Andrianov G N, Puyal J, Raymond J, Ventéo S, Demêmes D, Ryzhova I V
Laboratory of Physiology of Reception, Pavlov Institute of Physiology, Russian Academy of Sciences, Nab. Makarova 6, St. Petersburg 199034, Russia.
Hear Res. 2005 Jun;204(1-2):200-9. doi: 10.1016/j.heares.2005.02.003.
Using immunocytochemistry and multiunit recording of afferent activity of the whole vestibular nerve, we investigated the role of metabotropic glutamate receptors (mGluR) in the afferent neurotransmission in the frog semicircular canals (SCC). Group I (mGluR1alpha) and group II (mGluR2/3) mGluR immunoreactivities were distributed to the vestibular ganglion neurons, and this can be attributed to a postsynaptic locus of metabotropic regulation of rapid excitatory transmission. The effects of group I/II mGluR agonist (1S,3R)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (ACPD) and antagonist (R,S)-alpha-methyl-4-carboxyphenylglycine (MCPG) on resting and chemically induced afferent activity were studied. ACPD (10-100 microM) enhanced the resting discharge frequency. MCPG (5-100 microM) led to a concentration-dependent decrease of both resting activity and ACPD-induced responses. If the discharge frequency had previously been restored by L-glutamate (L-Glu) in high-Mg2+ solution, ACPD elicited a transient increase in the firing rate in the afferent nerve suggesting that ACPD acts on postsynaptic receptors. The L-Glu agonists, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) and N-methyl-D-aspartate (NMDA), were tested during application of ACPD. AMPA- and NMDA-induced responses were higher in the presence than absence of ACPD, implicating mGluR in the modulation of ionotropic glutamate receptors. These results indicate that activation of mGluR potentiates AMPA and NMDA responses through a postsynaptic interaction. We conclude that ACPD may exert modulating postsynaptic effects on vestibular afferents and that this process is activity-dependent.
我们运用免疫细胞化学技术以及对整个前庭神经传入活动的多单位记录，研究了代谢型谷氨酸受体（mGluR）在青蛙半规管（SCC）传入神经传递中的作用。I组（mGluR1α）和II组（mGluR2/3）mGluR免疫反应性分布于前庭神经节神经元，这可归因于代谢型调节快速兴奋性传递的突触后位点。研究了I/II组mGluR激动剂（1S,3R）-1-氨基环戊烷-反式-1,3-二羧酸（ACPD）和拮抗剂（R,S）-α-甲基-4-羧基苯甘氨酸（MCPG）对静息和化学诱导的传入活动的影响。ACPD（10 - 100微摩尔）提高了静息放电频率。MCPG（5 - 100微摩尔）导致静息活动和ACPD诱导反应均呈浓度依赖性降低。如果先前在高镁溶液中通过L-谷氨酸（L-Glu）恢复了放电频率，ACPD会引起传入神经放电率短暂增加，表明ACPD作用于突触后受体。在应用ACPD期间测试了L-Glu激动剂α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）和N-甲基-D-天冬氨酸（NMDA）。与不存在ACPD时相比，存在ACPD时AMPA和NMDA诱导的反应更高，这表明mGluR参与了离子型谷氨酸受体的调节。这些结果表明，mGluR的激活通过突触后相互作用增强了AMPA和NMDA反应。我们得出结论，ACPD可能对前庭传入神经发挥调节突触后效应，并且这个过程是活动依赖性的。
