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3B, C). From the 1/��[Ca2+]5APs?vs.��B relationship, ��S was found to be lower in the dendrites of BCs compared with those of SC-ACs (BCs: 65 (28�C88); SC-ACs: 171 (100�C201); Fig. 3B). Similarly, from the ��decay?vs.��B relationship, ��S was found to be lower in the dendrites of BCs (BCs: 82 (14�C114); SC-ACs: 187 (152�C189); Fig. 3C). These results suggest that the significantly larger amplitude and faster decay kinetics observed for AP-evoked Ca2+ rises in the dendrites of BCs compared with those of SC-ACs can arise from differences in the endogenous Ca2+ binding capacities between these cells. According to the results presented so far, dendritic Ca2+ transients evoked by backpropagating APs in two types http://en.wikipedia.org/wiki/NK_cells of hippocampal INs differ significantly due to the cell type-specific properties of Ca2+ handling, in particular to endogenous Ca2+ buffering capacities. To examine whether these quantitatively different CaTs may also involve distinct Ca2+ mechanisms, next we assessed their sensitivity http://www.selleckchem.com/products/Gefitinib.html to specific blockers of VSCCs and of intracellular Ca2+ stores (Fig. 4). Experiments were performed using Fluo-5F as a Ca2+ indicator. The L-type VSCC blocker nifedipine (10 ��m; Fig. 4Aa, Ba and C) decreased the AP-CaT amplitude to ?70% of that of the control in both cell types, indicating a significant contribution of L-type VSCCs to dendritic AP-CaTs in SC-ACs and BCs. However, the effects of the T-type VSCC blocker NNC 55-0396 (10 ��m; Fig. 4Ab, Bb and C), which is a modified mibefradil analogue that is exquisitely selective for T-type VSCCs when used at low concentration (Huang et al. 2004; Li et al. 2005), and of the P/Q-type VSCC blocker ��-agatoxin IVA (AgTx, 250 nm; Fig. 4Ac, Bc and C) were cell type specific. T-type VSCCs exhibited a significantly higher contribution in the dendrites of SC-ACs (SC-ACs, 39.6 �� 4.1% of AP-CaTs, n= 5; BCs, 20.5 �� 5.7% of AP-CaTs, n= 6; P http://www.selleckchem.com/products/DAPT-GSI-IX.html of BCs (SC-ACs, 2.5 �� 0.2% of AP-CaTs, n= 6; BCs, 28.2 �� 3.4% of AP-CaTs, n= 6; Fig. 4C). Furthermore, the inhibitors of R-type (SNX-482, 30 nm) and N-type (CTx, 250 nm) VSCCs had no effect in either cell type (Fig. 4Aa, Ba, Ac, Bc and C), suggesting that these channels do not contribute to dendritic AP-CaTs in SC-ACs and BCs. In addition, both cell types demonstrated a significant component mediated by the activation of intracellular Ca2+ stores (Fig. 4Ab, Bb and C), pointing to the Ca2+-induced Ca2+ release activated in IN dendrites by backpropagating APs. During theta rhythm in vivo, most hippocampal INs go through active and relatively silent states (Klausberger et al. 2003) during which the IN membrane potential should fluctuate from a relatively depolarized to a hyperpolarized level, respectively.