Experimental neurology
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Experimental neurology · Jul 2012
Spontaneous pain in partial nerve injury models of neuropathy and the role of nociceptive sensory cover.
Spontaneous pain is difficult to measure in animals. One proposed biomarker of spontaneous pain is autotomy, a behavior frequently observed in rats with complete hindpaw denervation (the neuroma model of neuropathic pain). A large body of evidence suggests that this behavior reflects spontaneous dysesthesic sensations akin to phantom limb pain or anesthesia dolorosa. ⋯ But the animal's pain experience was occult. The saphenous and sural nerves provided nociceptive sensory cover for the paw, preventing the behavioral expression of the spontaneous pain in the form of autotomy. The results support prior observations suggesting that partial nerve injury triggers spontaneous pain as well as allodynia, and illustrate the importance of nociceptive sensory cover in the prevention of self-inflicted limb injury.
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Experimental neurology · Jul 2012
Extensive respiratory plasticity after cervical spinal cord injury in rats: axonal sprouting and rerouting of ventrolateral bulbospinal pathways.
Spinal cord injury (SCI) causes an interruption of descending motor and autonomic nervous tracts. However, a partial injury, and particularly a unilateral section, is generally followed by spontaneous locomotor and respiratory recovery. Although locomotor functional recovery has been correlated to spontaneous anatomical plasticity of the corticospinal tract, the remodeling of the bulbospinal tract that sustains respiratory improvement is unknown and has therefore been investigated here after chronic lateral cervical injury in rats (90 days post-lesion by comparison to 7 days post-lesion). ⋯ Retrograde labeling of projections onto the phrenic nucleus revealed, after chronic injury, an increased recruitment of C1 propriospinal interneurons which moreover received more contacts from bulbospinal collaterals. This chronic remodeling was correlated with chronic diaphragm recovery under conditions of respiratory stress. Thus, despite extensive axonal loss and absence of direct phrenic reinnervation by bulbospinal respiratory neurons, sprouting processes toward cervical propriospinal neurons may contribute to the observed partial respiratory recovery.