| Project/Area Number |
17591953
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | The Nippon Dental University |
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Principal Investigator |
TAKEDA Mamoru The Nippon Dental University, School of Life Dentistry at Tokyo, Associate Professor (20227036)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,550,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥150,000)
Fiscal Year 2007: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2005: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Trigeminal ganglion / Glia / Hyperalciesia / Interleukin-1β / Perforated patch-clamp / Immunohistochemistry / Microiontophoresis / Extracellular recording / Interleukin-1β / 炎症 / マルチバレル / 微小電気泳動 / 免疫組織化学 |
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| Research Abstract |
The aim of the present study was to investigate whether neuron-glial cross talk in the trigeminal ganglia contribute to modulation of neuronal excitability of nociceptive trigeminal ganglion neurons during peripheral inflammation. Complete freund's adjuvant (CFA) was injected into rat facial skin to produce inflammation. The threshold for escape from mechanical stimulation applied to the whisker pad in inflamed rats was significantly lower than that in control. Two days after CFA injection, the mean percentage of TRG neurons encircled by glial fibrillary acidic protein (GFAP)/IL-1βimmunoreactivities were coexpressed in the same cells. Fluorogold labeling identified the site of inflammation. The number of FG-labeled IL-1 receptor type I (IL-1RI) small TRG neurons in inflamed rats was significantly greater than thai in control. In the FG labeled small TRG neurons, the size of IL-1β induced-depolarization in inflamed rats was larger than in control. Aσ-nociceptive TRG neurons responding to electrical stimulation of the whisker pad was recorded in pentobarbital-anesthetized rats. The number of Aσ-TRG neurons with spontaneous firings and their firing rate in inflamed rats were significantly larger than in control rats. The firing rates of the Aσ-TRG neuronal spontaneous activity were current-dependently decreased by local iontophoretic application of an interleukin I receptor type I antagonist (IL-1ra) in inflamed rats. The mechanical threshold of nociceptive-TRG neurons in inflamed rats was significantly lower than that in control rats, but was not significantly different between control rats and inflamed rats after iontophoretic application of an IL-1ra. These results suggest that under inflammation modulates the excitability of nociceptive Aσ-TRG neurons innervating the facial skin via IL-1β paracrine action within trigeminal ganglia. Such an IL-1β release could be important in determining trigeminal inflammatory hyperalgesia.
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