Studies on novel neuropeptide G-protein coupled receptors; Relaxin family peptide receptors, evolution, structure, function and drug development

PhD and Honours projects are available to study the expression, structure and function of these novel G-protein coupled receptors and their splice variants. Candidates will undergo training in various techniques including molecular cloning, cell biology, protein chemistry, site-directed mutagenesis, confocal microscopy, viral expression and animal behavioural phenotyping. Furthermore, candidates will be able to interact with industry partners with the opportunity to commercialize any of their research outcomes.

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Synaptic plasticity in pain pathways

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Targeted deletion of the CBP gene in brain nuclei involved in drug-seeking

Supervisors: Professor Andrew Lawrence, Dr Bianca Jupp

The transcription factor CREB has been implicated in the consolidation of neural plasticity associated with learning, memory and also drug addiction. However, CREB belongs to a family of related transcription factors so that genetic deletion of one gene may be compensated by up-regulation of related molecules. Importantly, all members of this family signal through a molecule known as the CREB binding protein (CBP) and so this represents a valid target to examine the involvement of a family of transcription factors in drug-seeking and drug-induced plasticity. To address this possibility, we are producing lines of double transgenic mice where the CBP gene has been deleted from defined populations of neurons. We will then assess the role of CBP in cocaine-seeking and cocaine-induced plasticity.

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Targeted dopamine D1 receptor-positive cell ablation in the brain of adult mice as a model of Parkinson-plus syndromes and Huntington’s disease.

Co-supervisor Dr Ilse Gantois
Parkinson’s plus syndromes are neurological conditions in which the clinical presentation resembles Parkinson’s disease but in which cells other than or in addition to the dopamine producing cells of the substantia nigra degenerate. Some of these syndromes are characterized as having death of cells that reside in the striatum. Another disease that is also known to have death of dopamine containing cells in striatum is Huntington’s disease.

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Temporal lobe epilepsy, the HPA axis and depression

Supervisors:Dr Mike Salzberg, Prof Terry O’Brien

The key structures involved in mesial temporal lobe epilepsy – the hippocampus and amygdala – are critical components in the central regulation of the HPA axis. The implications of this have hardly been studied at all. Does the HPA axis function normally when someone has mesial temporal sclerosis (the usual pathology underlying TLE)? What happens to HPA axis function when a temporal lobe is excised to treat intractable TLE (temporal lobectomy)? There are good reasons to think the answers to these questions are very important for several reasons, e.g., glucocorticoids and stress have been shown in animal models of this kind of epilepsy to aggravate the disorder, to speed up its rate of development.

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