Neural Structure and Function Laboratory - Honours in 2009

An Honours project undertaken in this lab would be administered by the Discipline of Anatomy & Histology.

Despite advances in the clinical management of acute pain, injury of the nervous system leads still, in a clinically significant number of cases, to chronic neuropathic pain and striking disabilities characterised by alterations in complex behaviours and physiological dysfunction. The combination of chronic neuropathic pain and disability is notoriously refractory to treatment. Traumatic injuries lead to an "acute phase" response characterised by inflammation, pain and the disruption of ongoing behaviours. This acute phase response is followed usually by a period of diminishing inflammation, reduced pain, healing of the injury and a return to normal function.

For a number of individuals however, pain and behavioural disruption persists beyond this acute phase and despite injury healing, results in a state of chronic pain and disability. Injury triggers neuroplastic changes provoking altered activity in both peripheral nerves and their spinal cord and brainstem projection targets. However, the specific neural adaptations leading to the development of a state of chronic or persistent pain and disability on the one hand, or to a complete recovery on the other, are not understood.

Injury, disability and chronic pain research

Supervisor + contact details:

• Associate Professor Kevin Keay

Recent work from our laboratory has demonstrated that nerve injury evokes both pain and disabilities (i.e., disrupted social behaviours, disrupted sleep-wake cycle, changed in appetite, metabolic and endocrine function, loss of the ability to cope effectively with stress/stressors) in a select subgroup of nerve-injured rats. We have therefore suggested that this model of nerve injury is closer to the human clinical presentation than previously appreciated. Our data suggest also that disabilities evoked by nerve damage reflect a specific and select neurobiological response to the injury. We have characterised using molecular biological (i.e., gene-chips, RT-PCR, Western blotting) and functional-anatomical (i.e., immunohistochemistry) techniques unique sets of neural adaptations in sciatic nerve recipient areas of the spinal cord, and the supraspinal areas which receive inputs from them in the subset of rats with pain and disability following injury.

The broad aims of our research is to identify the specific neural networks which undergo (mal)adaptation following injury and lead to both behavioural and physiological changes which characterise individuals with chronic pain and disability. Our research will contribute to a better understanding of the transition from acute injury to chronic pain and disability.