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Titlebook: Handbook of Neurotoxicity; Richard M. Kostrzewa Reference work 20141st edition Springer Science+Business Media New York 2014

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Reference work 20141st editionpectrum that might produce a dysfunction – akin to a neurotoxin’s effect. The Handbook of Neurotoxicity is thus an instructive and valuable guide towards understanding the role of neurotoxins/neurotoxicity in the expansive field of Neuroscience, andis an indispensable tool for laboratory investigators, neuroscientists, and clinical researchers.
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and valuable guide towards understanding the role of neurotoxins/neurotoxicity in the expansive field of Neuroscience, andis an indispensable tool for laboratory investigators, neuroscientists, and clinical researchers.978-1-4614-5836-4
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RCSN Cell System for Identifying Dopaminergic Neurotoxicitydopaminergic traits, including dopamine production and secretion, and the presence of catecholamine reuptake transporters. Notably, these properties have remained expressed in RCSN-3 cells for decades. This chapter also addresses the contribution of RCSN-3 to dopaminergic-mediated toxic phenomena, i
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Microglia: Neuroprotective and Neurodestructive Propertiesork during development and with repair, and to remove excess and aberrant proteins. Depending on the nature of the response and the physiological function of the microglia, a release of immune-related signaling factors can accompany a morphological change. It was initially thought that the immune-re
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6-Hydroxydopamine Lesioning of Dopamine Neurons in Neonatal and Adult Rats Induces Age-Dependent Connt to clinical symptoms modeled by the 6-OHDA treatment. In this chapter, behavioral, neurochemical, structural, and pharmacological studies carried out in adult and neonatal 6-OHDA-treated rats are reviewed, and findings are compared and contrasted. To date, age-dependent lesioning of DA neurons in
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Dopamine and L-dopa as Selective Endogenous Neurotoxinsating redox cycling with the concomitant depletion of energy and the formation of reactive oxygen species. L-dopa is also neurotoxic in cell cultures after oxidizing to a quinone species, but L-dopa seems to be a transient precursor of dopamine in that it is not able to induce neurotoxicity in vivo
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Nature of DSP-4-Induced Neurotoxicityhological changes of NE neurons with a pronounced decrease in NE levels in the cerebral cortex, hippocampus, spinal cord, and cerebellum. Less affected are the hypothalamus and pons-medulla. This process is not long lasting and after several months a regeneration of NE nerve terminals is observed. D
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