Wilsch V W, Behnisch T, Jäger T, Reymann K G, Balschun D
Leibniz Institute for Neurobiology, Department of Neurophysiology, D-39008 Magdeburg, Germany.
J Neurosci. 1998 Aug 15;18(16):6071-80. doi: 10.1523/JNEUROSCI.18-16-06071.1998.
The involvement of metabotropic glutamate receptors (mGluRs) in hippocampal long-term potentiation (LTP) is a matter of controversial debate. Using [Ca2+]i measurements by confocal laser scanning microscopy and field recordings of EPSPs (fEPSPs) in the hippocampal CA1-region, we found that the efficacy of the broad-spectrum mGluR-antagonist (S)-alpha-methyl-4-carboxyphenylglycine (MCPG) and of (S)-4-carboxy-phenylglycine (4-CPG), a selective antagonist at class I mGluRs, in LTP is contingent on the tetanization strength and the resulting [Ca2+]i response. As indicated by experiments in which we blocked voltage-dependent calcium channels (VDCCs) and intracellular Ca2+ stores (ICSs), the functional significance of class I mGluRs in LTP is confined to certain types of potentiation, which are induced by weak tetanization protocols and require the release of Ca2+ from ICSs for induction. During strong tetanic stimulation, this Ca2+ source is functionally bypassed by activating VDCCs.
代谢型谷氨酸受体(mGluRs)参与海马体长期增强效应(LTP)是一个存在争议的话题。通过共聚焦激光扫描显微镜测量[Ca2+]i以及记录海马体CA1区的兴奋性突触后电位(fEPSPs),我们发现广谱mGluR拮抗剂(S)-α-甲基-4-羧基苯甘氨酸(MCPG)和I类mGluRs的选择性拮抗剂(S)-4-羧基苯甘氨酸(4-CPG)对LTP的作用效果取决于强直刺激强度以及由此产生的[Ca2+]i反应。我们通过阻断电压依赖性钙通道(VDCCs)和细胞内钙库(ICSs)的实验表明,I类mGluRs在LTP中的功能意义仅限于某些类型的增强效应,这些增强效应由弱强直刺激方案诱导,并且诱导过程需要从ICSs中释放Ca2+。在强强直刺激期间,通过激活VDCCs,这种Ca2+来源在功能上被绕过。