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In the PNS, lesions cause RA\u2010induced gene transcription, intracellular translocation of retinoid receptors, and increased transcription of CRBP\u2010I, CRABP\u2010II, and retinoid receptors. The activation of RAR\u03b2 appears to be responsible for neurotrophic and neuritogenic effects of RA on dorsal root ganglia and embryonic spinal cord. While the physiological role of RA in the injured nervous system is still under investigation three domains of functions are suggested: (1) neuroprotection and support of axonal growth, (2) modulation of the inflammatory reaction by microglia\/macrophages, and (3) regulation of glial differentiation. 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