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PPAR\u03b3 activity has also been associated with neuroprotection in different neurological disorders, but the mechanisms involved in PPAR\u03b3 effects in the nervous system are still unknown. Here we describe a new functional role for PPAR\u03b3 in neuronal responses to injury. We found both PPAR transcripts and protein within sensory axons and observed an increase in PPAR\u03b3 protein levels after sciatic nerve crush. This was correlated with increased retrograde transport of PPAR\u03b3 after injury, increased association of PPAR\u03b3 with the molecular motor dynein, and increased nuclear accumulation of PPAR\u03b3 in cell bodies of sensory neurons. Furthermore, PPAR\u03b3 antagonists attenuated the response of sensory neurons to sciatic nerve injury, and inhibited axonal growth of both sensory and cortical neurons in culture. Thus, axonal PPAR\u03b3 is involved in neuronal injury responses required for axonal regeneration. Since PPAR\u03b3 is a major molecular target of the thiazolidinedione (TZD) class of drugs used in the treatment of type II diabetes, several pharmaceutical agents with acceptable safety profiles in humans are available. Our findings provide motivation and rationale for the evaluation of such agents for efficacy in central and peripheral nerve injuries. \u00a9 2015 Wiley Periodicals, Inc. 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