2007 Fiscal Year Final Research Report Summary
Postnatal developmental changes in synaptic molecules underlying maturation of excitatory synaptic transmission and synaptic regulation
| Project/Area Number |
17002013
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| Research Category |
Grant-in-Aid for Specially Promoted Research
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Doshisha University (2007)
The University of Tokyo (2005-2006) |
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Principal Investigator |
TAKAHASHI Tomoyuki Doshisha University, Faculty of Life and Medical Sciences, Professor (40092415)
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| Co-Investigator(Kenkyū-buntansha) |
TUJIMOTO Tetsuhiro University of Tokyo, Graduate School of Medicine, Lecturer (40212055)
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| Project Period (FY) |
2005 – 2007
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| Keywords | Potassium channcl / Ca^<2+>channel inactivation / Calyx of Held / Postnatal development / Transmitter release / Calmodulin / AMPA receptors / Residual Ca^<2+> |
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| Research Abstract |
(1) During the postnatal development Kv3 and Kv1 currents underwent a parallel increase, and became faster. Specific block of these channels indicated that the developmental changes of Kv3 and Kv1 contribute to establishment of reliable firing at high frequency, and stabilizing the nerve terminal, respectively (Nakamura & Takahashi, 2007)
(2) Bath-applied 4-CmC markedly increased the EPSC amplitude at the calyx of Held by inhibiting presynaptic voltage-gated K+currents, with no effect on voltage-gated Ca2+currents (Suzuki et al, 2007).
(3) The CaM-dependent IpCa inactivation during low-frequency stimulation, and the ensuing synaptic depression, occurs only at immature calyces, when a high intra-terminal Ca2+concentration can be attained during low frequency stimulation (Nakamura et al, 2008).
(4) Contribution of AMPAR desensitization to paired-pulse depression decreased after hearing onset, concomitantly with a developmental declines of GluR1 expression and transmitter release probability, indicating that both pre- and postsynaptic mechanisms contribute to the involvement of AMPAR desensitization in short-term synaptic depression (Koike-Tani et al, 2008).
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