Glia

In chronic pain conditions, such as fibromyalgia, the assumption that is classically made is that neurons cause the problem.  That is, the uncontrolled pain must be due to malfunctioning neurons in the pain pathway.  Linda Watkins, PhD, University of Colorado, offers a different view.  She postulates that non-neuronal cell types called glia may be the root of the problem.  Spinal cord glia (astrocytes and microglia) are immune-like cells which release an array of neuroexcitatory substances when these cells are triggered to activate.  Key among these spinally released substances are the proinflammatory cytokines:  Interleukin 1( IL-1), interleukin-6 ( IL-6) and tumor necrosis factor (TNF).  Evidence accruing across multiple laboratories over the past decade provide compelling support that activated glia, and their proinflammatory cytokine products, are key players in the creation and maintenance of diverse pathological pain states.  This profile suggests novel approaches to pain control where spinal cord glia and their proinflammatory cytokines are the therapeutic target, rather than neurons.  In animal models, this strategy is clearly successful.  A novel non-viral gene therapy approach (which constrains glial activation by driving the spinal production of the anti-inflammatory cytokine interleukin-10 ( IL-10), abolishes neuropathic pain for well over 3 months.  Indeed, once pain eventually returns, complete pain relief is again readily re-instated by simple follow-up IL-10 therapy.  This novel approach to pain and autoimmune function in fibromyalgia symptom management should stimulate some unique scientific research studies in the years ahead.