Fig. 5

NMDAR-LTD of prefrontal cortex-accumbal glutamatergic synapse was disrupted in CSDS mice. A Prefrontal cortex-accumbal field potential recordings of acute NAc slices reveal representative field excitatory postsynaptic potentials (fEPSPs) demonstrated respective recordings from sample experiments at 50 ms inter-pulse interval. B Paired-pulse facilitation (PPF) was recorded by changing intervals between pairs of salts. Paired-pulse ratios, that is to say, slope of fEPSPs no. 2/slope fEPSPs no. 1 were alike among control, CSDS, and d-serine treated slices (n = 8). C Prefrontal cortex-accumbal field potential recordings of acute brain slices exhibit the characteristic superposed fEPSPs by adding stimulation intensity. D Input–output curves illustrating the correlation between magnitudes of stimulation and evoked reaction for fEPSPs recorded from slices of control and CSDS mice. The CSDS decreased fEPSPs in NAc significantly, compared with control mice (n = 8). The d-serine treated slices increased fEPSPs in NAc significantly, compared with CSDS mice (n = 8). E Individual experiment traces showed that LTD was induced in control slices by low-frequency stimulation (LFS). The LFS consists of a 1-Hz, 900-pulse train, which has been used to cause NMDAR-LTD in prefrontal cortex-NAc synapse. F Averaged data demonstrated that LTD was induced in control slices by LFS. G Individual experiment traces showed that LTD was induced in CSDS slices by LFS. H Averaged data showed that LTD was induced in CSDS slices by LFS. I The column diagram demonstrated the level of LTD 40 min after LFS from control mice and CSDS mice. The NMDAR-LTD was impaired in CSDS mice compared with control mice. **P < 0 .01 vs. control group. The superimposed fEPSP in the upper portion is recording from representative experiments taken at the time indicated by the number. Each point was normalized mean ± SEM of eight slices