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Progressive tactile hypersensitivity: an inflammation-induced incremental increase in the excitability of the spinal cord.
Leukemia inhibitory factor is an anti-inflammatory and analgesic cytokine.
The progressive tactile hyperalgesia induced by peripheral inflammation is nerve growth factor dependent.
Interleukin-1beta-mediated induction of Cox-2 in the CNS contributes to inflammatory pain hypersensitivity.
Periganglionic inflammation elicits a distally radiating pain hypersensitivity by promoting COX-2 induction in the dorsal root ganglion.
Induction of the Oct-2 transcription factor in primary sensory neurons during inflammation is nerve growth factor-dependent.
Basal and touch-evoked fos-like immunoreactivity during experimental inflammation in the rat.
Nerve growth factor contributes to the generation of inflammatory sensory hypersensitivity.
Contribution of interleukin-1 beta to the inflammation-induced increase in nerve growth factor levels and inflammatory hyperalgesia.
ERK MAP kinase activation in superficial spinal cord neurons induces prodynorphin and NK-1 upregulation and contributes to persistent inflammatory pain hypersensitivity.
Silencing Nociceptor Neurons Reduces Allergic Airway Inflammation.
CD11b+Ly6G- myeloid cells mediate mechanical inflammatory pain hypersensitivity.
Neural Plasticity and Inflammatory Pain