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We speculated that PP-LTD was also dependent on the activation of Group I mGluR, including mGluR5 receptors. To test this possibility, we first examined whether the chemical activation of Group I mGluR could induce LTD. The application of 40 ��M of Group I mGluR agonist, DHPG, for 10 min resulted in significant LTD expression (65 �� 3% of [http://www.selleckchem.com/products/hydroxychloroquine-sulfate.html Hydroxychloroquine order] baseline, n = 6, P [http://www.selleckchem.com/products/Fasudil-HCl(HA-1077).html Fasudil research buy] LTD is independent of PKC activation (Schnabel et al.,1999,2001). We further examined the role of PKC in PP-LTD. Following the addition of 3 ��M chelerythrine, a PKC blocker, to the bath, PP-LTD was still inducible in CA1 areas (Fig. 2C, LTD = 78 �� 4% of baseline, n = 6, P [http://en.wikipedia.org/wiki/Oxygenase Oxygenase] of the mGluR5 pathway in CA1 areas (LTD = 74 �� 5% of baseline, n = 8 slices, P