Experimental neurology
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Experimental neurology · Aug 2012
Effect of subthalamic deep brain stimulation on turning kinematics and related saccadic eye movements in Parkinson disease.
Persons with Parkinson disease (PD) experience turning difficulty, often leading to freezing of gait and falls. Visual information plays a significant role in locomotion and turning, and while the effects of deep brain stimulation (DBS) on oculomotor function have been well documented, the effects of DBS on oculomotor function during turning and on turning itself have yet to be fully elucidated. ⋯ DBS significantly improves turn performance and related oculomotor performance. These findings add to the growing list of therapeutic benefits offered by DBS.
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Experimental neurology · Aug 2012
Inhibition of ROS-induced p38MAPK and ERK activation in microglia by acupuncture relieves neuropathic pain after spinal cord injury in rats.
Acupuncture (AP) is currently used worldwide to relieve pain. However, little is known about its mechanisms of action. We found that after spinal cord injury (SCI), AP inhibited the production of superoxide anion (O(2)·), which acted as a modulator for microglial activation, and the analgesic effect of AP was attributed to its anti-microglial activating action. ⋯ Furthermore, ROS produced after injury-induced p38MAPK and ERK activation in microglia, and mediated mechanical allodynia and thermal hyperalgesia, which were inhibited by AP or a ROS scavenger. AP also inhibited the expression of inflammatory mediators. Therefore, our results suggest that the analgesic effect of AP may be partly mediated by inhibiting ROS-induced microglial activation and inflammatory responses after SCI and provide the possibility that AP can be used effectively as a non-pharmacological intervention for SCI-induced chronic NP in patients.
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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.
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Experimental neurology · Jun 2012
ReviewRole of noncoding RNAs in trinucleotide repeat neurodegenerative disorders.
Increasingly complex networks of noncoding RNAs are being found to play important and diverse roles in the regulation of gene expression throughout the genome. Many lines of evidence are linking mutations and dysregulations of noncoding RNAs to a host of human diseases, and noncoding RNAs have been implicated in the molecular pathogenesis of some neurodegenerative disorders. The expansion of trinucleotide repeats is now recognized as a major cause of neurological disorders. Here we will review our current knowledge of the proposed mechanisms behind the involvement of noncoding RNAs in the molecular pathogenesis of neurodegenerative disorders, particularly the sequestration of specific RNA-binding proteins, the regulation of antisense transcripts, and the role of the microRNA pathway in the context of known neurodegenerative disorders caused by the expansion of trinucleotide repeats.