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. 2010 Apr 14;30(15):5176–5188. doi: 10.1523/JNEUROSCI.5351-09.2010

Figure 2.

Figure 2.

A, C, IBMAA is mediated by the activation of mGluR1. Example traces of IBMAA (A) and IGLU (C) on expanded time scale, in control and in the presence of glutamate receptor antagonists, were aligned on their rising phase. B, D, Histograms of IBMAA and IGLU amplitudes, expressed as percentage of controls, in the presence of glutamate receptor antagonists. CPCCOEt (A1) and, to a lesser extent, CNQX (A2) significantly reduced IBMAA (B, n = 24 for both). APV, MK801 (A3), and MPEP (A4) did not modify IBMAA (B, n = 6, 4, and 7, respectively). IGLU was significantly affected by all ionotropic (CNQX, MK801, APV, and CNQX plus MK801) receptor antagonists (C1, C2, D1, n = 10, 5, 6, 5, respectively). The IGLU sensitivity to mGluR antagonists was assessed in the presence of CNQX plus MK801 (D2). CPCCOEt (C3) significantly reduced IGLU (D2, n = 7), whereas MPEP (C4) left IGLU unaffected (D2, n = 3). **p < 0.01, #p < 0.0001.