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Sciatic Nerve Injury (sciatic + nerve_injury)
Selected AbstractsNeuropathic pain is enhanced in ,-opioid receptor knockout miceEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2006Xavier Nadal Abstract We have evaluated the possible involvement of ,-opioid receptor (DOR) in the development and expression of neuropathic pain. For this purpose, partial ligation of the sciatic nerve was performed in DOR knockout mice and wild-type littermates. The development of mechanical and thermal allodynia, as well as thermal hyperalgesia was evaluated by using the von Frey filament model, the cold-plate test and the plantar test, respectively. In wild-type and DOR knockout mice, sciatic nerve injury led to a neuropathic pain syndrome revealed in these nociceptive behavioural tests. However, the development of mechanical and thermal allodynia, and thermal hyperalgesia was significantly enhanced in DOR knockout mice. These results reveal the involvement of DOR in the control of neuropathic pain and suggest a new potential therapeutic use of DOR agonists. [source] Distribution and regulation of L-type calcium channels in deep dorsal horn neurons after sciatic nerve injury in ratsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2005E. Dobremez Abstract Deep dorsal horn neurons are involved in the processing of nociceptive information in the spinal cord. Previous studies revealed a role of the intrinsic bioelectrical properties (plateau potentials) of deep dorsal horn neuron in neuronal hyperexcitability, indicating their function in pain sensitization. These properties were considered to rely on L -type calcium currents. Two different isotypes of L -type calcium channel alpha 1 subunit have been cloned (CaV1.2 and CaV1.3). Both are known to be expressed in the spinal cord. However, no data were available on their subcellular localization. Moreover, possible changes in CaV1.2 and CaV1.3 expression had never been investigated in nerve injury models. Our study provides evidence for a differential expression of CaV1.2 and CaV1.3 subunits in the somato-dendritic compartment of deep dorsal horn neurons. CaV1.2 immunoreactivity is restricted to the soma and proximal dendrites whereas CaV1.3 immunoreactivity is found in the whole somato-dendritic compartment, up to distal dendritic segments. Moreover, these specific immunoreactive patterns are also found in electrophysiologically identified deep dorsal horn neurons expressing plateau potentials. After nerve injury, namely total axotomy or partial nerve ligation, CaV1.2 and CaV1.3 expression undergo differential changes, showing up- and down-regulation, respectively, both at the protein and at the mRNA levels. Taken together, our data support the role of L-type calcium channels in the control of intrinsic biolectrical regenerative properties. Furthermore, CaV1.2 and CaV1.3 subunits may have distinct and specific roles in sensory processing in the dorsal horn of the spinal cord, the former being most likely involved in long-term changes after nerve injury. [source] Differential activation of C1 complement components in rat spinal cord after sciatic nerve injuryJOURNAL OF NEUROCHEMISTRY, Issue 2003J. Mika Neuroimmune interactions are discussed to drive neuropathic pain. We used the Bennett model to correlate pain and cellular expression profiles of the complement factors C1q and C1q-associated serine proteases C1r/C1s in lumbar spinal cord. At 2 days C1q mRNA levels increased ipsilateral to the lesion, and peaked at 8 days when allodynia and severe walking problems were present. During regeneration walking problems disappeared together with C1q mRNA levels. C1q biosynthesis was restricted to microglia. Surprisingly, C1s/C1r biosynthesis was not increased after injury suggesting a role for C1q different from classical complement activation. Sustained C1q expression in spinal microglia after lesion in conjunction with pain behavior indicates that microglial C1q may be causally involved in the development and maintenance of neuropathic pain. Acknowledgements:, Supported by BMBF01GG9818, SFB297, DFGWE910/8-3, KBN3P05C00623. [source] Thyroid hormone enhances transected axonal regeneration and muscle reinnervation following rat sciatic nerve injuryJOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2010Petrica-Adrian Panaite Abstract Improvement of nerve regeneration and functional recovery following nerve injury is a challenging problem in clinical research. We have already shown that following rat sciatic nerve transection, the local administration of triiodothyronine (T3) significantly increased the number and the myelination of regenerated axons. Functional recovery is a sum of the number of regenerated axons and reinnervation of denervated peripheral targets. In the present study, we investigated whether the increased number of regenerated axons by T3-treatment is linked to improved reinnervation of hind limb muscles. After transection of rat sciatic nerves, silicone or biodegradable nerve guides were implanted and filled with either T3 or phosphate buffer solution (PBS). Neuromuscular junctions (NMJs) were analyzed on gastrocnemius and plantar muscle sections stained with rhodamine ,-bungarotoxin and neurofilament antibody. Four weeks after surgery, most end-plates (EPs) of operated limbs were still denervated and no effect of T3 on muscle reinnervation was detected at this stage of nerve repair. In contrast, after 14 weeks of nerve regeneration, T3 clearly enhanced the reinnervation of gastrocnemius and plantar EPs, demonstrated by significantly higher recovery of size and shape complexity of reinnervated EPs and also by increased acetylcholine receptor (AChRs) density on post synaptic membranes compared to PBS-treated EPs. The stimulating effect of T3 on EP reinnervation is confirmed by a higher index of compound muscle action potentials recorded in gastrocnemius muscles. In conclusion, our results provide for the first time strong evidence that T3 enhances the restoration of NMJ structure and improves synaptic transmission. © 2010 Wiley-Liss, Inc. [source] | ||||||||||