TY - JOUR
T1 - Neurotoxicity of dipiperidinoethane due to in vivo conversion to a selective cholinesterase inhibitor
AU - Baron, Bruce M.
AU - Kashman, Yoel
AU - Sokolovsky, Mordechai
PY - 1985/4/1
Y1 - 1985/4/1
N2 - 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.
AB - 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.
KW - cholinergic neurotoxin
KW - dipiperidinoethane
KW - dipiperidinoethane-N-oxide
KW - epileptogenic agent
KW - pharmacological action
UR - http://www.scopus.com/inward/record.url?scp=0021956595&partnerID=8YFLogxK
U2 - 10.1016/0006-8993(85)90728-0
DO - 10.1016/0006-8993(85)90728-0
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AN - SCOPUS:0021956595
SN - 0006-8993
VL - 331
SP - 164
EP - 167
JO - Brain Research
JF - Brain Research
IS - 1
ER -