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Science 31 July 1981:
Vol. 213. no. 4507, pp. 579 - 580
DOI: 10.1126/science.6894649

Articles

Science, Vol 213, Issue 4507, 579-580
Copyright © 1981 by American Association for the Advancement of Science


articles

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

CR Mantione, A Fisher, and I Hanin

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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