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Tolerance to Anesthesia Depends on Synaptic Proteins

Authors
  • Al-Hasan, Yazan M.1
  • Krishnan, Harish R.1
  • Ghezzi, Alfredo1
  • Prado, Francisco J. III1
  • Robles, Roseanna B.1
  • Atkinson, Nigel S.1
  • 1 The University of Texas at Austin, The Waggoner Center for Alcohol and Addiction Research, Section of Neurobiology, 1 University Station C0920, Austin, TX, 78712-0248, USA , Austin (United States)
Type
Published Article
Journal
Behavior Genetics
Publisher
Springer-Verlag
Publication Date
Feb 12, 2011
Volume
41
Issue
5
Pages
734–745
Identifiers
DOI: 10.1007/s10519-011-9451-8
Source
Springer Nature
Keywords
License
Yellow

Abstract

The hypnotic effects of anesthetics are caused by their interactions with neuronal components vital for proper signaling. An understanding of the adaptive mechanisms that lead to the development of anesthetic tolerance can offer insight into the regulation of neuroexcitability and plasticity that alter behavioral output. Here we use genetic and pharmacological manipulation of Drosophila to investigate the mechanisms of tolerance to benzyl alcohol. The mutants tested were temperature-sensitive paralytics that interfere with neuronal signaling: two mutations in dynamin that affect vesicle recycling, shits1 and shits2, and one that affects the voltage-activated Na+ channel, parats1. We also used N-ethylmaleimide (NEM) to pharmacologically interfere with synaptic function. We found that blocking the generation of action potentials using a temperature-sensitive paralytic mutation does not induce nor prevent the development of functional tolerance to benzyl alcohol, but that disruption of synaptic signaling using mutations in the dynamin gene or by NEM treatment inhibits the induction of tolerance.

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