cell type, specific neurotransmitter (via selective uptake channel), pharmacological and immunological targeting of identified receptors, or disruption of subcellular metabolic cell processes. These then provide powerful tools for making selective manipulations as the independent variable in physiological, pharmacological, and behavioral analyzes of normal and abnormal brain function in health and disease. Nevertheless, while most available toxins are effective in reproducing particular profiles of cell loss and features of cellular and subcellular pathology of the corresponding human disease, they frequently do not reproduce the neuropathogenic process accurately, and the lesions are typically acute rather than slowly progressive as is characteristic of most human neurodegenerative diseases. Consequently, neurotoxin-based lesions can provide effective models to study functional organization in the nervous system and have value for evaluating symptomatic and reparative approaches to treatment. However, such lesions are less suitable for the experimental analysis of neuropro-tective processes and for the development of therapeutic strategies to alter or reverse the progressive course of disease. For such applications, alternative genetic models are increasingly considered preferable.
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