Dr Tomris Mustafa
BSc (Hons) PhD (Melb)
Research Officer
Neuropeptides Group
Synaptic Neurobiology Laboratory
Joint appoint with the Howard Florey Institute and Mental Health Research Institute
Contact Details
Email: | |
Phone: | +61 (03) 8344 1867 (office) |
Phone: | +61 (03) 8344-5645 (laboratory) |
Research Interests
Understanding the link between G-protein coupled receptors and downstream signal transduction mechanisms in the central nervous system and how these are altered in neuropsychiatric illnesses, such as schizophrenia and depression.
Determining how abnormal functioning and dysregulation of GPCR-mediated calcium signalling required for neurotransmission and synaptic plasticity in both neurons and astrocyte can result in susceptibility to mental disorders such as schizophrenia.
Laboratory Techniques
- Molecular Biology
- Cell biology
- Receptor pharmacology and signalling
- Single cell calcium imaging
Additional Information
Tomris Mustafa completed her doctoral studies at the Howard Florey Institute under the supervision of Dr Anthony Albiston, characterising the human AT4/IRAP protein. She then commenced her postdoctoral training at the National Institutes of Mental Health with Dr Lee Eiden in Bethesda, Maryland. During this time she was awarded a Julie Axelrod Memorial Fellowship and cloned and characterised the PAC1 receptor variant expressed in chromaffin cells responsible for calcium-dependent catecholamine secretion. These studies focused on investigating the mechanisms utilised by GPCRs to regulate intracellular calcium signalling required for neuronal secretion, differentiation and gene transcription.
She then returned to Melbourne and joined Dr David Bowser’s laboratory on synaptic neurobiology, interested in determining how different cells in the brain communicate with each other and their local environment. Dr Tomris was then awarded the Ronald Phillip Griffith Research Fellowship, and together with Dr David Bowser, is currently investigating the ability of neurotransmitters and neuropeptides to influence neuronal excitability and plasticity though communication and modulation of astrocytes under both normal and pathological conditions.
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