Journal of the peripheral nervous system : JPNS
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J. Peripher. Nerv. Syst. · Sep 2006
Comparative StudyNociceptin and its receptor in rat dorsal root ganglion neurons in neuropathic and inflammatory pain models: implications on pain processing.
Nociceptin (NC), by activating its receptor, the opioid receptor-like 1 (ORL1) receptor, exerts an effect on a number of functions in the nervous system including locomotion, learning and memory, and processing of pain signals. Data on the expression of NC and ORL1 receptor in dorsal root ganglion (DRG) neurons and on its modulation after nerve injury and inflammation are controversial. We therefore sought to investigate the immunoreactivity (IR) of NC and ORL1 receptor in DRG neurons in two pain models, a pure neuropathic pain model, namely partial sciatic nerve transection (PST), and an inflammatory pain model, complete Freund's adjuvant (CFA) injection into the hindpaw. ⋯ Activating transcription factor 3 (ATF3), a neuronal marker of nerve injury, was induced in DRG neurons 7 and 14 days after PST and 7 days after CFA injection. Double labeling with ATF3 revealed expression of NC and ORL1 receptor in intact as well as in injured primary afferent neurons. Thus, NC and the ORL1 receptor may be involved in the modulation of neuropathic and inflammatory pain at the level of the primary afferent neuron.
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J. Peripher. Nerv. Syst. · Sep 2006
Comparative StudyEvidence for direct axonal toxicity in vincristine neuropathy.
There is a long-standing debate concerning the localization of the primary insult that results in distal axonal degeneration, or 'dying back' neuropathy. To address this question, we created an in vitro model of vincristine neuropathy in rat dorsal root ganglia (DRG). DRGs were grown in compartmentalized chambers, allowing for isolated exposure of the cell body or the axon to vincristine. ⋯ At this dose of 0.05 microM, exposure of the cell bodies had no effect on the growth of axons, whereas addition of vincristine to the axonal compartment caused axonal shortening without affecting the growth of unexposed 'sister' axons. Toxicity was seen only with exposure of the growing axonal tips. These data support localized axonal toxicity as a cause of distal axonal degeneration due to vincristine.