Jones M W, Headley P M
Department of Physiology, School of Medical Sciences, University of Bristol, UK.
Neuropharmacology. 1995 Aug;34(8):1025-31. doi: 10.1016/0028-3908(95)00055-b.
Microelectrophoretic application of the non-selective 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 [(RS)-3,5-DHPG] potentiated the responses of rat spinal neurones to the cyclically-ejected ionotropic excitatory amino acid (EAA) agonists NMDA, AMPA and kainate in vivo. Potentiation was not selective between the three ionotropic responses and was paralleled by an enhancement of background activity in spontaneously active cells. "Correcting" spike count data for this increase in background activity showed that the EAA responses were not potentiated beyond the apparent enhancement of cell excitability. Neither mGluR agonist produced potentiation when NMDA/AMPA cycling was superimposed on background discharge held constant with kainate. It is concluded that potentiation produced by both (1S,3R)-ACPD and (RS)-3,5-DHPG is secondary to an enhancement of cell excitability rather than being due to a specific interaction with ionotropic EAA receptors. The mechanism of excitability enhancement cannot be determined by extracellular recording, but group I mGluRs are most likely to be responsible.
非选择性代谢型谷氨酸受体（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[（RS）-3，5-DHPG]的微电泳应用增强了大鼠脊髓神经元在体内对周期性喷射的离子型兴奋性氨基酸（EAA）激动剂NMDA、AMPA和海人酸的反应。这种增强在三种离子型反应之间没有选择性，并且与自发活动细胞的背景活动增强同时出现。针对背景活动的这种增加对峰计数数据进行“校正”表明，EAA反应并未在细胞兴奋性明显增强之外得到进一步增强。当NMDA/AMPA循环叠加在由海人酸保持恒定的背景放电上时，两种mGluR激动剂均未产生增强作用。得出的结论是，（1S，3R）-ACPD和（RS）-3，5-DHPG产生的增强作用是细胞兴奋性增强的继发结果，而不是由于与离子型EAA受体的特异性相互作用。细胞兴奋性增强的机制无法通过细胞外记录确定，但I组mGluR最有可能是其原因。
