Neural proliferation in the dorsal root ganglia of the adult rat following capsaicin-induced neuronal death.
Glial proliferation is a major component of the nervous system's response to injury. In addition to glial proliferation, injury may induce neuronal proliferation in areas of the adult nervous system not considered neurogenic. We have previously reported increased neural proliferation within adult nodose ganglia following capsaicin-induced neuronal death. However, proliferation within the dorsal root ganglia (DRG) remains to be characterized. We hypothesized that capsaicin-induced neuronal death would increase proliferation of satellite glial cells (SGCs) within the DRG. To test this hypothesis, 6-week-old Sprague-Dawley rats received a neurotoxic dose of capsaicin, and proliferation was quantified and characterized at multiple time points thereafter. Proliferation of satellite glial cells expressing the progenitor cell marker nestin was increased at 1 and 3 days following capsaicin administration as shown by BrdU incorporation. In addition to SGCs was a large population of proliferating resident macrophages, as shown by retrovirally mediated expression of GFP. SGC proliferation at these early time points was followed by recovery of neuronal numbers after a loss of 40% of the neuronal population in the DRG. This recovery in neuronal number correlated with recovery of function as shown by paw withdrawal from a noxious heat source. Further understanding of the role that glial proliferation plays in the recovery of neuronal numbers and function may lead to the development of therapeutic treatments for neurodegenerative conditions.
Integrative Physiology and Neuroscience, College of Veterinary Medicine, Washington State University, Pullman, Washington, 99164-6520.
Zachary R
ZR
Gallaher
Stephen T
ST
Johnston
Krzysztof
K
Czaja
D000818:Animals; D001973:Bromodeoxyuridine / Q000378:metabolism; D002135:Calcium-Binding Proteins / Q000235:genetics / Q000378:metabolism; D002211:Capsaicin / Q000494:pharmacology*; D016923:Cell Death / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects*; D005727:Ganglia, Spinal / Q000166:cytology* / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D005974:Glutamate-Ammonia Ligase / Q000235:genetics / Q000378:metabolism; D008297:Male; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012190:Retroviridae / Q000502:physiology; D011984:Sensory Receptor Cells / Q000187:drug effects*; D018689:Sensory System Agents / Q000494:pharmacology*; D013997:Time Factors; D014162:Transfection
D002135:Calcium-Binding Proteins; D009419:Nerve Tissue Proteins; D018689:Sensory System Agents; D005974:Glutamate-Ammonia Ligase; D001973:Bromodeoxyuridine; D002211:Capsaicin
gliogenesis; macrophages; neural progenitors; proliferation; satellite glial cells