| First Author | Itoh S | Year | 2001 |
| Journal | Brain Res | Volume | 901 |
| Issue | 1-2 | Pages | 237-46 |
| PubMed ID | 11368972 | Mgi Jnum | J:69508 |
| Mgi Id | MGI:1934746 | Doi | 10.1016/s0006-8993(01)02373-3 |
| Citation | Itoh S, et al. (2001) Neuronal plasticity in hippocampal mossy fiber-CA3 synapses of mice lacking the inositol-1,4,5-trisphosphate type 1 receptor. Brain Res 901(1-2):237-46 |
| abstractText | In the present study, we used inositol-1,4,5-trisphosphate (IP(3)) type 1 receptor (IP(3)R1) knockout mice to examine the role of this receptor in the induction of LTP, LTD, and DP at mossy fiber-CA3 synapses. No difference in synaptically induced field-EPSPs was seen between the wild-type (IP(3)R1(+/+)) and IP(3)R1 knockout mice (IP(3)R1(-/-)), showing that basic synaptic transmission does not involve IP(3)R1 activation. Tetanus induced LTP in both wild-type and IP(3)R1(-/-) mice, but the magnitude of LTP was significantly greater in IP(3)R1(-/-) mice (149.8+/-3.5%, mean+/-S.E.M., n=15) than in wild-type mice (132.4+/-1.5%, n=17), suggesting that the IP(3)R1 has a suppressive effect on LTP induction. To determine whether this effect involved N-methyl-D-aspartate receptor (NMDAR)-dependent LTP, the effect of tetanus was tested in the present of the NMDAR antagonist, D,L-AP5 (50 &mgr;M); under these conditions, the LTP in both IP(3)R1(-/-) and IP(3)R1(+/+) mice was not significantly reduced. In addition, group I mGluR activation was shown to be necessary for LTP induction, as the LTP was almost blocked by the group I mGluR antagonist, RS-4CPG (500 &mgr;M) in both IP(3)R1(-/-) (117.6+/-1.7%, n=8) and IP(3)R1(+/+) (116.9+/-1.8%, n=5) mice. The IP(3)R1 also plays an essential role in LTD induction, as low-frequency stimulation (LFS) failed to induce LTD in the mutant mice (104.5+/-2.1%, n=10). DP was induced in both IP(3)R1(-/-) and wild-type mice. |
