Site-Selective Neurotoxicity (Cellular and Molecular by William Slikker Jr., David S Lester, William Slikker Jr,

By William Slikker Jr., David S Lester, William Slikker Jr, Philip Lazarovici

This distinctive quantity offers interdisciplinary insurance of the mechanistic viewpoint of neurotoxicity that makes a speciality of the location of motion of recognized neurotoxins. It presents the reader with an perception into the typical features of neurotoxin motion at the frightened process and examines websites of motion at 3 degrees of complexity: molecular, mobile, and mind, on the way to permit the improvement of extra particular healing and pharmacological rationales for remedy sooner or later. Site-Selective Neurotoxicity comprises precious details for graduate scholars and educational and business researchers within the fields of toxicology, pharmacology, neurosciences and medicine.

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Extra info for Site-Selective Neurotoxicity (Cellular and Molecular Mechanisms of Toxic Action)

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S. ), Handbook of Neurotoxicology, Vol. 2, Mercel Dekker, New York, pp. 845–870. Bowyer, J. , Davies, D. , Newport, G. , Scallet, A. C. , Jr. (1996) Parenterally administered d-nitropropionic acid and amphetamine can combine to produce damage to terminals and cell bodies in the striatum. , 712, 221–229. , Jenkins, B. , Hyman, B. , Ferrante, R. , Kowall, N. , Roy, D. R. F. (1993) Age-dependent vulnerability of the striatum to the mitochondrial toxin 3-nitropropionic acid. J. , 60, 359–366. , Di Monte, D.

1993). Harmaline has a hyperpolarizing effect on neurons of the inferior olive as well as a direct facilitation of low-threshold calcium conductance in these cells (Llinas, 1991). In addition, harmaline may act on gamma-aminobutyric acid (GABA) receptors that control the electronic coupling among olivary cells (Stratton and Lordon, 1991), thereby enhancing the synchronous rhythmic activity of populations of inferior olive neurons. These effects of olivary activity may then be transmitted to the cerebellar Purkinje cells by the climbing Site-selective action 21 fibers.

Free radicals are a product of the auto-oxidation of catecholamines such as epinephrine and dopamine (Freeman and Crapo, 1982). Arachidonic acid metabolism also generates free radical byproducts (Freeman and Crapo, 1982; Saunders and Horrocks, 1987). Another potential source of free radicals in the central nervous system is the activity of microglia, which like other phagocytic cells release reactive oxygen species when activated (Colton and Gilbert, 1987; Thomas, 1992). Free radical neuropathologies Under normal conditions, the free radicals generated in the central nervous system are well controlled by intrinsic scavenging systems.

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Site-Selective Neurotoxicity (Cellular and Molecular by William Slikker Jr., David S Lester, William Slikker Jr,
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