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. Author manuscript; available in PMC: 2010 Dec 21.
Published in final edited form as: J Neurophysiol. 2003 Mar;89(3):1308–1316. doi: 10.1152/jn.00644.2002

FIG. 2.

FIG. 2

Blockade of group II, but not group I or III mGluRs increases sEPSC amplitude. A: graphs of sEPSC amplitude vs. time for 3 cells, each exposed to an antagonist of a different metabotropic glutamate receptor (mGluR) group. After a 400-s pre-drug period, R(−)-1-amino-2,3-dihydro-1H-indene-1,5-dicarboxylic acid (AIDA, group I; 1 mM), 2S-2-amino-2-(1S,2S-2-carboxycyclopropyl-1-yl)-3-(xanth-9-yl)propanoic acid (LY341495, group II; 2 μM), and (R, S)-α-cyclopropyl-4-phosphonophenylglycine (CPPG, group III; 0.1 mM) were perfused for 400–500 s (□), followed by washout. ●, a single sEPSC. B: normalized mean sEPSC amplitude for groups of neurons exposed to mGluR antagonists. MCPG increased amplitude of sEPSCs (n = 15, P < 0.01); AIDA and (RS)-hexyl-HIBO (HIBO) decreased sEPSC amplitude (n = 14, results of 9 cells in AIDA and 5 cells in HIBO pooled, P < 0.001); LY341495 increased sEPSC amplitude (n = 11, P <0.01), while CPPG had no effect (−1.4 ± 4.4%, n = 7, P > 0.05). For wash values, see text.