Neurotoxicity of dipiperidinoethane due to in vivo conversion to a selective cholinesterase inhibitor

Bruce M. Baron, Yoel Kashman, Mordechai Sokolovsky*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Dipiperidinoethane (DPE) administration produces seizures and CNS lesions. Here we elucidate the cholinergic origin of DPE toxicity. DPE is both an acetylcholinesterase (AChE) inhibitor and a muscarinic antagonist. This dual action negates most of the toxic effects of the compound in vivo. The neurotoxicity is believed to arise from oxidative conversion to DPE-N-oxide, which selectively inhibits AChE. Cytotoxicity does not involve muscarinic neurons, since binding parameters were unchanged following in vivo exposure.

Original languageEnglish
Pages (from-to)164-167
Number of pages4
JournalBrain Research
Volume331
Issue number1
DOIs
StatePublished - 1 Apr 1985

Keywords

  • cholinergic neurotoxin
  • dipiperidinoethane
  • dipiperidinoethane-N-oxide
  • epileptogenic agent
  • pharmacological action

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