Effect of Diisopropylfluorophosphate on Synaptic Transmission and Acetylcholine Sensitivity in Neuroblastoma-Myotube Co-Culture

  • M. Adler
  • F.-C. T. Chang
  • D. Maxwell
  • G. Mark
  • J. F. Glenn
  • R. E. Foster
Part of the Advances in Behavioral Biology book series (ABBI, volume 30)


The toxicity of organophosphorous cholinesterase inhibitors is believed to result primarily from inhibition of acetylcholinesterase (AChE) and consequent increases in acetylcholine (ACh) lifetime (10). At the vertebrate neuromuscular junction, blockade of AChE leads to increases in the amplitude and time course of spontaneous miniature endplate potentials (MEPPs), evoked endplate potentials (EPPs) and their underlying currents (7, 9, 11). In mammalian but not amphibian preparations, anticholinesterase agents also cause repetitive antidromic firing in the presynaptic axon in response to a single conditioning stimulus (12). This phenomenon has been attributed to nerve terminal depolarization due to accumulation of Ach (17) or K+ (12) in the synaptic cleft following blockade of ACh hydrolysis.


AChE Activity Transmitter Diffusion Endplate Potential Desensitization Rate Glioma Hybrid Cell 
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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • M. Adler
    • 1
  • F.-C. T. Chang
    • 1
  • D. Maxwell
    • 1
  • G. Mark
    • 1
  • J. F. Glenn
    • 1
  • R. E. Foster
    • 1
  1. 1.Neurotoxicology BranchUnited States Army Medical Research Institute of Chemical DefenseAberdeen Proving GroundUSA

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