Omega-conotoxin GVIA blocks synaptic transmission in the CA1 field of the hippocampus.

The effects of omega-conotoxin GVIA (omega-CgTx), a peptide isolated from the venom of a marine mollusc, were studied in rat hippocampal neurons. Intracellular recordings from the CA1 area were made for the purpose in in vitro slice preparations. Omega-CgTx (0.1-1 microM) rapidly and irreversibly blocked the EPSP and the IPSPs elicited by electrical stimulation of Schaffer collaterals/commissural fibers. Omega-CgTx also blocked the slow cholinergic EPSP induced by electrical stimulation of cholinergic afferents. The postsynaptic effects of baclofen or carbachol remained unchanged in the presence of omega-CgTx and other postsynaptic calcium-dependent events such as afterhyperpolarization were not affected by omega-CgTx. These results suggest a presynaptic action of omega-CgTx through the blockade of neurotransmitter release. Omega-CgTx might act in the hippocampus by blocking presynaptic N-type voltage-sensitive calcium channels.