title: Persistent Ca2+ current contributes to a prolonged depolarization in Aplysia bag cell neurons.
abstract: Neurons may initiate behavior or store information by translating prior activity into a lengthy change in excitability. For example, brief input to the bag cell neurons of Aplysia results in an approximate 30-min afterdischarge that induces reproduction. Similarly, momentary stimulation of cultured bag cells neurons evokes a prolonged depolarization lasting many minutes. Contributing to this is a voltage-independent cation current activated by Ca(2+) entering during the stimulus. However, the cation current is relatively short-lived, and we hypothesized that a second, voltage-dependent persistent current sustains the prolonged depolarization. In bag cell neurons, the inward voltage-dependent current is carried by Ca(2+); thus we tested for persistent Ca(2+) current in primary culture under voltage clamp. The observed current activated between -40 and -50 mV exhibited a very slow decay, presented a similar magnitude regardless of stimulus duration (10-60 s), and, like the rapid Ca(2+) current, was enhanced when Ba(2+) was the permeant ion. The rapid and persistent Ca(2+) current, but not the cation current, were Ni(2+) sensitive. Consistent with the persistent current contributing to the response, Ni(2+) reduced the amplitude of a prolonged depolarization evoked under current clamp. Finally, protein kinase C activation enhanced the rapid and persistent Ca(2+) current as well as increased the prolonged depolarization when elicited by an action potential-independent stimulus. Thus the prolonged depolarization arises from Ca(2+) influx triggering a cation current, followed by voltage-dependent activation of a persistent Ca(2+) current and is subject to modulation. Such synergy between currents may represent a common means of achieving activity-dependent changes to excitability.
authors.affiliation: Department of Physiology, Queen's University, Kingston, Ontario, Canada.
authors.forename: Alan K H
authors.initials: AK
authors.lastname: Tam
authors.forename: Julia E
authors.initials: JE
authors.lastname: Geiger
authors.forename: Anne Y
authors.initials: AY
authors.lastname: Hung
authors.forename: Chris J
authors.initials: CJ
authors.lastname: Groten
authors.forename: Neil S
authors.initials: NS
authors.lastname: Magoski
mesh_terms: D000818:Animals; D001048:Aplysia / Q000166:cytology*; D055592:Biophysical Phenomena / Q000502:physiology*; D001703:Biophysics; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects; D002478:Cells, Cultured; D004558:Electric Stimulation / Q000379:methods; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D007477:Ions / Q000378:metabolism / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D009532:Nickel / Q000494:pharmacology; D018408:Patch-Clamp Techniques / Q000379:methods; D026902:Potassium Channel Blockers / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000031:analogs & derivatives / Q000494:pharmacology; D019789:Tetraethylammonium / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D007477:Ions; D026902:Potassium Channel Blockers; C020922:4-O-methyl-12-O-tetradecanoylphorbol 13-acetate; D019789:Tetraethylammonium; D009532:Nickel; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium