The study of mechanisms underlying pain
Many of us expect our aches and pains to be readily treated by aspirin-like drugs. And, for effective control of more serious pain conditions, we have morphine-like drugs. So, why are we still looking to develop new anti-inflammatory and analgesic drugs? Well, aspirin and morphine-like drugs have many drawbacks, especially if needed to treat chronic severe pain conditions. Nerve injury-induced pain, also known as neuropathic pain, is perhaps the least well controlled of all chronic pain syndromes; it can result from trauma to the spinal cord and/or peripheral nerves, and is a frequent consequence of shingles (varicella zoster) infection in the elderly. Neuropathic pain is associated with persistent inflammatory reactions and immune responses at the site of injury and/or in nearby dorsal root ganglia (DRG) which house the cell bodies of primary sensory neurons. These responses result in abnormal spontaneous discharges of the injured nerve, and long-term plasticity changes in dorsal horn neurons of the spinal cord and neurons of the DRG resulting in the subsequent abnormal perception of pain.
The work of the Wise lab involves the study of cell signaling mechanisms involved in mediating responses in inflammatory pain and neuropathic pain conditions. We study cells isolated from the DRG of adult rats, and are particularly interested in cell-cell communication between the DRG neurons and non-neuronal satellite glial cells (SGCs). The SGCs tightly ensheathe the neuronal cell bodies, and become activated in response to nerve injury. Our work shows the control of neuronal cell survival by glial cells, and conversely, the control of glial cell activity by DRG neurons. One goal of our current research is to determine why and how neurons keep their associated glial cells under control. The research area of neuron-glial cell interactions should provide interesting targets for the future development of novel analgesics and anti-inflammatory drugs.