Ugolini A, Corsi M, Bordi F
Pharmacology Dept, GlaxoWellcome Medicines Research Centre, Verona, Italy.
Neuropharmacology. 1997 Aug;36(8):1047-55. doi: 10.1016/s0028-3908(97)00103-2.
Application of the metabotropic glutamate receptor (mGluR) agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) and the Group I selective mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) potentiated NMDA- and AMPA-induced potential changes recorded from ventral roots of the isolated hemisected baby rat spinal cord. Potentiation produced by 1S,3R-ACPD was completely abolished by the Group I selective mGluR antagonists (S)-4-carboxyphenylglycine (4CPG) or (+)-alpha-methyl-4-carboxyphenylglycine (MCPG). In addition, the protein kinase C (PKC) blockers staurosporine or chelerythrine chloride were able to antagonize the 1S,3R-ACPD-induced potentiation of both NMDA and AMPA response, suggesting that the enhancing effect induced by Group I mGluRs is modulated by a PKC-mediated mechanism. The mGluRs-induced potentiation of NMDA and AMPA responses may be important in modulating various forms of synaptic plasticity and nociceptive processes.
代谢型谷氨酸受体（mGluR）激动剂（1S，3R）-1-氨基环戊烷-1，3-二羧酸（1S，3R-ACPD）和I组选择性mGluR激动剂（RS）-3，5-二羟基苯甘氨酸（DHPG）的应用增强了从分离的半切新生大鼠脊髓腹根记录到的NMDA和AMPA诱导的电位变化。I组选择性mGluR拮抗剂（S）-4-羧基苯甘氨酸（4CPG）或（+）-α-甲基-4-羧基苯甘氨酸（MCPG）完全消除了1S，3R-ACPD产生的增强作用。此外，蛋白激酶C（PKC）阻滞剂星形孢菌素或氯化白屈菜红碱能够拮抗1S，3R-ACPD诱导的NMDA和AMPA反应增强，这表明I组mGluRs诱导的增强作用是由PKC介导的机制调节的。mGluRs诱导的NMDA和AMPA反应增强在调节各种形式的突触可塑性和伤害性过程中可能很重要。
