A re-excitation mechanism for strychnine-induced doublets in molluscan neurons.
The effects of strychnine on Aplysia R2 neurons were evaluated using simultaneous intracellular recordings of the soma and axon potentials. 1 mM strychnine produced a slight enlargement of the somatic spike and a large increase of the axon spike duration. Following direct stimulation, the soma displayed depolarizing afterpotentials ( DAPs ) which might trigger extra-spikes, both produced electronically by long-lasting axon spikes. Cobalt suppressed both the axon spike lengthening and the somatic extra-spikes or DAPs , and induced large depolarizing shifts in the soma. The region of largest spike lengthening (proximal axon) had a large density of Ca channels. The different effects of strychnine on the soma and on the axon were assumed to result from a selective blockage of the V-dependent K channels which would predominate in the axon whereas Ca-activated K channels would predominate in the soma.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001048:Aplysia / Q000187:drug effects / Q000502:physiology*; D001369:Axons / Q000187:drug effects; D003035:Cobalt / Q000494:pharmacology; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D011188:Potassium / Q000378:metabolism; D013331:Strychnine / Q000494:pharmacology*
D007473:Ion Channels; D003035:Cobalt; D013331:Strychnine; D011188:Potassium