J.-C.H. and S.-J.C. contributed equally to this work.
Bidirectional synaptic plasticity induced by conditioned stimulations with different number of pulse at hippocampal CA1 synapses: Roles ofN-methyl-D-aspartate and metabotropic glutamate receptors
Article first published online: 10 MAR 2011
Copyright © 2011 Wiley-Liss, Inc.
Volume 65, Issue 8, pages 795–803, August 2011
How to Cite
Hsu, J.-C., Cheng, S.-J., Yang, H.-W., Wang, H.-J., Chiu, T.-H., Min, M.-Y. and Lin, Y.-W. (2011), Bidirectional synaptic plasticity induced by conditioned stimulations with different number of pulse at hippocampal CA1 synapses: Roles ofN-methyl-D-aspartate and metabotropic glutamate receptors. Synapse, 65: 795–803. doi: 10.1002/syn.20906
- Issue published online: 1 JUN 2011
- Article first published online: 10 MAR 2011
- Accepted manuscript online: 7 JAN 2011 11:59PM EST
- Manuscript Accepted: 27 DEC 2010
- Manuscript Received: 3 OCT 2010
- China Medical University Hospital. Grant Numbers: DMR-99-158, DOH100-TD-B-111-004
- pulse number;
In the mammlian brain, the hippocampus has been established as a principle structure for learning and memory processes, which involve synaptic plasticity. Althought a relationship between synaptic plasticity and stimulation frequency has been reported in numerous studies, little is known about the importance of pulse number on synaptic plasticity. Here we investigated whether the pulse number can modulate bidirectional plasticity in hippocampal CA1 areas. When a CA1 area was induced by a paired-pulse (PP) with a 10-ms interval, the strength of the synapse was altered to form a long-term depression (LTD), with a 68 ± 4% decrease in expression. The PP-induced LTD (PP-LTD) was blocked by the metabotropic glutamate receptors subtype 5 (mGluR5) antagonist MPEP, suggesting that the PP-LTD relied on the activation of GluR5. In addition, this modulation of LTD was protein kinase C (PKC)- and Group II mGluR-independent. However, when increasing the pulse number to 4 and 6, potentiated synaptic strength was observed, which was N-methyl-D-aspartate receptor (NMDAR)-dependent but mGluR5-independent. Surprisingly, when blocking mGluR, the synaptic efficacy induced by triple-pulse stimulation was altered to form a long-term potentiation (LTP) with a 142 ± 7% enhancement, and was further blocked by NMDA antagonist APV. Following treatment with APV and PKC blocker chelerythrine, the LTP expression induced by 4- and 6-pulse stimulation was switched to LTD. We suggest that CA1 synaptic plasticity is regulated by the result of competition between NMDA and mGluR5 receptors. We suggest that the pulse number can bidirectionally modulate synaptic plasticity through the activation of NMDA and mGluR5 in hippocampal CA1 areas. Synapse , 2011. © 2011 Wiley-Liss, Inc.