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ENGLISH ABSTRACT
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
[Changes in long-term synaptic plasticity in the spinal dorsal horn of neuropathic pain rats].
OBJECTIVE: To observe the change in induction of long-term potentiation (LTP) of C-fiberevoked potentials in the spinal dorsal horn of neuropathic pain rats, examine the changes in plasticity of synaptic transmission, and explore the effects and mechanisms of central sensitization and neuropathic pain following noxious stimulation or nerve injury.
METHODS: Neuropathic pain model was produced by tight ligation of the L5/L6 spinal nerve in Sprague-Dawley rats and the control group rats were received sham operation. The C-fiber-evoked field potentials in rat spinal dorsal horn were recorded by extracellular recording techniques. The differences in induction of LTP of C-fiber dorsal horn field potentials in sham-operated and neuropathic pain rats were compared.
RESULTS: (1) In neuropathic pain rats, the LTP in the dorsal horn was induced by high-frequency, low-intensity conditioning stimulation (100 Hz, 10 V, 0.5 ms, given in 4 trains of 1 s duration at 10 s intervals) of the sciatic nerve, while the same stimulation couldn't induce LTP in sham-operated rats. The LTP could only be induced by high-frequency, high-intensity conditioning stimulation (100 Hz, 30-40 V, 0.5 ms, given in 4 trains of 1 s duration at 10 s intervals) of the sciatic nerve in these control rats. (2) The thresholds for evoking C-fiber dorsal horn field potentials were significantly lower and the amplitudes tended to be higher in neuropathic pain rats as compared to controls.
CONCLUSION: These data suggest that the nerve injury itself is likely to induce a state of hyperexcitability at the spinal nociceptive synapses, and further support the notion that the long-term synaptic plasticity and the central sensitization may contribute to the development of neuropathic pain.
METHODS: Neuropathic pain model was produced by tight ligation of the L5/L6 spinal nerve in Sprague-Dawley rats and the control group rats were received sham operation. The C-fiber-evoked field potentials in rat spinal dorsal horn were recorded by extracellular recording techniques. The differences in induction of LTP of C-fiber dorsal horn field potentials in sham-operated and neuropathic pain rats were compared.
RESULTS: (1) In neuropathic pain rats, the LTP in the dorsal horn was induced by high-frequency, low-intensity conditioning stimulation (100 Hz, 10 V, 0.5 ms, given in 4 trains of 1 s duration at 10 s intervals) of the sciatic nerve, while the same stimulation couldn't induce LTP in sham-operated rats. The LTP could only be induced by high-frequency, high-intensity conditioning stimulation (100 Hz, 30-40 V, 0.5 ms, given in 4 trains of 1 s duration at 10 s intervals) of the sciatic nerve in these control rats. (2) The thresholds for evoking C-fiber dorsal horn field potentials were significantly lower and the amplitudes tended to be higher in neuropathic pain rats as compared to controls.
CONCLUSION: These data suggest that the nerve injury itself is likely to induce a state of hyperexcitability at the spinal nociceptive synapses, and further support the notion that the long-term synaptic plasticity and the central sensitization may contribute to the development of neuropathic pain.
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