| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4344625 | Neuroscience Letters | 2012 | 6 Pages |
The calcium control hypothesis posits that postsynaptic calcium increases are required to trigger synaptic plasticity, with large increases inducing LTP and small increases inducing LTD. In CA1 of the hippocampus, however, LTD induced by chemical activation of metabotropic glutamate receptors (agonist-LTD) is independent of increases in postsynaptic calcium. Here we tested whether LTD induced by pairing of presynaptic stimulation with postsynaptic depolarization (synaptic-LTD) is similarly calcium-independent. This protocol induced an NMDA-dependent LTP when paired at 0 mV, which was converted to mGluR-dependent LTD when paired at −20 mV. The LTD was not blocked by calcium chelation, blockers of L- or T-type voltage-dependent calcium channels, or hyperpolarization to −70 mV. We conclude that synaptically induced mGluR-dependent LTD, like agonist induced mGluR LTD, does not require calcium influx for its induction.
► mGluR-dependent LTD was evoked in CA1 in a calcium-independent manner. ► This form of mGluR-dependent LTD also did not require postsynaptic depolarization. ► mGluR-dependent LTD expression is not reversed in whole-cell voltage-clamp.
