Date Published:

Abstract:

Neurons and satellite glial cells (SGCs) in sensory ganglia maintain bidirectional communications that are believed to be largely mediated by chemical messengers. Nerve injury leads to SGC activation, which was proposed to be mediated by nitric oxide (NO) released from active neurons, but evidence for this is lacking. Here we tested the idea that increased neuronal firing is a major factor in NO release. We activated neurons in isolated dorsal root and trigeminal ganglia from mice with capsaicin (5 µM), which acts on transient receptor potential vanilloid type 1 (TRPV1) channels in small neurons. We found that capsaicin induced SGC activation, as assayed by glial fibrillary acidic protein (GFAP) upregulation, and an NO-donor had a similar effect. Incubating the ganglia in capsaicin in the presence of the NO-synthase inhibitor L-NAME (100 µM) prevented the GFAP upregulation. We also found that capsaicin caused an increase in SGC-SGC coupling, which was shown previously to accompany SGC activation. To test the contribution of ATP to the actions of capsaicin, we incubated the ganglia with capsaicin in the presence of P2 purinergic receptor inhibitor suramin (100 µM), which prevented the capsaicin-induced GFAP upregulation. Size analysis indicated that although capsaicin acts mainly on small neurons, SGCs around neurons of all sizes were affected by capsaicin, suggesting a spread of signals from small neurons to neighboring cells. We conclude that neuronal excitation leads to NO release, which induces SGCs activation. It appears that ATP participates in NO's action, possibly by interaction with TRPV1 channels.