Molecular mechanisms that contribute to skeletal pain
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Head of Laboratory
Associate Professor Jason Ivanusic+61 3 8344 7254
Project Details
Skeletal pain is transmitted by two classes of peripheral nociceptors. Aδ nociceptors are medium-diameter myelinated neurons that transmit fast, intense pain, of the sort experienced in fracture and breakthrough cancer pain. C nociceptors are small-diameter unmyelinated neurons that encode slow, burning pain, of the sort experienced in cancer and osteoarthritis. A number of ion channels and receptors are emerging as important modulators of the activity of peripheral bone nociceptors. Identifying these regulators of nerve activity and better understanding their role in generation of bone pain could open up avenues for development of tools to selectively manipulate pain originating from bone. In this project, we will use a variety of techniques and animal models to explore roles for different ion channels and receptors in generating and/or maintaining skeletal pain. We are currently interested in modelling experimental inflammation of the bone marrow, osteoarthritis and bone cancer induced skeletal pain. Depending on the particular ion channel or receptor that is being explored, students can expect to gain experience in working with animals models of skeletal pathology, an in vivo electrophysiological bone-nerve preparation, neuroanatomical tracing and immunohistochemistry, small animal handing, anaesthesia, surgery and/or dissection.
Researchers
Associate Professor Jason Ivanusic
Michael Morgan, Postdoctoral Research Fellow
Jenny Thai, Research Support Officer
Vida Nazemian, PhD Student
Kelly Effendi, Honours Student
Mohamed Habib, Honours Student
Paul Trinh, Honours Student
Collaborators
Associate Professor James Brock
Associate Professor Michael Barrington
Associate Professor Stuart Mazzone
Dr. Alice McGovern