Fig. 2.

Long-term potentiation of cortico/thalamostriatal EPSP in cholinergic interneurons requires an increase in postsynaptic Ca²⁺. BMI (30 μm) was added to the bath solution throughout the experiments. Aa, EPSPs evoked before and after tetanic stimulation. Sweeps (4 min average) were taken at the times indicated on the graph in Ab (1 and2). Calibration: 1 mV, 25 msec. Ab, Percentage of each EPSP slope compared with the control values measured 10 min before the tetanus is plotted against time. Note that LTP occurred after the tetanus in the presence of BMI in the cholinergic interneuron. B, Average normalized EPSP slopes are plotted in the presence of BMI (○). Differences of the mean EPSP slopes between before and after HFS were statistically significant throughout the experiment (0–5 min after HFS, p < 0.05, paired t test; after 5 min, p< 0.001, paired t test; n = 20). Loading cells with BAPTA (20 mm) blocked the induction of LTP (▴). Pretreatment with Ni²⁺ (50 μm) and nimodipine (10 μm) also failed to induce LTP (▾). Thus, an increase in intracellular Ca²⁺ is required for LTP induction. When the experiment with BMI (○) was regarded as the control, the differences between the control and the experiment with Ni²⁺ and nimodipine became statistically significant throughout 10 min after the tetanus (p < 0.05, unpairedt test; p = 0.0083, ANOVA;n = 14). Differences between the control and the experiment with BAPTA were statistically significant all the time after 10 min (10–25 min after HFS, p < 0.05, unpairedt test; 30 min after HFS, p < 0.01, unpaired t test; p < 0.0001, ANOVA;n = 10). Statistical significance is indicated byasterisks on the graph: *p < 0.05, **p < 0.01. C, Treatment withd-APV (50 μm; ▵; n = 7) 10 min before HFS did not block LTP induction (p = 0.0586, ANOVA).