(A) Representative mEPSC traces from WT and hippocampal neurons in the presence of 10 μM bicuculline (Bic) and 1 μM tetrodotoxin (TTX)

(B) Cumulative probability of mEPSC amplitude in WT (gray) and (black) mice. (inset) The quantitative results of amplitude; no difference was found between WT and mice. (C) Cumulative distribution of mEPSC frequency in WT (gray) and (black) mice. Inset shows that the lack of dysbindin notably decreased the mean frequency of mEPSCs. (D) Histograms display quantitative analysis of HHD, RT, and charge of mEPSCs, showing that the lack of dysbindin slows the kinetics and increases the charge of single vesicle release. Data are from 238 spikes (7 cells, WT) and 112 spikes (6 cells, ). (E) Analysis of decay time constant (τ) was performed on averaged mEPSCs obtained from 50 individual events. The decay time was best fitted with a single exponential function. The decay of EPSCs in neurons (black) was slower than that in WT (gray). (F) Averaged evoked EPSC waveforms of WT and cells from 10 traces. (G) Comparison of the amplitude, RT, charge transfer, or decay time constant (τ) of evoked EPSCs between WT (gray) and (black) cells. The lack of dysbindin resulted in reduced amplitude and slower decay time without affecting the amount of release as measured by the charge transfer. Data are from 17 cells (WT) and 16 cells (). *, P < 0.05; ***, P < 0.001. Error bars indicate the mean ± SEM.<p><b>Copyright information:</b></p><p>Taken from ", a schizophrenia susceptibility gene, affects kinetics of transmitter release"</p><p></p><p>The Journal of Cell Biology 2008;181(5):791-801.</p><p>Published online 2 Jun 2008</p><p>PMCID:PMC2396815.</p><p>