G alpha(q)-deficient mice lack metabotropic glutamate receptor-dependent long-term depression but show normal long-term potentiation in the hippocampal CA1 region

Long-term potentiation (LTP) and depression (LTD) are potential cellular me chanisms involved in learning and memory. Group I metabotropic glutamate re ceptors (mGluR), which are linked to heterotrimeric G-proteins of the G(q) family (G(q) and G(11)), have been reported to facilitate both hippocampal LTP and LTD. To evaluate their functional role in synaptic plasticity, we s tudied LTD and LTP in the CA1 region of the hippocampus from wild-type, G a lpha (q)(-/-), and G alpha (11)(-/-) mice. Basic parameters of the synaptic transmission were not altered in G alpha (q),(-/-) and G alpha (11)(-/-) m ice. 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 ago nist or by paired-pulse low-frequency stimulation (PP-LFS) was absent in G alpha (q)(-/-) mice. Moreover, PP-LFS caused potentiation of the synaptic t ransmission 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 membe r of the G(q) family.