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. 2010 May 14;4:12. doi: 10.3389/fncel.2010.00012

Figure 4.

Figure 4

The impact of molecular/cellular mechanisms on GrC synaptic excitation in the network. (A) Response of GrCs activated by a mf burst (five spikes at 100 Hz on eight contiguous mfs). Each group of traces corresponds to the same 52 GrCs sharing a common bursting mf. The underlying PSTH reports the probability of spike occurrence in 1-ms bins for all (250) GrCs responding to the mf burst. Note that the switch-off of GABA-A α6 receptors and even more of GABA-A α1 + GABA-A α6 receptors, which control the fast and slow components of inhibition, considerably enhances spike generation protracting the duration of the output burst. Blocking the NMDA receptors prevents EPSP temporal summation reducing the GrC response. Decreasing release probability slows down temporal summation while increasing release probability accelerates temporal summation, with opposite effects on the rate of the GrC resposne. (B) The raster-plot shows the timing of individual spikes in different conditions for the same 52 GrCs shown in (A) and for 5 GoC. Note that GoCs, through GABA-A α1 and α6 receptors, regulate the duration of the time window for GrC discharge, which normally lasts 5–10 ms from the stimulus. Repetitive GrC firing is prevented by the block of NMDA receptors and by a low release probability.