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The possibility that R-type calcium channels contribute to fast glutamatergic transmission in the hippocampus has been assessed using low concentrations of NiCl2 and the peptide toxin SNX 482, a selective antagonist of the pore-forming α1E subunit of R-type calcium channel. EPSPs or EPSCs were recorded in the whole-cell configuration of the patch-clamp technique mainly from CA3 hippocampal neurons. Effects of both NiCl2 and SNX 482 were tested on large (composite) EPSCs evoked by mossy and associative–commissural fiber stimulation. NiCl2 effects were also tested on minimal EPSPs–EPSCs. Both substances reduced the amplitude of EPSPs–EPSCs. This effect was associated with an increase in the number of response failures of minimal EPSPs–EPSCs, an enhancement of the paired-pulse facilitation ratios of both minimal and composite EPSCs, and a reduction of the inverse squared coefficient of variation (CV−2). The reduction of CV−2 was positively correlated with the decrease in EPSC amplitude. The inhibitory effect of NiCl2 was occluded by SNX 482 but not by ω-conotoxin-MVIIC, a broad-spectrum antagonist thought to interact with N- and P/Q-type calcium channels, supporting a specific action of low concentrations of NiCl2 on R-type calcium channels. Together, these observations indicate that both NiCl2 and SNX 482 act at presynaptic sites and block R-type calcium channels with pharmacological properties similar to those encoded by the α1E gene. These channels are involved in fast glutamatergic transmission at hippocampal synapses.

Presynaptic R-Type Calcium Channels Contribute to Fast Excitatory Synaptic Transmission in the Rat Hippocampus