| Project/Area Number |
11556008
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
植物保護
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| Research Institution | RIKEN (The Institute of Physical and Chemical Research) |
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Principal Investigator |
NAGATA Keiichi Laboratory for Memory and Learning, BSI, RIKEN Researcher, 記憶学習機構研究チーム, 研究員 (40282321)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUDA Kazuhiko Faculty of Agriculture, Kinki University, Assistant professor, 農学部, 助教授 (00199796)
OZOE Yoshihisa Life and Environmental Science, Shimane University, 生物資源科学部, 教授 (80112118)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1999: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | Ion channel / Insecticides / Patch clamp method / Electroohysiology sinele-channel / Acetylcholine / GABA |
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| Research Abstract |
The neuronal nicotinic acetylcholine receptor-channels (AChR) play a vital role in the central nervous system in a complicated manner. Several ion channels including NMDA and GABA(A) receptors are modulated by Ca2+ ions which enter through the neuronal nicotinic AChRs in the presynaptic membranes. In order to clarify the detailed mechanism of action of insecticides on the neuronal nicotinic AChR, effects of imidacloprid, cartap, neostigmine and carbaryl were studied using the whole-cell and single-channel patch clamp techniques. Results indicate that these four insecticides modulate nicotinic AChR by different mechanisms of action. Imidacloprid acts as a partial agonist generating predominantly subconductance state currents, whereas cartap acts as an open channel blocker at the nicotinic AChR. Neostigmine and carbaryl directly block the nicotinic AChR similar to cartap. Nitenpyram, (E)-N-(6-chloro-3-pyridylmethyl)-N-ethyl-N '-methyl-2-nitro-vinylidenediamine, is known to act on the nic
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otinic acetylcholine receptor-channel (AChR). We examined the effects of nitenpyram on the neuronal type of the nicotinic AChR in rat clonal phaeochromocytoma PC 12 cells using a patch clamp technique to clarify the mechanisms of action at the single-channel level. Nitenpyram itself induced single-channel currents mediated by the neuronal nicotinic AChR. Co-application of ACh and nitenpyram opened the channels exhibiting the two conductance states. The proportion of main conductance levels was decreased and that of subconductance levels was increased in the presence of nitenpyram. The open time and closed time distribution, but not for the burst duration, for the main conductance state currents with co-application of ACh and nitenpyram were similar to those of Ach-induced current. These changes of single-channel kinetics result in a decrease in probability of openings of main conductance state currents explaining the effects of nitenpyram on the neuronal nicotinic AChR. The effects of nitenpyram on the acetylcholine-induced current are deemed directly responsible for the toxic actions in animals. Less
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