Abstract
Injury or inflammation in the peripheral branches of neurons of sensory ganglia causes changes in neuronal properties, including excessive firing, which may underlie chronic pain. The main types of glial cell in these ganglia are satellite glial cells (SGCs), which completely surround neuronal somata. SGCs undergo activation following peripheral lesions, which can enhance neuronal firing. How neuronal injury induces SGC activation has been an open question. Moreover, the mechanisms by which the injury is signaled from the periphery to the ganglia are obscure and may include electrical conduction, axonal and humoral transport, and transmission at the spinal level. We found that peripheral inflammation induced SGC activation and that the messenger between injured neurons and SGCs was nitric oxide (NO), acting by elevating cyclic guanosine monophosphate (cGMP) in SGCs. These results, together with work from other laboratories, indicate that a plausible (but not exclusive) mechanism for neuron-SGCs interactions can be formulated as follows: Firing due to peripheral injury induces NO formation in neuronal somata, which diffuses to SGCs. This stimulates cGMP synthesis in SGCs, leading to their activation and to other changes, which contribute to neuronal hyperexcitability and pain. Other mediators such as proinflammatory cytokines probably also contribute to neuron-SGC communications.
Highlights
The effects of injury to peripheral nerves on neuronal cell bodies in the peripheral and central nervous systems has been a major research topic because it is related to both important clinical and basic biological questions
The questions that will be addressed in this article are: what are the possible pathways between the periphery and the ganglionic neurons, and what is the signaling mechanism between the neurons and the satellite glial cells (SGCs)? The discussion below is an attempt to combine the available information with some novel ideas
Dai et al [11] stimulated the peripheral end of a rat sciatic nerve electrically, chemically and physiologically, and detected an increased level of phosphorylated ERK (pERK) in dorsal root ganglia (DRG) neurons within 2 min
Summary
The effects of injury to peripheral nerves on neuronal cell bodies in the peripheral and central nervous systems has been a major research topic because it is related to both important clinical and basic biological questions. Peripheral injury induces numerous alterations in sensory ganglia, in particular in the sensory neurons and the satellite glial cells (SGCs) that surround them [4,5]. These changes include augmented neuronal firing and activation (gliosis) of SGCs. The questions that will be addressed in this article are: what are the possible pathways between the periphery and the ganglionic neurons, and what is the signaling mechanism between the neurons and the SGCs?
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