The effect of ω‐conotoxin GVIA on synaptic transmission within the nucleus accumbens and hippocampus of the rat in vitro

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Abstract
1 The actions of two calcium channel antagonists, the N-channel blocker ω-conotoxin GVIA (ω-CgTx) and the L-channel antagonist nisoldipine, on synaptic transmission were investigated in the hippocampus and nucleus accumbens of the rat in vitro. 2 ω-CgTx (100 nm for 10 min) produced a marked and irreversible reduction of focally evoked population spikes and intracellularly recorded excitatory postsynaptic potentials (e.p.s.ps) in the nucleus accumbens, which could not be overcome by increasing the stimulus strength. 3 Nisoldipine (10 μm for 10 min) had no effect on population spikes in the nucleus accumbens or the CA1 of the hippocampus. 4 In the hippocampus, population spikes were not irreversibly reduced by ω-CgTx (100 nm for 10 min) but rather, multiple population spikes were produced along with spontaneous synchronous discharges. This indicated that inhibitory synaptic transmission was being preferentially reduced. 5 Intracellular recordings demonstrated that ω-CgTx powerfully reduced inhibitory synaptic transmission in an irreversible manner and that excitatory transmission was also reduced but to a lesser extent. Unlike excitatory transmission in the nucleus accumbens and inhibitory transmission in the hippocampus, increasing the stimulus strength overcame the reduction of hippocampal excitatory transmission. 6 It is concluded that ω-CgTx-sensitive calcium channels are involved in the calcium entry that precedes the synaptic transmission in all these synapses. The apparent lower sensitivity of the hippocampal excitatory fibres to ω-CgTx may indicate that calcium entry that promotes transmitter release at central synapses may be mediated by pharmacologically distinct calcium channels.