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PubMed · 6894649

The AF64a-treated mouse: possible model for central cholinergic hypofunction.

C R Mantione·A Fisher·I Hanin
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Abstract

A loss in the number of functional, sodium ion-dependent, high-affinity choline transport sites was observed in the cortex and hippocampus of mice given an intracerebroventricular injection of 65 nanomoles of AF64A (ethylcholine mustard aziridinium ion) 3 days earlier. Such an effect was not observed in the striatum. This effect of AF64A represents a long-term neurochemical deficit at cholinergic nerve terminals in some brain regions which can lead to a persistent deficiency in central cholinergic transmission. The AF64A-treated animal may thus be a model for certain psychiatric or neurological disorders that appear to involve central cholinergic hypofunction.

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AnimalsAziridinesAzirinesBiological TransportBrainCerebral CortexCholineCorpus StriatumHippocampusKineticsMiceSodiumSynaptosomesJournal ArticleResearch Support, U.S. Gov't, P.H.S.

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C R Mantione, A Fisher, I Hanin. 1981-07-31. The AF64a-treated mouse: possible model for central cholinergic hypofunction.. https://doi.org/10.1126/science.6894649

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