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The Journal of Neuroscience, July 15, 2001, 21(14):4943-4948

G_q-Deficient Mice Lack Metabotropic Glutamate Receptor-Dependent Long-Term Depression But Show Normal Long-Term Potentiation in the Hippocampal CA1 Region

Thomas Kleppisch¹, Viktor Voigt¹, Rüdiger Allmann¹, and Stefan Offermanns²

¹ Institut für Pharmakologie und Toxikologie, Technische Universität München, 80802 München, Germany, and ² Pharmakologisches Institut, Abteilung Molekulare Pharmakologie, Universität Heidelberg, 69120 Heidelberg, Germany

Long-term potentiation (LTP) and depression (LTD) are potential cellular mechanisms involved in learning and memory. Group I metabotropic glutamate receptors (mGluR), which are linked to heterotrimeric G-proteins of the G_q family (G_q and G₁₁), have been reported to facilitate both hippocampal LTP and LTD. To evaluate their functional role in synaptic plasticity, we studied LTD and LTP in the CA1 region of the hippocampus from wild-type, G_q(/), and G₁₁(/) mice. Basic parameters of the synaptic transmission were not altered in G_q(/) and G₁₁(/) mice. Moreover, these mice showed normal LTP in response to a strong tetanus and to a weak tetanus. However, LTD induced either by a group I mGluRs agonist or by paired-pulse low-frequency stimulation (PP-LFS) was absent in G_q(/) mice. Moreover, PP-LFS caused potentiation of the synaptic transmission in these mice that was not affected by the NMDAR antagonist AP-5. These results show that G_q plays a crucial role in the mGluR-dependent LTD, whereas hippocampal LTP is not affected by the lack of a single member of the G_q family.

Key words: synaptic plasticity; hippocampus; metabotropic glutamate receptor; GTP-binding protein; gene targeting; mouse

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21144943-06$05.00/0

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