脊髄クモ膜下腔内 Ca^<2+> チャネル阻害薬 cilnidipine 投与によるラット神経因性疼痛の調節
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The neuropathic pain developed following peripheral nerve injury may be mediated by upregulated synaptic transmission of spinal cord. N-type Ca^<2+> channel localized in pre-synaptic terminals has been shown to modulate the release of neurotransmitter. Previous studies have demostrated that N-type Ca^<2+> channel blockers suppress peripheral nerve neuroplasticityinduced neuropathic pain. Cilnidipine is a newly synthesized 1, 4-dihydropyridine (DHP)-type Ca^<2+> channel blocker. This study analyzed that effect of intrathecal infusion of cilnidipine on the response to thermal stimulation and histo-pathological changes after chronic constriction injury (CCI) in rats. Male Sprague-Dawley rats was implanted with intrathecal (I.T.) catheters under 2∿3% halothane anesthesia according to the modified method of Yaksh and Rudy (1976). The left sciatic nerve of rats was ligated under 2∿3% halothane anesthesia. Paw withdrawal latency times (PWL) of response to thermal stimulation were measured in these rats by using the planter test equipment before CCI (pre) and at 3, 5, 6, 8, and 10 days after CCI. Rats were separated into three groups. : 1) saline 10μl 2) L-, N-type Ca^<2+> channel blocker cilnidipine 100ng/10μl 3) L-type Ca^<2+> channel activater BayK8644 100ng/10μl+cilnidipine 100ng/10μl. Each drug group was injected by I.T. catheter, everyday from 5 days after CCI. Histochemical analysis for apoptosis (TUNEL stain) and neuronal degeneration (HE stain) in the laminae I-II, III-IV in spinal cord (L3-5) in rats was performed with light microscope (40 and 400 times) at the 6 and 10 days after CCI, respectively. The left paw withdrawal latency time was significantly increased on thermal stimulation by intrathecal infusion of cilnidipine than saline. Apoptic and necrotic neuronal degeneration was significantly decreased at the lamine I-II and III-IV by intrathecal infusion of cilnidipine than saline. The present results clearly demonstrated that cilnidipine prevents the sensitization evoked by thermal stimulation which is associated with effect on apoptotic and necrotic neuronal degeneration. This effects were not antago-nized by giving L-type Ca^<2+> channel agonist, BayK-8644. These results showed that cilnidipine may regulate pain sensitization produced by sciatic nerve ligation, suggesting that cilnidipine has beneficial effect in developing thermal neuropatic pain via mechanism by inhibiting N-type Ca^<2+> channel.
- 九州歯科学会の論文
- 2000-02-25
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