Abstract Following peripheral nerve injury, neuronal cell functions in sensory ganglia shift from normal maintenance and neurotransmission toward survival and regeneration. A rapid modulation of glial cell activity, which is related to changes in neuronal-support cell interaction, also occurs after nerve injury. Nerve growth factor (NGF) is required for the survival and maintenance of specific populations of sensory and sympathetic 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. A similar role for NGF in modulating support cell responses to peripheral nerve injury, however, has not been demonstrated. Using an autoimmune model, we assessed the effects of NGF depletion in adult rats on the injury-induced expression of glial fibrillary acid protein immunoreactivity (GFAP-IR) in the ipsilateral and contralateral trigeminal ganglia (TG). Unilateral inferior alveolar nerve crush resulted in a bilateral,NGF-dependent trigeminal satellite cell response. In control rats there was a widespread induction of GFAP-IR in the ipsilateral as well as the contralateral TG. In contrast, GFAP-IR was reduced to the mandibular division of the ipsilateral TG in NGF-depleted rats, and the contralateral up-regulation of GFAP-IR was entirely abolished. Bilateral sympathectomy failed to mimic the effects of autoimmunization. Our results provide evidence that NGF depletion inhibits injury-induced satellite cell responses, independent of its effects on sympathetic nerve function.