Abstract
The stimulation of the Schaffer collateral/commissural fibers at low frequency (1 Hz) for 3–5 min can trigger a slow‐onset form of low‐frequency stimulation (LFS)‐long‐term potentiation (LTP) (LFS‐LTP) in the CA1 area of the adult rat hippocampus. Here we have examined the developmental profile of this plasticity. In 9–15 day‐old rats, the application of 1 Hz for 5 min induced long‐term depression (LFS‐LTD). In 17–21 day‐old rats, 1 Hz stimulation had no effect when applied for 5 min but mediated LTD when stimulus duration was increased to 15 min. Over 25 day‐old, 1 Hz stimulation mediated LFS‐LTP. LFS‐LTD was dependent on both N‐methyl‐D‐aspartate (NMDA) and mGlu5 receptor activation. Antagonists of mGlu1α and cannabinoid type 1 receptor were ineffective to block LTD induction. LFS‐LTD was not associated with a change in paired‐pulse facilitation ratio, suggesting a postsynaptic locus of expression of this plasticity. Next, we examined whether LFS‐LTD was related to ‘chemical’ LTDs obtained by the direct stimulation of mGlu5 and NMDA receptors. The saturation of LFS‐LTD completely occluded NMDA‐ and (RS)‐2‐Chloro‐5‐hydroxyphenylglycine (CHPG)‐induced LTD. CHPG‐LTD and NMDA‐LTD occluded each other. In addition, we observed that NMDA‐LTD was dependent on mGlu5 receptor activation in 9–12 day old rats while it was not in animals older than 15 day‐old. Therefore we postulate that during LFS application, NMDA and mGlu5 receptor could interact to trigger LTD. Low‐frequency‐mediated synaptic plasticity is subject to a developmental switch from NMDA‐ and mGlu5 receptor‐dependent LTD to mGlu5 receptor‐dependent LTP with a transient period (17–21 day‐old) during which LFS is ineffective. © 2006 Wiley‐Liss, Inc.