Different glutamate receptor mechanisms in long-term depression induced by different stimulus patterns in the CA1 area of adult rat hippocampus.
- Author:
Li CHEN
1
;
Tai-Zhen HAN
;
Ma-Li JIANG
Author Information
1. Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, Xi'an 710061, China.
- Publication Type:Journal Article
- MeSH:
2-Amino-5-phosphonovalerate;
pharmacology;
Animals;
CA1 Region, Hippocampal;
physiology;
Glycine;
analogs & derivatives;
pharmacology;
Long-Term Synaptic Depression;
Rats;
Receptors, Metabotropic Glutamate;
antagonists & inhibitors;
Receptors, N-Methyl-D-Aspartate;
antagonists & inhibitors
- From:
Acta Physiologica Sinica
2008;60(2):270-274
- CountryChina
- Language:English
-
Abstract:
Previous reports suggested that a novel stimulus pattern of multi-train stimulus at low-frequency (2-Hz or 5-Hz) could induce stable long-term depression (LTD) in the CA1 area of adult rat hippocampus. In the present study, in order to determine the mechanism in LTD induced by the two novel tetanus patterns, changes in the population spikes (PS) in the hippocampal CA1 area of adult rats following the multi-train stimulus in the presence of AP5 [antagonist of N-methyl-D-aspartate receptors (NMDARs)] or MCPG [antagonist of type I/II metabotropic glutamate receptors (mGluRs)] were recorded. The results showed that both AP5 and MCPG inhibited the LTD induced by 2-Hz multi-train stimulus. The mean amplitude of population spikes (PSA) normalized to the baseline was (96.0±3.5)% after applying AP5 (n=10) and (95.7±4.1)% after applying MCPG (n=8), respectively, measured at 20 min post-tetanus. While 5-Hz multi-train tetanus failed to induce LTD in the presence of MCPG. The mean PSA was (73.6±4.4)% (n=10) and (98.2±8.9)% (n=8) in the presence of AP5 and MCPG, respectively, measured at 35 min post-tetanus. So it is suggested that LTD induced by 2-Hz multi-train tetanus involves co-activation of NMDARs and mGluRs, while LTD induced by 5-Hz multi-train tetanus is only related to activation of mGluRs.
