Abstract:
Current information indicates that glial cells participate in most normal and pathological processes of the central nervous system. Although much less is known about satellite glial cells (SGCs) in sensory ganglia, it appears that these cells share many characteristics with their central counterparts. We found that SGCs in sensory ganglia of mice undergo major changes in a variety chronic of pain models such as axotomy, local and systemic inflammations, neuropathy induced by chemotherapeutic drugs, and diabetic neuropathy. These changes include upregulation of the glial marker glial fibrillary acidic protein (GFAP), increased cell coupling by gap junctions, and augmented responses to ATP via P2 receptors.
We also showed that intercellular communications in the ganglia are mediated by calcium waves, which depend on gap junctions and P2 receptors. Our main hypothesis is that augmentation of these two factors leads to increased excitability of sensory neurons and pain. In support of this idea, blocking gap junctions reduced neuronal excitability and pain. We propose that SGCs play a major role in chronic pain and may be a suitable target for pain therapy.
