Skip Navigation

American Zoologist 2001 41(4):1009-1025; doi:10.1093/icb/41.4.1009
© 2001 by The Society for Integrative and Comparative Biology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Yu, B.
Right arrow Articles by Blankenship, J. E.
Right arrow Search for Related Content
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Serotonin Directly Increases a Calcium Current in Swim Motoneurons of Aplysia brasiliana1

Baojian Yu1, Georgi N. Gamkrelidze2, Paul J. Laurienti3 and James E. Blankenship2,4
1 Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, Texas 77555-1031
2 Lucent Technologies, Bell Labs, Biological Computational Research Department, 600 Mountain Avenue, P.O. Box 636, Murray Hill, New York 07974-0636
3 {ddagger}Department of Radiology, Wake Forest University, School of Medicine, Medical Center Blvd., Winston-Salem, North Carolina 27157-1010
4 Marine Biomedical Institute, University of Texas Medical Branch, 301 University Blvd., Galveston, Texas 77555-1069

Muscle fibers in the swim appendages of the mollusk Aplysia brasiliana are innervated by cholinergic motoneurons. Serotonin (5-HT) causes an increase in amplitude of junctional potentials and muscle contractions at this neuromuscular synapse. We studied motoneurons with intracellular current-clamp recording and single-electrode voltage-clamp analysis to determine the effects of 5-HT on somatic currents in these presynaptic neurons. Serotonin was found to have no effect on action potential duration in motoneurons bathed in normal seawater, and no effect of 5-HT could be detected on K+ currents, indicating that 5-HT does not indirectly enhance calcium currents by prolonging the action potential. Calcium currents were isolated by replacing extracellular sodium with TEA and adding tetrodotoxin and other K+-channel blockers. Under these conditions motoneuron action potentials were greatly prolonged and could be blocked with Co2+ or Cd2+. Addition of 5-HT increased the duration of these Ca2+ spikes by about 35%. In motoneurons studied with voltage clamp, the amine produced a 58% increase in total inward calcium current. Use of the calcium channel blockers nifedipine, nimodipine, {omega}-conotoxin GVIA, and {omega}-agatoxin TK revealed that motoneurons express varying amounts of L-, N- and P-like calcium channels, but only an agatoxin-sensitive, P-type channel is sensitive to 5-HT. It is concluded that 5-HT acts directly to increase a P-type Ca2+ current during a normal spike. The resulting increase in intracellular calcium could contribute to an increase in transmitter release and account for the increase in junctional potentials in swim muscles.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.