Lee Ok kyung, Lee Chang-Joong, Choi Sukwoo
Department of Neuroscience, Ewha Institute of Neuroscience (EIN), School of Medicine, Ewha Womans University, Jongno-Gu, Jongno-6-Ga, 70, Ewha Dong-Dae-Mun Hospital, Seoul 110-783, South Korea.
Neuroreport. 2002 Apr 16;13(5):685-91. doi: 10.1097/00001756-200204160-00030.
L-LTP (late-phase long-term potentiation) at thalamo-amygdala synapses is thought to be critical for auditory fear conditioning, but it has not been clear what kinds of surface receptors and channels are involved in the induction phase of the L-LTP. Here we report that the NMDA receptor antagonist D-AP5 (50 microM), the L-type calcium channel antagonist nifedipine (30 microM) and the metabotropic glutamate receptor 5 antagonist MPEP (10 microM) prevented L-LTP induction when each antagonist was separately applied at saturating concentrations before and during repeated tetanus. By contrast, the mGluR1 antagonist CPCCOEt (80 microM) failed to show any effects on L-LTP induction. Neither D-AP5 nor MPEP produced any significant effects on potentiated synaptic responses when applied after L-LTP had been established. Thus, our data suggest that NMDA receptors, L-type calcium channels and mGluR5 are involved in L-LTP induction in the thalamo-amygdala pathway.
丘脑-杏仁核突触处的晚期长时程增强（L-LTP）被认为对听觉恐惧条件反射至关重要，但尚不清楚在L-LTP的诱导阶段涉及哪些类型的表面受体和通道。在此我们报告，当在重复强直刺激之前和期间分别以饱和浓度单独应用每种拮抗剂时，NMDA受体拮抗剂D-AP5（50微摩尔）、L型钙通道拮抗剂硝苯地平（30微摩尔）和代谢型谷氨酸受体5拮抗剂MPEP（10微摩尔）可阻止L-LTP的诱导。相比之下，mGluR1拮抗剂CPCCOEt（80微摩尔）对L-LTP的诱导未显示任何作用。当在L-LTP建立后应用时，D-AP5和MPEP对增强的突触反应均未产生任何显著影响。因此，我们的数据表明，NMDA受体、L型钙通道和mGluR5参与了丘脑-杏仁核通路中L-LTP的诱导。
