title: Barium action potentials in regenerating axons of the lamprey spinal cord.
abstract: Intracellular recordings were obtained from growing tips of regenerating giant axons in the lamprey spinal cord, the recording sites verified by Lucifer yellow injection. In the presence of extracellular Ba++ (3-6 mM), tetraethylammonium (10-15 mM), and 4-aminopyridine (4-6 mM), action potentials showed prolonged plateaus. The fast initial phase of the action potential, but not the plateau (Ba++-spike), was blocked by tetrodotoxin (10(-6) gm/ml). The Ba++ spike was associated with increased membrane conductance and could be terminated with hyperpolarizing current pulses. Normal axons did not generate similar Ba++ spikes. However, TTX-resistant, voltage-dependant conductance changes could be elicited in normal axons if much higher concentrations of Ba++ (18-30 mM) were used. Their rate of rise was slower than in regenerating axons (0.6 V/sec vs 3.2 V/sec; n = 5), and the response did not outlast the current pulse. The Ba++ responses in normal and regenerating axons were blocked by ions known to block voltage-gated Ca++ conductances (Co++, Ni++, or Cd++). Therefore, these spikes probably represent Ba++ entry through voltage-dependent Ca++ channels, suggesting the presence of a higher-than-average voltage-dependent Ca++ conductance in the growing axon. However, Ca++-dependent spikes could not be obtained under any conditions in either normal or regenerating axons. Simultaneous intracellular recordings from growth cones and axons indicated that the Ba++ spike was initiated, in most cases, at the growth cone. The Ba++ spikes were recorded in regenerating axons for as long as 50 days following cord transection and were not correlatable with the "dying-back" phenomenon in cut axons, which usually is over before day 6. The concept of a higher-than-average voltage-dependent Ca++ conductance in growing tips of regenerating axons is in agreement with the hypothesis that Ca++ is important in regeneration and that regeneration may be related to the process of chemical synaptic transmission.
authors.forename: B A
authors.initials: BA
authors.lastname: MacVicar
authors.forename: R R
authors.initials: RR
authors.lastname: Llinás
mesh_terms: D015761:4-Aminopyridine; D000200:Action Potentials / Q000187:drug effects*; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D001369:Axons / Q000502:physiology*; D001464:Barium / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004553:Electric Conductivity; D007473:Ion Channels / Q000502:physiology; D007546:Isoquinolines; D007798:Lampreys; D008839:Microelectrodes; D009416:Nerve Regeneration; D013116:Spinal Cord / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D000631:Aminopyridines; D007473:Ion Channels; D007546:Isoquinolines; D013757:Tetraethylammonium Compounds; D001464:Barium; D013779:Tetrodotoxin; D019789:Tetraethylammonium; C017475:lucifer yellow; D015761:4-Aminopyridine