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The Use of AF64A (Ethylcholine Aziridinium Ion) to Model Alzheimer’s Disease

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Toxin-Induced Models of Neurological Disorders

Abstract

Natural and synthetic toxins have been valuable tools for exploring the morphological, biochemical, and molecular correlates of brain function. Compounds that disrupt specific ion channels, axoplasmic transport processes, neuronal populations, or neurotransmitter systems have helped to characterize the fundamental neurobiology of brain cells and the principles of synaptic transmission (McGeer et al., 1987). For example, neurotoxins have been used to (1) identify the steps involved in the synthesis, storage, and release of neurotransmitters, (2) determine how a transmitter interacts with specific receptors and ion channels, (3) examine plasticity of a given brain system and the nature and extent of neural reorganization following its injury, (4) examine the covariation between altered neurotransmitter dynamics and behavior, and finally (5) develop animal models of neurological disorders such as Parkinson’s disease, Huntington’s disease, and temporal lobe epilepsy (Sanberg and Coyle, 1984).

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Walsh, T.J., Opello, K.D. (1994). The Use of AF64A (Ethylcholine Aziridinium Ion) to Model Alzheimer’s Disease. In: Woodruff, M.L., Nonneman, A.J. (eds) Toxin-Induced Models of Neurological Disorders. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1447-7_9

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