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Modulation of Formalin-Evoked Hyperalgesia by Intrathecal N-Type Ca Channel and Protein Kinase C Inhibitor in the Rat

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Abstract

1. ω-CgTx attenuated formalin-evoked biphasic flinches, while PKC inhibitor (STU) attenuated phase 2 and was reversed by PDBu.

2. ω-CgTx and STU suppressed the increase in CSF-glutamate after formalin injection.

3. Morphine completely suppressed both increased flinching and CSF glutamate release.

4. Thus, ω-CgTx (N-type Ca channels) may regulate neurotransmitter release evoked by C fiber activation and the formalin-evoked hyperalgesia may possibly be provoked as a result of PKC activation elicited by both presynaptic neurotransmitter release and activation of NMDA receptors in the spinal neurons.

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Correspondence to Toshizo Ishikawa.

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Nakanishi, O., Ishikawa, T. & Imamura, Y. Modulation of Formalin-Evoked Hyperalgesia by Intrathecal N-Type Ca Channel and Protein Kinase C Inhibitor in the Rat. Cell Mol Neurobiol 19, 191–197 (1999). https://doi.org/10.1023/A:1006937209676

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  • DOI: https://doi.org/10.1023/A:1006937209676

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