Thomas Bishop

TL;DR: The chemokine CCL2, produced by both damaged and undamaged primary sensory neurons in neuropathic pain states in rats, is released in an activity dependent manner from the central terminals of these fibres and provides a mechanism for immune activation, which in turn regulates the sensitivity of pain signaling systems in neuropathy pain states.

TL;DR: Investigation of the ability of intrathecal neurotrophin-3 (NT3) to promote axonal regeneration across the dorsal root entry zone (DREZ) and functional recovery in adult rats found it to allow sensory axons to overcome inhibition present at the DREZ and may serve to promote functional recovery following dorsal root avulsions in humans.

TL;DR: It is concluded that UVB inflammation produces a dose‐dependent hyperalgesic state sensitive to established analgesics, which suggests thatUVB inflammation in the rat may represent a useful translational tool in the study of pain and the testing of analgesic agents.

TL;DR: It is suggested that UVB inflammation, at least using moderate doses produces sensory changes primarily by sensitising peripheral pain processing in the relative absence of alterations in central pain processing.

TL;DR: It is concluded that UVB‐induced mechanical hyperalgesia may be explained by a net shift in peripheral nociceptor response properties and alteration in mechanical responses of A&dgr;‐ and heat‐insensitive C‐nocicePTors were particular to stronger stimuli.