Research groups
Greg Weir
Post-doctoral Research Fellow
My research interests centre on understanding sensory neuron biology in health and disease. Sensory neurons of the dorsal root ganglia are an incredibly heterogeneous population of neurons; tasked with detecting a range of sensations including touch, itch, warmth and nociception. While much knowledge has been accrued as to the molecular profile of neurochemically distinct sensory neurons, the functional roles they play in normal sensation are still unclear. Less still is understood as to which populations contribute to different aspects of pathological pain following inflammation or damage to the nervous system. Better knowledge of the neural circuits underlying normal nociception and pathological pain states will undoubtedly lead to advances in the development of novel and specific analgesics.
I am particularly interested in using new tools available to neuroscience in order to control the activity of discreet neuronal populations. In doing so we can begin to ask fundamental questions as to the role of specifically targeted neurons. We have used a chemogenetic approach to remotely silence sensory neurons in a non-biased manner. This strategy has efficacy in reversing pain-related hypersensitivity in a preclinical nerve injury model. Our current work involves targeting our silencing to discreet populations in order to understand their function in normal and diseased states.
Recent publications
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The Genetics of Neuropathic Pain from Model Organisms to Clinical Application
Journal article
Calvo M. et al, (2019), Neuron, 104, 637 - 653
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The Role of TRESK in Discrete Sensory Neuron Populations and Somatosensory Processing
Journal article
CADER M. et al, (2019), Frontiers in Molecular Neuroscience
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Defining the Functional Role of NaV1.7 in Human Nociception
Journal article
McDermott LA. et al, (2019), Neuron, 101, 905 - 919.e8
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Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability
Journal article
Dawes JM. et al, (2018), Neuron, 97, 806 - 822.e10
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Mutations in DNM1L, as in OPA1, result in dominant optic atrophy despite opposite effects on mitochondrial fusion and fission
Journal article
Gerber S. et al, (2017), Brain, 140, 2586 - 2596