N-type Ca 2+ channels mediate transmitter release at the electromotoneuron-electrocyte synapses of the weakly electric fish Gymnotus carapo

Abstract

The effects of ω-conotoxin-GVIA (ω-CgTX) on synaptic transmission were studied in the electromotoneuron-electrocyte synapses of the electric organ (EO) of the weakly electric fish Gymnotus carapo. ω-CgTX selectively and irreversibly blocked excitatory postsynaptic potentials (EPSPs) in a dose dependent-manner. The toxin had no effect on: (a) resting postsynaptic membrane potential and conductance; (b) postsynaptic action potentials elicited by depolarizing transmembrane current pulses; (c) the action potential conduction in the presynaptic fiber; (d) acetylcholine (ACh)-induced postsynaptic responses. Nifedipine — a selective dihydropyridine antagonist of the L-type voltage-dependent Ca 2+ channels (VDCCs) — did not affect synaptic transmission. Transmission was also undisturbed by the peptide ω-Agatoxin (ω-Aga-IVA), the low molecular weight polyamine, funnel-web toxin (FTX) — both included in the venom of the spider Agelenopsis aperta — and its synthetic analog sFTX, all selective blockers of P-type VDCCs. Since ω-CgTX irreversibly blocks the N-type VDCCs, we conclude that presynaptic N-type VDCCs mediate transmitter release at electromotoneuron-terminals. The VDCCs involved in fish peripheral electromotoneuron-electrocyte presynaptic transmitter release are therefore similar to those in amphibian, reptilian and avian peripheral synapses, but differ from mammalian and invertebrate motoneuron terminals.