Abstract

Peripheral nerve injury results in sprouting of nerve fibers in the spinal cord dorsal horn, which may result in neuropathic pain. It has been reported that rat dorsal root ganglion neurons showed an enhancement of axonal sprouting when expression of syntaxin1A, a SNARE protein that was shown to be involved in transmitter release, was inhibited by an application of antisense oligonucleotide. In the present study, we investigated the effects of peripheral nerve injury on the expression of syntaxin1A mRNA in the spinal cord dorsal horn using real time quantitative RT-PCR. We also recorded the miniature excitatory postsynaptic currents (mEPSCs) from neurons in the superficial dorsal horn neurons by patch clamp methods, and analyzed the effects of nerve injury on mEPSCs. Mechanical allodynia appeared immediately after nerve ligation and continued for 20 days, which was accompanied with the reduction of syntaxin1A mRNA expression. The frequency of mEPSCs significantly increased in the peripheral nerve-ligated mouse. This increase in the frequency of mEPSCs may underlie the cellular mechanism of allodynia development. The reduced expression of syntaxin1A concurrent with the allodynia and increased frequency of mEPSC may indicate a potential role for syntaxin1A in the development of allodynia, possibly through axonal sprouting in the spinal cord dorsal horn.

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