Anwyl R
Department of Physiology, Trinity College, Dublin, Ireland.
Brain Res Brain Res Rev. 1999 Jan;29(1):83-120. doi: 10.1016/s0165-0173(98)00050-2.
Electrophysiological research on mGluRs is now very extensive, and it is clear that activation of mGluRs results in a large number of diverse cellular actions. Studies of mGluRs and on ionic channels has clearly demonstrated that mGluR activation has a widespread and potent inhibitory action on both voltage-gated Ca2+ channels and K+ channels. Inhibition of N-type Ca2+ channels, and inhibition of Ca(++)-dependent K+ current, IAHP, and IM being particularly prominent. Potentiation of activation of both Ca2+ and K+ channels has also been observed, although less prominently than inhibition, but mGluR-mediated activation of non-selective cationic channels is widespread. In a small number of studies, generation of an mGluR-mediated slow excitatory postsynaptic potential has been demonstrated as a consequence of the effect of mGluR activation on ion channels, such as activation of a non-selective cationic channels. Although certain mGluR-modulation of channels is a consequence of direct G-protein-linked action, for example, inhibition of Ca2+ channels, many other effects occur as a result of activation of intracellular messenger pathways, but at present, little progress has been made on the identification of the messengers. The field of study of the involvement of mGluRs in synaptic plasticity is very large. Evidence for the involvement of mGluRs in one form of LTD induction in the cerebellum and hippocampus is now particularly impressive. However, the role of mGluRs in LTP induction continues to be a source of dispute, and resolution of the question of the exact involvement of mGluRs in the induction of LTP will have to await the production of more selective ligands and of selective gene knockouts.
目前，对代谢型谷氨酸受体（mGluRs）的电生理研究非常广泛，很明显，mGluRs的激活会导致大量多样的细胞活动。对mGluRs与离子通道的研究清楚地表明，mGluR激活对电压门控Ca2+通道和K+通道都有广泛而有效的抑制作用。对N型Ca2+通道的抑制，以及对Ca(++)依赖性K+电流、IAHP和IM的抑制尤为突出。虽然不如抑制作用明显，但也观察到了mGluRs对Ca2+和K+通道激活的增强作用，不过mGluR介导的非选择性阳离子通道激活很普遍。在少数研究中，由于mGluR激活对离子通道的影响，如激活非选择性阳离子通道，已证明会产生mGluR介导的缓慢兴奋性突触后电位。虽然某些mGluR对通道的调节是直接G蛋白偶联作用的结果，例如对Ca2+通道的抑制，但许多其他效应是细胞内信使途径激活的结果，不过目前在信使的鉴定方面进展甚微。mGluRs参与突触可塑性的研究领域非常广阔。目前，mGluRs参与小脑和海马体中一种形式的长时程抑制（LTD）诱导的证据尤其令人印象深刻。然而，mGluRs在长时程增强（LTP）诱导中的作用仍然存在争议，要解决mGluRs在LTP诱导中的确切作用问题，还得等待更具选择性的配体和选择性基因敲除的产生。
