Fig. 2.
Types of presynaptic Ca2+channels controlling neurotransmitter release in the hippocampal medial perforant pathway. A, Time courses of [Capre]t and fEPSP in response to 1 μm ω-CgTx GVIA, the N-type Ca2+channel blocker, in the hippocampal medial perforant pathway. The toxin substantially reduced [Capre]t but had only a minor effect on synaptic transmission. The mean inhibition of [Capre]t and fEPSP by ω-CgTx GVIA was ∼31 ± 6 and 12 ± 3% (n = 9). Although the amount of [Capre]t reduced by the toxin at this synapse was comparable with that measured at the hippocampal CA3–CA1 synapse of the same species, much less effect of N-type Ca2+ channel blockade on synaptic transmission was observed here. Inset shows sample traces taken during steady-state periods in the control solution and after application of ω-CgTx GVIA. B, Time courses of [Capre]t and fEPSP in response to 1 μm ω-Aga IVA, the P/Q-type Ca2+channel blocker. Application of the toxin strikingly reduced [Capre]t and potently inhibited synaptic transmission. On average, ω-Aga IVA reduced [Capre]t by 53 ± 5% (n = 3) and inhibited the fEPSP by 86 ± 2% (n = 3). These data indicate that, similar to other excitatory central synapses studied to date, Ca2+entering through P/Q-type channels is the major source of Ca2+ triggering release of neurotransmitter in the hippocampal medial perforant pathway. Inset shows sample traces taken during steady-state periods in the control solution and after application of ω-Aga IVA.