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In sensory ganglia each nerve cell body is usually enveloped by a satellite glial cell (SGC) sheath, sharply separated from sheaths encircling adjacent neurons by connective tissue. However, following axon injury SGCs may form bridges connecting previously separate perineuronal sheaths. Each sheath consists of one or several layers of cells that overlap in a more or less complex fashion; sometimes SGCs form a perineuronal myelin sheath. SGCs are flattened mononucleate cells containing the usual cell organelles. Several ion channels, receptors and adhesion molecules have been identified in these cells. SGCs of the same sheath are usually linked by adherent and gap junctions, and are functionally coupled. Following axon injury, both the number of gap junctions and the coupling of SGCs increase markedly. The apposed plasma membranes of adjacent cells are separated by 15-20 nm gaps, which form a potential pathway, usually long and tortuous, between connective tissue and neuronal surface. The boundary between neuron and SGC sheath is usually complicated, mainly by many projections arising from the neuron. The outer surface of the SGC sheath is covered by a basal lamina. The number of SGCs enveloping a nerve cell body is proportional to the cell body volume; the volume of the SGC sheath is proportional to the volume and surface area of the nerve cell body. In old animals, both the number of SGCs and the mean volume of the SGC sheaths are significantly lower than in young adults. Furthermore, extensive portions of the neuronal surface are not covered by SGCs, exposing neurons of aged animals to damage by harmful substances.

Current information indicates that glial cells participate in all the 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. This review presents information that has been accumulated recently on the physiology and pharmacology of SGCs. It appears that SGCs carry receptors for numerous neuroactive agents (e.g., ATP, bradykinin) and can therefore receive signals from other cells and respond to changes in their environment. Activation of SGCs might in turn influence neighboring neurons. Thus SGCs are likely to participate in signal processing and transmission in sensory ganglia. Damage to the axons of sensory ganglia is known to contribute to neuropathic pain. Such damage also affects SGCs, and it can be proposed that these cells have a role in pathological changes in the ganglia.

Slender projections, similar to microvilli, are the main specialization of the perikaryal surface of sensory ganglion neurons. The extent of these projections correlates closely with the volume of the corresponding nerve cell body. It is likely that the role of perikaryal projections of sensory ganglion neurons, which lack dendrites, is to maintain the surface-to-volume ratio of the nerve cell body above some critical level for adequate metabolic exchange. Satellite cells probably have the ability to promote, or provide a permissive environment for, the outgrowth of these projections. It is not yet known whether the effect of satellite cells is mediated by molecules associated with their plasma membrane or by diffusible factors. Furthermore, receptor molecules for numerous chemical agonists are located on the nerve cell body surface, but it is not known whether certain molecules are located exclusively on perikaryal projections or are also present on the smooth surface between these projections. Further study of the nerve cell body surface and of the influence that satellite cells exert on it will improve our understanding of the interactions between sensory ganglion neurons and satellite neuroglial cells.