Neuropathic pain is a common diabetic complication, with as many as 50% of patients suffering from sensory complications (burning pain, pins and needles). To date the efficacy and longevity of many current pain-killing drugs is poor. This is due to the majority of patients not getting adequate pain relief and those few who do get benefit, suffer from adverse side effects therefore cannot stay on the medication long-term.
This problem is exacerbated as the mechanisms by which diabetic neuropathic pain occurs and the site of action is still unclear. Only by improving our understanding and advancing our knowledge of the underlying systems by which pain is caused, can we be successful in treating diabetic neuropathic pain. Recent evidence suggests that processing of sensory information at the level of the spinal cord is a key site by which diabetic neuropathic pain manifests.
It is widely known that the plasticity of the central nervous system strongly underpins neuropathic pain through changes in the organisation, morphology and excitability of spinal neurons resulting in the summation and amplification of sensory signals. Our work to date highlights that in diabetics there is a significant alteration in how the spinal cord sensory neurons modulates sensory information following alterations in neurovascular coupling. We wish to establish how hyperglycaemia drives sensory neuron excitability in the spinal cord to develop new treatment approaches for diabetic neuropathic pain. We utilise cell and rodent based assays inclusive of histology, behavioural assessment and electrophysiological studies incorporating biochemical techniques.
Applicants should have a 2:1 or 1st class honours degree in a subject relevant to the proposed project. A 2:2 degree may be considered only where applicants also offer a Masters degree with Merit.
Fees and funding
This is a self-funded PhD opportunity
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