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      Spinal Cord Injury: A Model of Central Neuropathic Pain


      S. Karger AG

      Spinal cord injury, Central pain, Excitotoxicity, Plasticity, Secondary injury

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          The condition of pain after spinal cord injury (SCI) affects the life quality of nearly 70% of individuals with SCI. Clinical studies over the past decade have provided important insights into the complexities of the clinical and psychosocial characteristics of this debilitating consequence of SCI. The use of experimental models developed to study at-level or below-level pain has provided an appreciation for the mechanism(s) responsible for the onset and progression of these conditions. Important to the studies related to SCI pain has been the focus on the molecular, biochemical, anatomical, and functional consequences of SCI that have identified potential therapeutic targets for the design of novel treatment strategies.

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          Most cited references 48

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          Central sensitization and LTP: do pain and memory share similar mechanisms?

          Synaptic plasticity is fundamental to many neurobiological functions, including memory and pain. Central sensitization refers to the increased synaptic efficacy established in somatosensory neurons in the dorsal horn of the spinal cord following intense peripheral noxious stimuli, tissue injury or nerve damage. This heightened synaptic transmission leads to a reduction in pain threshold, an amplification of pain responses and a spread of pain sensitivity to non-injured areas. In the cortex, LTP - a long-lasting highly localized increase in synaptic strength - is a synaptic substrate for memory and learning. Analysis of the molecular mechanisms underlying the generation and maintenance of central sensitization and LTP indicates that, although there are differences between the synaptic plasticity contributing to memory and pain, there are also striking similarities.
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            Transcriptional and posttranslational plasticity and the generation of inflammatory pain.

            Inflammatory pain manifests as spontaneous pain and pain hypersensitivity. Spontaneous pain reflects direct activation of specific receptors on nociceptor terminals by inflammatory mediators. Pain hypersensitivity is the consequence of early posttranslational changes, both in the peripheral terminals of the nociceptor and in dorsal horn neurons, as well as later transcription-dependent changes in effector genes, again in primary sensory and dorsal horn neurons. This inflammatory neuroplasticity is the consequence of a combination of activity-dependent changes in the neurons and specific signal molecules initiating particular signal-transduction pathways. These pathways phosphorylate membrane proteins, changing their function, and activate transcription factors, altering gene expression. Two distinct aspects of sensory neuron function are changed as a result of these processes, basal sensitivity, or the capacity of peripheral stimuli to evoke pain, and stimulus-evoked hypersensitivity, the capacity of certain inputs to generate prolonged alterations in the sensitivity of the system. Posttranslational changes largely alter basal sensitivity. Transcriptional changes both potentiate the system and alter neuronal phenotype. Potentiation occurs as a result of the up-regulation in the dorsal root ganglion of centrally acting neuromodulators and simultaneously in the dorsal horn of their receptors. This means that the response to subsequent inputs is augmented, particularly those that induce stimulus-induced hypersensitivity. Alterations in phenotype includes the acquisition by A fibers of neurochemical features typical of C fibers, enabling these fibers to induce stimulus-evoked hypersensitivity, something only C fiber inputs normally can do. Elucidation of the molecular mechanisms responsible provides new opportunities for therapeutic approaches to managing inflammatory pain.
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              Superficial NK1-expressing neurons control spinal excitability through activation of descending pathways.

              The increase in pain sensitivity that follows injury is regulated by superficially located projection neurons in the dorsal horn of the spinal cord that express the neurokinin-1 (NK1) receptor. After selective ablation of these neurons in rats, we identified changes in receptive field size, mechanical and thermal coding and central sensitization of deeper dorsal horn neurons that are important for both pain sensations and reflexes. We were able to reproduce these changes by pharmacological block of descending serotonergic facilitatory pathways. Using Fos histochemistry, we found changes in the activation of serotonergic neurons in the brainstem as well as evidence for a loss of descending control of spinal excitability. We conclude that NK1-positive spinal projection neurons, activated by primary afferent input, project to higher brain areas that control spinal excitability--and therefore pain sensitivity--primarily through descending pathways from the brainstem.

                Author and article information

                S. Karger AG
                October 2005
                13 October 2005
                : 14
                : 4
                : 182-193
                Comprehensive Center for Pain Research and the McKnight Brain Institute University of Florida, Gainesville, Fla., USA
                87657 Neurosignals 2005;14:182–193
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 3, References: 84, Pages: 12


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