Chronic pain circuits

Chronic pain is a major global health burden, affecting nearly 20% of the Australian population. This debilitating condition results in hypersensitivity to sensory input so a normally innocuous stimulus can be painful (allodynia) or a moderately noxious stimulus causes excessive pain (hyperalgesia). Many chronic pain states are linked to neural circuit dysfunction, which can be traced back to the spinal level in the majority of cases. We have recently identified a subset of interneurons in the spinal cord dorsal horn that are selectively altered in an experimental model of chronic pain (Imlach et al. 2016, PMID: 27841371). These neurons are optimally positioned to act as a ‘gate’ that determines how sensory input (pain, touch) are relayed through pain pathways to the brain. In order to genetically target these neurons in vivo (eg: opto- or chemogenetics), we need to identify markers that are specific to this neuronal subtype. The aim of this project will be to determine which neuronal markers, or combination of markers, can be used to specifically identify these neurons. This will involve screening candidate markers in spinal cord tissue using immunohistochemical labelling and confocal imaging. If time permits, changes in the expression of candidate markers and receptors in the spinal cord will be investigated following the development of chronic pain. This will reveal elements within the circuitry that may be responsible of abnormal sensory processing in pain states.