کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2199448 | 1099449 | 2006 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Group-II metabotropic glutamate receptors negatively modulate NMDA transmission at striatal cholinergic terminals: Role of P/Q-type high voltage activated Ca++ channels and endogenous dopamine Group-II metabotropic glutamate receptors negatively modulate NMDA transmission at striatal cholinergic terminals: Role of P/Q-type high voltage activated Ca++ channels and endogenous dopamine](/preview/png/2199448.png)
Striatal cholinergic nerve terminals express functional group-II metabotropic (mGlu) and NMDA glutamate receptors. To investigate whether these receptors interact to regulate ACh release, LY354740 (a group-II mGlu receptor agonist) and NMDA were co-applied in striatal synaptosomes and slices. LY354740 prevented the NMDA-evoked [3H]-choline release from synaptosomes and ACh release from slices. In synaptosomes, this modulation was prevented by ω-agatoxin IVA, suggesting that it was mediated by P/Q-type high voltage activated Ca++ channels. In slices, LY341495 (a group-II mGlu receptor antagonist) enhanced the NMDA-induced ACh release, suggesting that group-II mGlu receptor activation by endogenous glutamate inhibits NMDA transmission. Co-immunoprecipitation studies excluded direct group-II mGlu-NMDA receptor interactions. Finally, group-II mGlu negative modulation of NMDA transmission was abolished in dopamine-depleted synaptosomes and slices, suggesting that it relied on endogenous dopamine. We conclude that group-II mGlu receptors attenuate NMDA inputs at striatal cholinergic terminals via Ca++ channel modulation and dopamine-sensitive pathways.
Journal: Molecular and Cellular Neuroscience - Volume 31, Issue 2, February 2006, Pages 284–292