Chamberlain Sophie E L, Yang Jian, Jones Roland S G
Department of Pharmacy and Pharmacology, University of Bath, Claverton Down, Bath, UK.
Neural Plast. 2008;2008:872456. doi: 10.1155/2008/872456. Epub 2008 Oct 29.
We have previously shown that spontaneous release of glutamate in the entorhinal cortex (EC) is tonically facilitated via activation of presynaptic NMDA receptors (NMDAr) containing the NR2B subunit. Here we show that the same receptors mediate short-term plasticity manifested by frequency-dependent facilitation of evoked glutamate release at these synapses. Whole-cell patch-clamp recordings were made from layer V pyramidal neurones in rat EC slices. Evoked excitatory postsynaptic currents showed strong facilitation at relatively low frequencies (3 Hz) of activation. Facilitation was abolished by an NR2B-selective blocker (Ro 25-6981), but unaffected by NR2A-selective antagonists (Zn(2+), NVP-AAM077). In contrast, postsynaptic NMDAr-mediated responses could be reduced by subunit-selective concentrations of all three antagonists. The data suggest that NMDAr involved in presynaptic plasticity in layer V are exclusively NR1/NR2B diheteromers, whilst postsynaptically they are probably a mixture of NR1/NR2A, NR1/NR2B diheteromers and NR1/NR2A/NR2B triheteromeric receptors.
我们之前已经表明,内嗅皮质(EC)中谷氨酸的自发释放通过激活含有NR2B亚基的突触前NMDA受体(NMDAr)而受到持续性促进。在此我们表明,相同的受体介导了短期可塑性,表现为这些突触处诱发的谷氨酸释放的频率依赖性促进。在大鼠EC切片的V层锥体神经元上进行全细胞膜片钳记录。诱发的兴奋性突触后电流在相对较低的激活频率(3 Hz)下表现出强烈的促进作用。NR2B选择性阻断剂(Ro 25 - 6981)可消除促进作用,但不受NR2A选择性拮抗剂(Zn(2+)、NVP - AAM077)的影响。相反,所有三种拮抗剂的亚基选择性浓度均可降低突触后NMDAr介导的反应。数据表明,参与V层突触前可塑性的NMDAr仅为NR1/NR2B二聚体,而在突触后它们可能是NR1/NR2A、NR1/NR2B二聚体和NR1/NR2A/NR2B三聚体受体的混合物。