Astrocytes but not microglia express NADPH-diaphorase activity after motor neuron injury in the rat.
The purpose of this study was to identify cellular sources of nitric oxide (NO) after injury to rat facial motor neurons using NADPH-diaphorase histochemistry. We employed intraneural injections of either saline or toxic ricin, followed by nerve crush, in order to produce regeneration or degeneration of facial motor neurons (FMNs), respectively. Reactive astrocytes responding to ricin-induced degeneration of FMNs showed increased NADPH-diaphorase activity while reactive astrocytes responding to axotomy (saline injection) did not. Reactive microglial cells were found not to express NADPH-diaphorase in either one of these two paradigms. We conclude that irreversible neuron injury resulting in neurodegeneration causes increased production of NO by reactive astrocytes.
McElhaney
M R
MR
Department of Comparative and Experimental Pathology, College of Veterinary Medicine, University of Florida, Gainesville 32610.
Chandler
L J
LJ
Streit
W J
WJ
D000818:Animals; D001253:Astrocytes / Q000201:enzymology*; D005154:Facial Nerve / Q000166:cytology / Q000201:enzymology; D006651:Histocytochemistry; D008024:Ligands; D008297:Male; D017628:Microglia / Q000201:enzymology*; D009046:Motor Neurons / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D009252:NADPH Dehydrogenase / Q000096:biosynthesis*; D009409:Nerve Crush; D009410:Nerve Degeneration / Q000187:drug effects; D009416:Nerve Regeneration / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012276:Ricin / Q000633:toxicity
D008024:Ligands; D012276:Ricin; D009252:NADPH Dehydrogenase