Event Details

Friday, 06 October 2017
12:30 pm - 1:30 pm
Queensland Bioscience Precinct Auditorium - Building 80, The University of Queensland
UQ Location:
Queensland Bioscience Precinct (St Lucia)
Event category(s):

Event Contact

Ms Katrina Garner-Moore
3346 2110
Org. Unit:
Institute for Molecular Bioscience

Event Description

Full Description:
The somatosensory nervous system perceives and transfers sensory modalities such as pain, itch, and temperature from the periphery to the central nervous system. Voltage-gated sodium (Nav) channels are vital for action potential generation, and are key players in this signal transmission process. Recent discoveries identified new roles for particular Nav channel subtypes in pain and other modalities. First, we will discuss how a spider toxin revealed a role for Nav1.1-expressing fibers in eliciting profound hypersensitivity to mechanical stimuli. In the gut, high-threshold mechanosensitive fibers also express Nav1.1 and possess enhanced toxin sensitivity in a mouse model of chronic visceral hypersensitivity. A small-molecule compound that inhibits Nav1.1 activity now shows promise as a drug candidate for mechanical pain and irritable bowel syndrome.
Accumulating evidence suggests a prominent role for Nav1.9 in nociception. Challenges in expressing this channel in a heterologous system and a poor understanding of its tissue distribution complicate the formation of a hypothesis about the role of Nav1.9 in transmitting sensory modalities. To overcome these obstacles, we developed a Nav1.9 stable cell line and generated an EGFP-tagged Nav1.9 mouse line, which allows us to refine tissue distribution and function of this channel in particular cell types. Moreover, Nav1.9-/- mouse behavior reveals a role for this particular subtype in regulating sensory modalities other than pain. We are currently exploring the neuronal circuitry underlying these observations.

Directions to UQ

Google Map:
To St Lucia Campus, UQ Ipswich, and UQ Gatton.

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