SELECTIVE BLOCKADE OF SPINAL REFLEXES BY OMEGA-CONOTOXIN IN THE ISOLATED SPINAL-CORD OF THE NEONATAL RAT

High-voltage-activated calcium currents can be pharmacologically separated into two components: omega-conotoxin-sensitive, dihydropyridine resistant (N-type) and dihydropyridine sensitive, omega-conotoxin-resistant (L-type). In the present study, omega-conotoxin completely blocked spinal monosynaptic responses and long-latency electrically evoked polysynaptic reflexes were 93% blocked. Short-latency electrically evoked and capsaicin-evoked polysynaptic reflexes were partially blocked (39 and 37% block, respectively). Nifedipine, a dihydropyridine type antagonist, had no effect on any evoked responses and Bay K 8644, a dihydropyridine agonist, only increased spontaneous firing. Dynorphin A blocks N currents, but its depressant effects were not altered by irreversible blockade of omega-conotoxin-sensitive N channels. These results demonstrate that omega-conotoxin-sensitive N channels play a major role in the synaptic transmission that mediates monosynaptic and electrically evoked slow polysynaptic reflexes, and a lesser but significant role in fast and capsaicin-evoked polysynaptic spinal reflexes. L-type channels play a minor role. Furthermore, dynorphin A depresses synaptic transmission by blockade of high threshold calcium channels that are distinct from the omega-conotoxin-sensitive N channel, or by a mechanism that does not directly involve calcium channels.