Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 24, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/ijms24032677
Keywords
dorsal root ganglia; neurons; dye coupling; intracellular recording; membrane excitability; aging; pain; gap junctions
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This study focused on age-related changes in dorsal root ganglia (DRG) neurons and satellite glial cells (SGCs) in mice. It was found that in aged mice, there was a higher level of coupling between DRG neurons and SGCs, and the membrane excitability of DRG neurons increased with age. These changes may be caused by low-grade inflammation associated with aging and contribute to pain behavior.
The effects of aging on the nervous system are well documented. However, most previous studies on this topic were performed on the central nervous system. The present study was carried out on the dorsal root ganglia (DRGs) of mice, and focused on age-related changes in DRG neurons and satellite glial cells (SGCs). Intracellular electrodes were used for dye injection to examine the gap junction-mediated coupling between neurons and SGCs, and for intracellular electrical recordings from the neurons. Tactile sensitivity was assessed with von Frey hairs. We found that 3-23% of DRG neurons were dye-coupled to SGCs surrounding neighboring neurons in 8-24-month (Mo)-old mice, whereas in young adult (3 Mo) mice, the figure was 0%. The threshold current for firing an action potential in sensory neurons was significantly lower in DRGs from 12 Mo mice compared with those from 3 Mo mice. The percentage of neurons with spontaneous subthreshold membrane potential oscillation was greater by two-fold in 12 Mo mice. The withdrawal threshold was lower by 22% in 12 Mo mice compared with 3 Mo ones. These results show that in the aged mice, a proportion of DRG neurons is coupled to SGCs, and that the membrane excitability of the DRG neurons increases with age. We propose that augmented neuron-SGC communications via gap junctions are caused by low-grade inflammation associated with aging, and this may contribute to pain behavior.
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