N-TYPE CA2-ELECTROCYTE SYNAPSES OF THE WEAKLY ELECTRIC FISH GYMNOTUS-CARAPO( CHANNELS MEDIATE TRANSMITTER RELEASE AT THE ELECTROMOTONEURON)

The effects of omega-conotoxin-GVIA (omega-CgTX) on synaptic transmiss ion were studied in the electromotoneuron-electrocyte synapses of the electric organ (EO) of the weakly electric fish Gymnotus carapo. omega -CgTX selectively and irreversibly blocked excitatory postsynaptic pot entials (EPSPs) in a dose dependent-manner. The toxin had no effect on : (a) resting postsynaptic membrane potential and conductance; (b) pos tsynaptic action potentials elicited by depolarizing transmembrane cur rent pulses; (c) the action potential conduction in the presynaptic fi ber; (d) acetylcholine (ACh)-induced postsynaptic responses. Nifedipin e - a selective dihydropyridine antagonist of the L-type voltage-depen dent Ca2+ channels (VDCCs) - did not affect synaptic transmission. Tra nsmission was also undisturbed by the peptide omega-Agatoxin (omega-Ag a-IVA), the low molecular weight polyamine, funnel-web toxin (FTX) - b oth included in the venom of the spider Agelenopsis aperta - and its s ynthetic analog sFTX, all selective blockers of P-type VDCCs. Since om ega-CgTX irreversibly blocks the N-type VDCCs, we conclude that presyn aptic N-type VDCCs mediate transmitter release at electromotoneuron te rminals. The VDCCs involved in fish peripheral electromotoneuron-elect rocyte presynaptic transmitter release are therefore similar to those in amphibian, reptilian and avian peripheral synapses, but differ from mammalian and invertebrate motoneuron terminals.