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. 2016 Dec 15;23(2):145–154. doi: 10.1111/cns.12663

Figure 5.

Figure 5

Decrease in glutamatergic synaptic activity of IC neurons by BBG in NMD rats. (A) Representative traces illustrating sEPSCs of an IC neuron before and after the addition of BBG (1 μM). (B) Cumulative fraction of peak amplitude of sEPSCs in an IC pyramidal neuron under the pre‐ and postdrug conditions (left); bar plot showing no significant change in sEPSC peak amplitude by BBG (right). (C) Cumulative fraction of interevent intervals of sEPSCs under the pre‐ and postdrug conditions (left); bar plot showing the significant decrease in sEPSC frequency by BBG (right). n = 6 cells, *P < 0.05 versus pre. (D) Representative traces illustrating mEPSCs of an IC neuron before and after the addition of BBG (1 μM); TTX (1 μM) was used to block action potentials. (E) Cumulative fraction of peak amplitude of mEPSCs in one IC pyramidal neuron under the pre‐ and postdrug conditions (left); bar plot showing no significant change in mEPSC peak amplitude by BBG (right). (F) Cumulative fraction of interevent intervals of mEPSCs under the pre‐ and postdrug conditions (left); bar plot showing that mEPSC frequency was remarkably decreased by BBG treatment (right). Peak amplitude and frequency of BBG‐treated neurons were normalized by those from the same neuron before BBG treatment. n = 6 cells, *P < 0.05 versus pre.