We investigate the role of redox signaling for the manifestation and maintenance of neuropathic pain and specifically address the potential modulation caused by tetrahydrobiopterin and nitric oxide (BH4/NO). In a mouse model for neuropathic pain we analyze changes of the redox balance including live cell imaging of redox sensitive GFP in parallel to calcium currents and redox-proteomic screens to detect modified proteins. Behavioral correlates of neuropathic pain will be analyzed in a cre-loxP mediated specific knockout of HIF-1alpha which is a downstream target of BH4/NO.

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