Fig. 8.

Selective Ca²⁺ channel blockers do not prevent spike-associated Ca²⁺ release in the presence of 30 μmt-ACPD.A, A train of 10 backpropagating spikes evoked at 30 msec intervals caused a rapid [Ca²⁺]_iincrease at a location close to the soma in the apical dendrites. The amplitude of this change was approximately constant when these trains were evoked at 30 sec intervals (1). The addition of 100 μm NiCl₂ to the ACSF reduced the amplitude of this increase without changing the shape of the transient (2). When t-ACPD was added to this solution, a secondary [Ca²⁺]_i increase was observed (3). B–D, Similar experiments are shown with 1 μm ω-CTX-GVIA, 10 μm nimodipine, and 400 nm ω-Aga-IVA. None of these agents prevented release by t-ACPD (B, D) or CCh (C). ω-CTX-GVIA reduced the spike-associated [Ca²⁺]_i in normal ACSF, whereas nimodipine and ω-Aga-IVA did not. For the experiment with ω-Aga-IVA, fura-6F was the Ca²⁺ indicator, resulting in faster transients.