Figure 5.
Calcium signals underlying GABA release during lateral feedback. A, Glutamate-evoked lateral feedback IPSCs were strongly reduced by the nonselective Cav channel blocker, Cd2+ (200 μm). The Cd2+-insensitive component of the IPSCs was eliminated by additional inclusion of PhTx (1 μm). B, Summarized drug effects (mean ± SD) on feedback IPSCs. C, Feedback IPSCs evoked in the presence of PhTx (to eliminate Ca2+ influx through AMPARs; control trace) were strongly, but not completely, reduced by coapplication of either N- or L-type Cav channel antagonists (ω-conotoxin GVIA, 10 nm, or isradipine, 10 μm, respectively). D, Summarized effects of Cav channel blockers (mean ± SD) on feedback IPSCs evoked in the presence of 1 μm PhTx. E, Feedback IPSCs were reduced by bath application of the RyR antagonist, RR (40 μm), but not the IP3R antagonist XeC (3 μm). F, Summarized data (mean ± SD) showing that RyRs, but not IP3Rs, contribute to the Ca2+ signaling underlying lateral GABA release. All experiments were performed in the presence of strychnine (3 μm) and DHT (50 μm). **p < 0.01; ***p < 0.001. Israd, Isradipine; Mibef, mibefradil; Aga, agatoxin IVA; thap, thapsigargin.