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AF64A

Known as: AF64A-picrylsulfonate 
National Institutes of Health

Related topics

Related topics

1 relation

Broader (1)

ethylcholine aziridinium

Papers overview

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Highly Cited
2012
Highly Cited
2012
Human neural stem cells over-expressing choline acetyltransferase restore cognition in rat model of cognitive dysfunction
Highly Cited
2010
Highly Cited
2010
Piperine, the main alkaloid of Thai black pepper, protects against neurodegeneration and cognitive impairment in animal model of cognitive deficit like condition of Alzheimer's disease.
Highly Cited
2004
Highly Cited
2004
Neuronal gelsolin prevents apoptosis by enhancing actin depolymerization
Highly Cited
2002
Highly Cited
2002
Effects of the destruction of starburst-cholinergic amacrine cells by the toxin AF64A on rabbit retinal directional selectivity
The effects of intraocular injections of ethylcholine mustard aziridinium ion (AF64A), an irreversible inhibitor of choline… 
Review
1988
Review
1988
Animal models of Alzheimer's disease: experimental cholinergic denervation
Highly Cited
1988
Highly Cited
1988
Evidence for dopamine D-2 receptors on cholinergic interneurons in the rat caudate-putamen.
1985
1985
Regional differences in ethylcholine mustard aziridinium ion (AF64A)-induced deficits in presynaptic cholinergic markers for the rat central nervous system.
Several highly selective biochemical markers were used to assess the persistent central cholinergic dysfunction which accompanies… 
Highly Cited
1983
Highly Cited
1983
Selective Presynaptic Cholinergic Neurotoxicity Following Intrahippocampal AF64A Injection in Rats
Abstract: Compound AF64A, ethylcholine mustard aziridinium ion (0.4–8 nmol) was stereotaxically administered into rat dorsal… 
Highly Cited
1982
Highly Cited
1982
Long-term central cholinergic hypofunction induced in mice by ethylcholine aziridinium ion (AF64A) in vivo.
Ethylcholine mustard aziridinium ion (AF64A), a neurotoxic choline analog, was evaluated for its interactions with the… 
Highly Cited
1981
Highly Cited
1981
The AF64a-treated mouse: possible model for central cholinergic hypofunction.
A loss in the number of functional, sodium ion-dependent, high-affinity choline transport sites was observed in the cortex and… 
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