Persistent Ca2+ Current Contributes to a Prolonged Depolarization in Aplysia Bag Cell Neurons

• Published in: Journal of neurophysiology Vol. 102; no. 6; pp. 3753 - 3765
• Main Authors: Tam, Alan K. H, Geiger, Julia E, Hung, Anne Y, Groten, Chris J, Magoski, Neil S
• Format: Journal Article
• Language: English
• Published: United States Am Phys Soc 01.12.2009
• Subjects: Animals; Aplysia - cytology; Biophysical Phenomena - physiology; Biophysics; Calcium - metabolism; Calcium Channel Blockers - pharmacology; Calcium Signaling - drug effects; Cells, Cultured; Electric Stimulation - methods; Ion Channel Gating - drug effects; Ion Channel Gating - physiology; Ions - metabolism; Ions - pharmacology; Membrane Potentials - drug effects; Membrane Potentials - physiology; Neurons - physiology; Nickel - pharmacology; Patch-Clamp Techniques - methods; Potassium Channel Blockers - pharmacology; Tetradecanoylphorbol Acetate - analogs & derivatives; Tetradecanoylphorbol Acetate - pharmacology; Tetraethylammonium - pharmacology
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.00669.2009

Department of Physiology, Queen's University, Kingston, Ontario, Canada Submitted 28 July 2009; accepted in final form 8 October 2009 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. Address for reprint requests and other correspondence: N. S. Magoski, Dept. of Physiology, Queen's University, 4th Floor, Botterell Hall, 18 Stuart St., Kingston, ON K7L 3N6, Canada (E-mail: magoski{at}queensu.ca ).