| Project/Area Number |
11480245
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B).
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
神経・脳内生理学
|
|---|
| Research Institution | THE UNIVERSITY OF TOKYO |
|---|
Principal Investigator |
TACHIBANA Masao Univ of Tokyo, Graduate School of Humanities and Sociology, Professor, 大学院・人文社会系研究科, 教授 (60132734)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TSUKAMOTO Yoshihiko Hyogo College of Medicine, Medical School, Professor, 医学部, 教授 (20104250)
|
|---|
| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥15,600,000 (Direct Cost: ¥15,600,000)
Fiscal Year 2000: ¥5,200,000 (Direct Cost: ¥5,200,000)
Fiscal Year 1999: ¥10,400,000 (Direct Cost: ¥10,400,000)
|
|---|
| Keywords | RETINA / SYNAPSE / EXOCYTOSIS / GLUTAMATE / GABA / PROTEIN KINASE C / GLUTAMATE TRANSPORTER / BIPOLAR CELL / アマクリン細胞 / グルタミン酸受容体 / GABA受容体 / フィードバック / シナプス小胞 / エクソサイトーシス / 興奮性シナプス後電流 |
|---|
| Research Abstract |
Mechanisms of transmitter release from retinal bipolar cells were investigated electrophysiologically and morphologically. We obtained the following results.
1. Axon terminals of goldfish bipolar cells were whole-cell clamped, and the membrane capacitance changes associated with exocytosis were measured. The released glutamate was simultaneously monitored electrophysiologically with a glutamate receptor rich neuron as a sensor. Prolonged depolarization of bipolar terminals resulted in a phasic release of glutamate (due to the first and second pools), which was followed by a small tonic release, suggesting the presence of the third pool.
2. Activation of protein kinase C (PKC) in the presynaptic terminals of goldfish bipolar cells increased the amount of glutamate release. The double-pulse experiments revealed that the increase was ascribed to the increase in the pool size of the second pool. EM studies indicated that synaptic vesicles accumulated near the synaptic ribbons after the PKC activation.
3. A pair of bipolar and ganglion cells was simultaneously whole-cell clamped in the slice preparation of the newt retina. Depolarization of a bipolar cell evoked an EPSC in the ganglion cell. Blockade of glutamate transporters resulted in the prolongation of the evoked EPSC.Glutamate transporters actually contribute to the shaping of the evoked EPSC and the light-induced responses.
4. The function of GABA_c-receptors at bipolar terminals was examined in the slice preparation of the mouse retina. When GABA_c-receptors were intact, the light-induced current in amacrine cells composed mainly of the AMPA-receptor mediated current. After the blockage of GABA_c receptors, the light-induced current composed of the AMPA-receptor mediated current, which was followed by the NMDA-receptor mediated current. GABA_c-mediated feedback from amacrine cells regulate the amount of glutamate release from bipolar cells.
|
