Brain research bulletin
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Brain research bulletin · Jan 2009
ReviewBody weight supported gait training: from laboratory to clinical setting.
After spinal cord injury (SCI) of the cat or rat neuronal centres below the level of lesion exhibit plasticity that can be exploited by specific training paradigms. In individuals with complete or incomplete SCI, human spinal locomotor centers can be activated by appropriate afferent input. This includes to facilitate and assist stepping movements of the legs and to provide body weight support (BWS) standing on a moving treadmill. ⋯ Since several years driven gait orthoses can provide a standardized locomotor training. In the future, if regeneration approaches can successfully be applied in human SCI, even individuals with complete SCI may recover walking ability with locomotor training. Presently, individuals with complete SCI, spinal neuronal circuits undergo a degradation of their function 1 year after injury.
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Brain research bulletin · Nov 2008
Extracellular signal-regulated kinases mediate melittin-induced hypersensitivity of spinal neurons to chemical and thermal but not mechanical stimuli.
Subcutaneous melittin injection causes central plasticity at the spinal level in wide-dynamic-range (WDR) neurons, which are hypersensitive to various nociceptive stimuli. Previous behavioral studies demonstrated that the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase 1/2(ERK1/2), p38 MAPK, and c-Jun N-terminal kinase are involved in both peripheral and spinal processing of melittin-induced nociception and hypersensitivity. Yet the functional roles of the three MAPKs vary among different stimulus modalities, and must be further studied at the cellular level in vivo. ⋯ Melittin-induced enhancement of thermal hypersensitivity was also greatly inhibited by a single dose of capsazepine, a thermal nociceptor (TRPV1) blocker. These results suggest that activation of the ERK signaling pathway in the periphery is likely necessary for maintenance of a spinally sensitized state; activation of ERK1/2 in the primary injury site may regulate TRPV1, leading to dorsal horn hypersensitivity to thermal and chemical stimuli. ERK signaling pathways are not likely to be associated with melittin-induced dorsal horn hypersensitivity to mechanical stimuli.
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Brain research bulletin · Nov 2008
Tumor necrosis factor-α of Red nucleus involved in the development of neuropathic allodynia.
The pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) is associated with the generation of inflammatory and neuropathic pain. The current study aims to investigate the expression of TNF-α in the brain of rats with spared nerve injury (SNI), a neuropathic pain model with the lesion of common peroneal and tibial nerves. Two weeks following SNI, the immunohistochemical results identified that the expression level of TNF-α in the Red nucleus (RN) of SNI rats was apparently higher than that of sham-operated rats. ⋯ The results showed that the 50% paw withdrawal threshold (von Frey test) of SNI rats were increased by 20 and 2.0 μg/ml anti-TNF-α antibody as compared with that of the basic value and control groups (P<0.05), the analgesic effect lasted for 50 and 30 min, respectively. However, no significant analgesic effect was observed after 0.2 μg/ml antibody was microinjected into the RN. These results suggest that the TNF-α of RN is involved in the development of neuropathic allodynia in SNI rats.
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Brain research bulletin · Oct 2008
Upregulation of Ryk expression in rat dorsal root ganglia after peripheral nerve injury.
To study changes of Ryk expression in dorsal root ganglia (DRG) after peripheral nerve injury, we set up an animal model of unilateral sciatic nerve lesioned rats. Changes of Ryk protein expression in DRG neurons after unilateral sciatic nerve injury were investigated by immunostaining. Changes of Ryk mRNA were also tested by semi-quantitative PCR concurrently. ⋯ Ryk mRNA levels increased slightly from 1 to 2 weeks, decreased then by 3 weeks post-lesion. These results indicate that Ryk might be involved in peripheral nerve plasticity after injury. This is a novel function apart from its well-known fundamental activity as a receptor mediating axon guidance and outgrowth.