| Project/Area Number |
03670066
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Kurume University |
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Principal Investigator |
TOKIMASA Takayuki (1992) Kurume University School of Medicine, Associate Professor, 医学部, 助教授 (50155511)
蓮尾 博 (1991) 久留米大学, 医学部, 講師 (90172882)
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| Co-Investigator(Kenkyū-buntansha) |
時政 孝行 久留米大学, 医学部, 助教授 (50155511)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1992: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1991: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Central nervous system / Septal nuclei / Patch-clamp / Excitatory amino acid / Synaptic transmission / Modulation / Metabotropic glutamate receptor / Long-term potentiation / 伝達修飾作用 |
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| Research Abstract |
Intracellular and voltage-clamp recordings were made from neurons in rat brain slices containing dorsolateral septal nucleus (DLSN), in vitro. In DLSN neurons, excitatory and two components of inhibitory postsynaptic potentials (EPSP, IPSP and LHP) were evoked by stimulations of fimbria/fornix pathway. The present experiment clearly demonstrated that these synaptic potentials may be modulated by several neurotransmitters and/or modulators existing in DLSN. Effects of adenosine were extensively examined and clarified that adenosine inhibits the synaptic potentials in rat septal nucleus neurons mediated through pre-and postsynaptic A_1-adenosine receptors. Presynaptic A_1 receptors seems to be located on the excitatory nerve terminals but not on the inhibitory one in DLSN. Our data suggest that postsynaptic effect of adenosine is mediated by activation of GTP-binding proteins which coupled to a potassium conductance system. However the presynaptic mechanism is still unknown at present. A
… More
nother line of experiments, we demonstrated that trans-ACPD, a selective metabotropic glutamate receptor agonist, shows biphasic actions on the EPSP. Trans-ACPD suppressed the EPSP presynaptically during application and produced long-lasting potentiation of the EPSP after wash out. This potentiation was compared with the long-term potentiation evoked by tetanic stimulation of fimbria/fornix pathway. Under a certain stimulus condition, only the LHP was potentiated due presumably to the long-lasting potentiation of the EPSP of the inhibitory interneurons. In most of the neurons tested, the induction of the LTP was blocked by APV, an NMDA receptor antagonist. However, the involvement of metabotropic receptor activation could not be ruled out. Indeed, the LTP was induced in the presence of APV in some neurons. Possible mechanisms underlying the effects of these neurotransmitters and/or modulators described above have now been subjected to further investigation by means of the whole-cell patch-clamp. Less
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