2005 Fiscal Year Final Research Report Summary
Effects of spatio-temporal changes in intracellular free-calcium concentration in central nerve system on signal transmission and anesthetic action
| Project/Area Number |
15390471
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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 | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Niigata University |
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Principal Investigator |
FUJIWARA Naoshi Niigata University, Institute of Medical and Dentistry, Professor, 医歯学系, 教授 (70181419)
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| Co-Investigator(Kenkyū-buntansha) |
SEO Kenji Niigata University, Institute of Medical and Dentistry, Associate Professor, 医歯学系, 助教授 (40242440)
OKAMOTO Manabu Niigata University, Medical and Dental Hospital, Lecturer, 医歯学総合病院, 講師 (70303146)
WATANABE Yoko Niigata University, Institute of Medical and Dentistry, Assistant, 医歯学系, 助手 (80018853)
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| Project Period (FY) |
2003 – 2005
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| Keywords | cortical slices / hippocampal slices / membrane potential imaging / calcium imaging / glutamate receptor / calcium channel / ω-agatoxin |
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| Research Abstract |
Signal transmissions in the cerebral cortex, hippocampus, trigeminal subnucleus caudalis and spinal cord were spatio-temporally characterized using a high-speed optical imaging technique. (1)Slice preparations of the mouse cerebral cortex were stained with a voltage sensitive dye RH414 or a Ca^<2+> indicator Rhod-2 for fluorescence imaging. Electrical single-pulse stimulation to the layer V evoked transient depolarization in the layer V, and then this excitatory response propagated to the layers II-III and widely expanded in these layers. The excitation in the layers II-III was inhibited by an AMPA/kainate receptor antagonist, CNQX, and a P/Q-type Ca^<2+> channel antagonist, ω-agatoxin IVA. Intracellular Ca^<2+> level elevated in the layer V and layers II-III in response to the stimulation. The Ca^<2+> responses were insensitive to CNQX but were profound inhibited by ω-agatoxin IVA and partially by an NMDA receptor antagonist, MK-801. Thus, excitation propagation in the layers II-III m
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ay be mediated by the post-synaptic AMPA/kainate receptors. Ca^<2+> influx through P/Q-type Ca^<2+> channels may play an important role in an intracellular Ca^<2+> elevation inducing pre-synaptic glutamate release. (2)In hippocampal slices, excitation propagation in the CA1 region was also inhibited by CNQX. Ca^<2+> elevation in response to single-pulse stimulation was not so sensitive to MK-801 or Ca^<2+> antagonists at the same concentrations as applied to the cortical slices. (3)In the trigeminal subnucleus caudalis, both excitation propagation and Ca^<2+> elevations in response to single-pulse stimulation were inhibited by CNQX. The results suggest that processes of the Ca^<2+> elevation by single-pulse stimulation were different among the regions of the central nerve system. (4)Slow excitation propagation expanded to the deeper laminae was elicited by high-frequent pulse-train stimulation to the dorsal root. The propagation was enhanced by iteration of the high-frequent stimulation. This enhanced response may correspond to hyper-excitability known as "wind-up" phenomenon. Less
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