Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA.
Hippocampus. 2011 Dec;21(12):1302-17. doi: 10.1002/hipo.20842. Epub 2010 Sep 7.
Stratum lacunosum-moleculare interneurons (L-Mi) in hippocampal area CA3 target the apical dendrite of pyramidal cells providing feedforward inhibition. Here we report that selective activation of group III metabotropic glutamate receptors (mGluRs) 4/8 with L(+)-2-amino-4-phosphnobytyric acid (L-AP4; 10 μM) decreased the probability of glutamate release from the mossy fiber (MF) terminals synapsing onto L-Mi. Consistent with this interpretation, application of L-AP4 in the presence of 3 mM strontium decreased the frequency of asynchronous MF EPSCs in L-Mi. Furthermore, the dose response curve showed that L-AP4 at 400 μM produced no further decrease in MF EPSC amplitude compared with 20 μM L-AP4, indicating the lack of mGluRs 7 at these MF terminals. We also found that one mechanism of mGluRs 4/8-mediated inhibition of release is linked to N-type voltage gated calcium channels at MF terminals. Application of the group III mGluR antagonist MSOP (100 μM) demonstrated that mGluRs 4/8 are neither tonically active nor activated by low and moderate frequencies of activity. However, trains of stimuli to the MF at 20 and 40 Hz delivered during the application of MSOP revealed a relief of inhibition of transmitter release and an increase in the overall probability of action potential firing in the postsynaptic L-Mi. Interestingly, the time to first action potential was significantly shorter in the presence of MSOP, indicating that mGluR 4/8 activation delays L-Mi firing in response to MF activity. Taken together, our data demonstrate that the timing and probability of action potentials in L-Mi evoked by MF synaptic input is regulated by the activation of presynaptic high affinity group III mGluRs.
CA3 区的腔隙分子层中间神经元(L-Mi)靶向锥体神经元的树突顶,提供前馈抑制。我们报告说,选择性激活代谢型谷氨酸受体 3 型(mGluR)4/8 型(L(+)-2-氨基-4-磷酸丁酸(L-AP4;10 μM))可降低苔藓纤维(MF)末梢与 L-Mi 突触谷氨酸释放的概率。这一解释与以下事实一致:在 3 mM 锶存在下应用 L-AP4 降低了 L-Mi 中的异步 MF EPSC 频率。此外,剂量反应曲线表明,与 20 μM L-AP4 相比,400 μM L-AP4 对 MF EPSC 幅度没有进一步降低,表明这些 MF 末梢缺乏 mGluR7。我们还发现,mGluR4/8 介导的释放抑制的一种机制与 MF 末梢的 N 型电压门控钙通道有关。应用 III 组 mGluR 拮抗剂 MSOP(100 μM)表明,mGluR4/8 既不是紧张性活动,也不受低和中等频率活动的激活。然而,在 MSOP 应用期间,MF 以 20 和 40 Hz 的频率刺激串发现,递质释放的抑制作用得到缓解,并且在突触后 L-Mi 中的动作电位总体发射概率增加。有趣的是,在存在 MSOP 的情况下,第一个动作电位的时间明显缩短,表明 mGluR4/8 的激活延迟了 L-Mi 对 MF 活动的反应。总之,我们的数据表明,MF 突触输入诱发的 L-Mi 中的动作电位的时间和概率受到前突触高亲和力 III 组 mGluR 的激活的调节。