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BJA Advance Access originally published online on May 27, 2005
British Journal of Anaesthesia 2005 95(2):216-221; doi:10.1093/bja/aei163
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2005. All rights reserved. For Permissions, please e-mail: journal.permissions@oupjournals.org

Volatile anaesthetic effects on phospholipid binding to synaptotagmin 1, a presynaptic Ca2+ sensor

D. Fu1, P. Vissavajjhala1 and H. C. Hemmings, Jr1,2,*

Departments of 1 Anesthesiology and 2 Pharmacology, Weill Medical College of Cornell University, New York, NY, USA

* Corresponding author: Department of Anesthesiology, Box 50, Weill Cornell Medical College, 525 E. 68th Street, New York, NY 10021, USA. E-mail: hchemmi{at}med.cornell.edu

Background. Volatile anaesthetics have important effects on synaptic transmission in the CNS. Depression of excitatory transmission involves reduced transmitter release via unidentified presynaptic mechanisms. Synaptotagmin 1 is a synaptic vesicle-associated protein that regulates Ca2+-evoked transmitter release involving critical Ca2+/phospholipid interactions within its C2 domains.

Methods. We analysed the effects of halothane and isoflurane on the binding of purified recombinant rat synaptotagmin 1 C2A, C2B and C2AB domains to radiolabelled phospholipid liposomes.

Results. Halothane and isoflurane had no significant effects on the maximal binding or Ca2+ dependence of binding of synaptotagmin 1 C2 domains to mixed phospholipid vesicles composed of either phosphatidylserine/phosphatidylcholine or phosphatidylinositol/phosphatidylcholine.

Conclusions. Inhibition of synaptic vesicle exocytosis by volatile anaesthetics does not appear to involve an effect on the critical Ca2+/phospholipid binding properties of synaptotagmin 1, a Ca2+ sensor involved in regulating evoked Ca2+-dependent neurotransmitter release.


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