Whole-cell patch-clamp recordings of non-NMDA glutamatergic EPSCs were made from identified cholinergic neurones in slices of basal forebrain (BF) of young rats (P13-P18), to investigate the subtypes of calcium channels involved in dopamine D1-like receptor-mediated presynaptic inhibition of the EPSCs. The BF cholinergic neurones were pre-labeled by intra-cerebroventricular injection of a fluorescent marker, Cy3-192IgG. A D1-like receptor agonist, SKF 81297 (30 µM) suppressed the EPSCs reversibly by the extent about 30 %, and this inhibition was reproducible. Calcium channel subtypes involved in the glutamatergic transmission were elucidated using selective Ca2+ channel blockers. The N-type Ca2+ channel blocker, -conotoxin (-CgTX, 3 µM), suppressed the EPSCs by 57.5 %, whereas the P/Q-type channel selective blocker, -Agatoxin-TK (-Aga-TK, 200 nM), suppressed the EPSCs by 68.9 %. Simultaneous application of both blockers suppressed the EPSCs by 96.1 %. The R-type Ca2+ channel blocker, SNX-482 (300 nM) suppressed the EPSCs by 18.4 %, whereas nifedipine, the L-type Ca2+ channel blocker, (10 µM) had little effect. In the presence of -Aga-TK, SKF81297, a dopamine D1-like receptor agonist had no effect on the EPSCs. On the other hand, SKF81297 could still inhibit the EPSCs in the presence of either -CgTX, SNX-482 or nifedipine. SKF 81297 had no further effect on the EPSCs when external Ca2+ concentration was raised to 7.2 mM in the presence of -Aga-TK, but could still inhibit the EPSCs in high Ca2+ solution after -CgTX application. Forskolin (FK, 10 µM), an activator of adenylyl cyclase pathway, suppressed the EPSCs, and FK-induced effect was mostly blocked in the presence of -Aga-TK but not that of -CgTX. These results suggest that D1-like receptor activation selectively blocks P/Q-type calcium channels to reduce glutamate release onto BF cholinergic neurones.