Morishita W, Alger B E
Department of Physiology, University of Maryland School of Medicine, Baltimore 21201, USA.
Hippocampus. 2000;10(3):261-8. doi: 10.1002/1098-1063(2000)10:3<261::AID-HIPO6>3.0.CO;2-1.
We investigated the role of metabotropic glutamate receptors in the mediation of depolarization-induced suppression of inhibition (DSI), using whole-cell electrophysiological techniques in rat hippocampal slice preparation. In a previous work, we showed that a retrograde signal travels from CA1 pyramidal cells to GABA interneurons and prevents them from releasing GABA for tens of seconds at 30 degrees C. The resulting suppression of inhibition is DSI. The retrograde signal appeared to be glutamate, or a glutamate analog, which acted on group I metabotropic receptors on the interneurons. It is not known if DSI occurs in hippocampal subregions besides CA1. If DSI does occur in other regions, it will be important to know if the role of metabotropic glutamate receptors (mGluRs) in mediating DSI is the same everywhere. The distribution of mGluR subtypes varies among hippocampal subregions. In the CA3 region, unlike CA1, group II mGluRs are prevalent. It was possible, therefore, that in CA3, the group II mGluRs would mediate DSI. We have begun to investigate these issues. We now report that: 1) DSI does occur in CA3. 2) Carbachol induces IPSC activity that can be recorded in CA1 and CA3a. This carbachol-induced activity can be reduced by the selective group II mGluR agonist, DCG-IV, and by DSI. 3) Evoked IPSCs in CA3a, but not in CA1, can be reduced by DCG-IV; hence the interneurons activated by carbachol may reside in CA3a. 4) Despite the group II mGluR agonist sensitivity of CA3a interneurons, DSI in this region is not affected by a group II mGluR antagonist, CPPG, and therefore does not appear to be mediated by group II mGluRs.
我们采用大鼠海马脑片制备中的全细胞电生理技术，研究了代谢型谷氨酸受体在去极化诱导的抑制性突触后电位抑制（DSI）介导过程中的作用。在之前的一项研究中，我们发现一种逆行信号从CA1锥体细胞传导至GABA能中间神经元，并在30℃时阻止它们释放GABA达数十秒之久。由此产生的抑制性突触后电位抑制即为DSI。这种逆行信号似乎是谷氨酸或谷氨酸类似物，作用于中间神经元上的I组代谢型受体。目前尚不清楚除CA1外，DSI是否在海马其他亚区发生。如果DSI确实在其他区域发生，那么了解代谢型谷氨酸受体（mGluRs）在介导DSI过程中的作用在各处是否相同将很重要。mGluR亚型在海马各亚区的分布有所不同。在CA3区，与CA1不同，II组mGluRs占主导。因此，在CA3区，II组mGluRs有可能介导DSI。我们已开始研究这些问题。我们现在报告如下：1）DSI确实在CA发生。2）卡巴胆碱可诱导IPSC活性，该活性可在CA1和CA3a中记录到。这种卡巴胆碱诱导的活性可被选择性II组mGluR激动剂DCG-IV和DSI降低。3）DCG-IV可降低CA3a区诱发的IPSC，但不能降低CA1区的，因此被卡巴胆碱激活的中间神经元可能位于CA3a区。4）尽管CA3a区中间神经元对II组mGluR激动剂敏感，但该区域的DSI不受II组mGluR拮抗剂CPPG的影响，因此似乎不是由II组mGluRs介导的。
