| Project/Area Number |
63570075
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Neurophysiology and muscle physiology
|
|---|
| Research Institution | TOKYO METROPOLITAN INSTITUTE FOR NEUROSCIENCES |
|---|
Principal Investigator |
MIWA Akiko Tokyo Metrop. Inst. for Neurosci., Dept. Neurobiol. staff Scientist, 病態神経生理学研究室, 主事研究員 (60142155)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SAHARA Yoshinori Tokyo Metrop. Inst. for Neurosci., Dept. Neurobiol. staff Scientist, 病態神経生理学研究室, 流動研究員 (40206008)
|
|---|
| Project Period (FY) |
1988 – 1989
|
| Project Status |
Completed (Fiscal Year 1989)
|
| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1989: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1988: ¥1,400,000 (Direct Cost: ¥1,400,000)
|
|---|
| Keywords | Nerve terminal / L-Glutamic acid / G-protein / GTPgammaS / Glutamate_B receptor / Neuromuscular junction / Gーprotein / シナプス前神経 / GABA / シナプス後電位 / イセエビ歩脚 |
|---|
| Research Abstract |
The role of GTP binding protein in the presynaptic membrane was investigated by use of intra-axonal recording near the nerve terminal of lobster neuromuscular synapse. L-glutamate activated the presynaptic glutamate receptor. (glutamate B receptor), inducing a hyperpolarizing current carried by K ion. This presynaptic glutamate potential was effectively blocked by pertussis toxin (IAP), indicating mediation by GTP-protein. Injection of GTPYS, a non-hydrolysable analog of GTP, hyperpolarized the presynaptic membrane and mimicked the presynaptic glutamte potential.
The effect of GTP_<gamma>S injection on synaptic transmission was studied by recording the excitatory postsynaptic current (EPSC) with macro-patch recording. After injection GTP_<gamma>S in the presynaptic axon, the amplitude of the EPSC was gradually and irreversively diminished. Quantal analysis of EPSCs revealed that after GTP_<gamma>S injection quantal content was much reduced, whereas unit quantal size was unchanged.
The results suggest that glutamate B receptor in the presynaptic membrane gives rise to a presynaptic inhibitory effect on transmitter release by activating GTP-binding protein.
|
