Ito I, Sugiyama H
Department of Biology, Faculty of Science, Kyushu University, Fukuoka, Japan.
Neuroreport. 1991 Jun;2(6):333-6. doi: 10.1097/00001756-199106000-00008.
We have investigated the roles of glutamate (Glu) receptors in the mechanism of long-term potentiation observed in rat hippocampal mossy fiber synapses (MF-LTP). The mossy fiber responses were almost completely suppressed by ionotropic Glu receptor (iGluR) antagonists both before and after the induction of LTP. However, tetanic stimulation produced robust LTP even when the synaptic transmission was blocked postsynaptically by iGluR antagonists. In contrast, when the transmission was blocked presynaptically by Ca(2+)-free media, tetanic stimulation produced no LTP. D,L-2-amino-3-phosphono-propionate(D,L-AP3), a metabotropic Glu receptor (mGluR) antagonist, inhibited the induction of MF-LTP. Perfusion with ibotenate, a mGluR agonist, induced long-lasting enhancement of the mossy fiber responses without tetanic stimulation, and this ibotenate-induced potentiation was antagonized by D,L-AP3.
我们研究了谷氨酸（Glu）受体在大鼠海马苔藓纤维突触（MF-LTP）中观察到的长时程增强机制中的作用。在LTP诱导之前和之后，离子型Glu受体（iGluR）拮抗剂几乎完全抑制了苔藓纤维反应。然而，即使突触传递被iGluR拮抗剂在突触后阻断，强直刺激仍能产生强烈的LTP。相反，当突触传递被无钙培养基在突触前阻断时，强直刺激不会产生LTP。代谢型Glu受体（mGluR）拮抗剂D，L-2-氨基-3-膦酰丙酸（D，L-AP3）抑制了MF-LTP的诱导。用mGluR激动剂碘代谷氨酸灌注，在没有强直刺激的情况下诱导了苔藓纤维反应的持久增强，并且这种碘代谷氨酸诱导的增强被D，L-AP3拮抗。
