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 o xide (NO) after injury to rat facial motor neurons using NADPH-diaphor ase histochemistry. We employed intraneural injections of either salin e or toxic ricin, followed by nerve crush, in order to produce regener ation or degeneration of facial motor neurons (FMNs), respectively. Re active astrocytes responding to ricin-induced degeneration of FMNs sho wed increased NADPH-diaphorase activity while reactive astrocytes resp onding to axotomy (saline injection) did not. Reactive microglial cell s were found not to express NADPH-diaphorase in either one of these tw o paradigms. We conclude that irreversible neuron injury resulting in neurodegeneration causes increased production of NO by reactive astroc ytes.