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The effect of ω‐conotoxin GVIA on synaptic transmission within the nucleus accumbens and hippocampus of the rat in vitro
Author(s) -
Horne A.L.,
Kemp J.A.
Publication year - 1991
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1991.tb09855.x
Subject(s) - excitatory postsynaptic potential , nucleus accumbens , neurotransmission , neuroscience , inhibitory postsynaptic potential , chemistry , population , calcium channel , population spike , hippocampal formation , voltage dependent calcium channel , calcium , biology , dopamine , biochemistry , receptor , medicine , environmental health , organic chemistry
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 n m 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 μ m 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 n m 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.