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

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.

• Authors: B M Baron, Y Kashman, M Sokolovsky
• Journal: Brain research (Brain Res) Vol. 331 Issue 1 Pg. 164-7 (Apr 01 1985) ISSN: 0006-8993 [Print] Netherlands
• PMID: 3986560 (Publication Type: Journal Article)

Chemical References

• Cholinesterase Inhibitors
• Convulsants
• Piperidines
• Receptors, Muscarinic
• dipiperidinoethane
• dipiperidinoethane-di-N-oxide

Topics

• Animals
• Brain (drug effects)
• Cerebral Cortex (enzymology)
• Cholinesterase Inhibitors
• Convulsants (pharmacology)
• Oxidation-Reduction
• Piperidines (metabolism, pharmacology)
• Rats
• Receptors, Muscarinic (drug effects)