title: Selective blockade of spinal reflexes by omega-conotoxin in the isolated spinal cord of the neonatal rat.
abstract: 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.
authors.affiliation: Neuroimaging and Drug Action Section, National Institute on Drug Abuse, Baltimore, MD 21224.
authors.forename: J A
authors.initials: JA
authors.lastname: Bell
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002211:Capsaicin / Q000494:pharmacology; D004399:Dynorphins / Q000494:pharmacology; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology; D010456:Peptides, Cyclic / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012018:Reflex / Q000187:drug effects*; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D020960:omega-Conotoxins
chemical_list: D002121:Calcium Channel Blockers; D007473:Ion Channels; D010456:Peptides, Cyclic; D020960:omega-Conotoxins; C053423:Conus magus toxin; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D004399:Dynorphins; D009543:Nifedipine; D002211:Capsaicin