The progressive tactile hyperalgesia induced by peripheral inflammation is nerve growth factor dependent.
Inflammatory pain hypersensitivity mediated by phenotypic switch in myelinated primary sensory neurons.
Progressive tactile hypersensitivity: an inflammation-induced incremental increase in the excitability of the spinal cord.
Collateral sprouting of uninjured primary afferent A-fibers into the superficial dorsal horn of the adult rat spinal cord after topical capsaicin treatment to the sciatic nerve.
Zinc reduces the hyperalgesia and upregulation of NGF and IL-1 beta produced by peripheral inflammation in the rat.
Peripheral cell types contributing to the hyperalgesic action of nerve growth factor in inflammation.
Phenotypic modification of primary sensory neurons: the role of nerve growth factor in the production of persistent pain.
Induction of the Oct-2 transcription factor in primary sensory neurons during inflammation is nerve growth factor-dependent.
