Control of Intrarenal Blood Flow
• 1999 Fayez Hammad, Department of Physiology, University of Otago — The Role of Endothelins in Cold Ischaemia — Reperfusion Injury in Renal Transplantation
• 1997 Refik Kanjhan, Department of Physiology, University of Auckland — The Conundrum of P2X2R Expression in the CNS.