NGF DEPLETION REDUCES IPSILATERAL AND CONTRALATERAL TRIGEMINAL SATELLITE CELL REACTIONS AFTER INFERIOR ALVEOLAR NERVE INJURY IN ADULT RATS

Following peripheral nerve injury, neuronal cell functions in sensory ganglia shift from normal maintenance and neurotransmission toward sur vival and regeneration, A rapid modulation of glial cell activity, whi ch is related to changes in neuronal-support cell interaction, also oc curs after nerve injury. Nerve ,growth factor (NGF) is required for th e survival and maintenance of specific populations of sensory and symp athetic neurons, and changes in neuronal gene expression after axonal injury are due in part to a loss of NGF retrograde transport from the periphery to the cell body. ii similar role for NGF in modulating supp ort cell responses to peripheral nerve injury, however; has mot been d emonstrated. Using an autoimmune model, we assessed the effects of NGF depletion in adult rats on the injury-induced expression of glial fib rillary acid protein immunoreactivity (GFAP-IR) in the ipsilateral and contralateral trigeminal ganglia (TG). Unilateral inferior alveolar n erve crush resulted in a bilateral, NGF-dependent trigeminal satellite cell response. In control rats there was a widespread induction of GF AP-IR in the: ipsilateral al as well as the contralateral TG. In contr ast, GFAP-IR mas reduced to the mandibular division of the ipsilateral TG; in NGF-depleted rats, and the contralateral up-regulation of GFAP -IR Nas entirely abolished. Bilateral sympathectomy failed to mimic th e effects of autoimmunization. Our results provide evidence that NGF d epletion inhibits injury-induced satellite cell responses, independent of its effects on sympathetic nerve function. (C) 1998 Academic Press .