Figure 1. Activation of mGluR7 reduced NMDAR currents in BF neurons, which was selectively impaired by Aβ in BF cholinergic neurons. A, Immunocytochemical images showing the costaining of MAP2 (blue, a marker for neurons) and ChAT (green, a marker for cholinergic neurons) of acutely isolated neurons from NBM in BF. Arrow points to a ChAT+ neuron; arrowheads point to two ChAT− neurons. B, Single-cell RT-PCR showing the expression of ChAT mRNA in acutely dissociated BF neurons. C, Plot of normalized peak VDCCs showing the effect of carbachol (20 μm), a cholinergic receptor agonist, in dissociated BF large neurons (cholinergic) and small neurons (noncholinergic). Inset, Representative VDCC traces evoked by a voltage ramp (at time points denoted by #). Calibration: 0.2 nA, 25 ms. D, Cumulative data (mean ± SEM) showing the percentage reduction of VDCC by carbachol in BF large (cholinergic) and small (noncholinergic) neurons. *p < 0.01 (ANOVA). E, F, Plot of normalized peak NMDAR currents showing the l-AP4 (200 μm) effect in BF cholinergic (E) and noncholinergic (F) neurons isolated from slices treated with or without oligomeric Aβ (1 μm, 2 h). The fast washout of l-AP4 in dissociated neurons led to the speedy recovery of NMDAR currents. G, Representative current traces taken from the records used to construct E and F. Calibration: 0.1 nA, 1 s. H, Cumulative data (mean ± SEM) showing the percentage reduction of NMDAR currents by l-AP4 or 8-OH-DPAT (5-HT1A agonist, 20 μm) in BF cholinergic and noncholinergic neurons with or without Aβ treatment. *p < 0.005 (ANOVA).