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. Author manuscript; available in PMC: 2007 Apr 10.
Published in final edited form as: Nat Med. 2005 Aug 14;11(9):973–981. doi: 10.1038/nm1277

Figure 2.

Figure 2

PDSs are mediated by release of glutamate from action potential-independent sources. (a) Representative traces of field potential recording in 4-AP; 4-AP and TTX; 4-AP, TTX, APV (50 μM), and CNQX (20 μM). (b) Frequency, amplitude and area (amplitude × duration) plotted as a function of time (n = 7). Spontaneous field potential events were observed in all slices exposed to 4-AP. The frequency and amplitude of PDSs were reduced by 20–35% by TTX and by 85–90% by APV and CNQX. (c) Normalized mean values of frequency, amplitude, and area (amplitude × duration) during exposure to 4-AP, 4-AP + TTX, 4-AP + TTX + APV/CNQX, during washout of APV/CNQX (4-AP + TTX), and during washout of TTX (4-AP) (n = 7). (d) The cocktail of VGCC blockers (Nifedipine, Mibefradil, Omega-Conotoxin MVIIC, Omega-Conotoxin GVIA, SNX-482, same concentration as in Fig. 1 and TTX did not decrease the frequency or amplitude of PDSs compared with TTX alone (n = 5). (e) D,L-threo-beta-benzyloxyaspartate (TBOA, a glutamate transport inhibitor, 100 μM) did not reduce the occurrence of PDSs, but increased the frequency, amplitude and area of PDSs significantly suggesting that inverted transport of glutamate did not contribute to PDSs (n = 6). (f) (S)-Alpha-methyl-4-carboxy-phenylglycine ((S)-MCPG, a non-selective mGluR antagonist, 1 mM) did not decrease the frequency or amplitude of PDSs compared with TTX alone (n = 7). (g) CNQX alone significantly reduced PDSs (n = 6). (h) APV alone highly significantly reduced PDSs (n = 6). (i) TTX added before (10–15 min) had no effect on frequency of PDSs, but significantly reduced the amplitude of PDSs compared with slices first exposed to TTX 20 min after addition of 4-AP (n = 7). *, P < 0.05; **, P < 0.001; student's t-test; mean ± s.d..