By Hyman M. Schipper
256 pages, sixty seven figures, 6 tables, hardcover This monograph is the 1st of its sort to concentration particularly at the function of astroglia in aging-related human neurodegenerative problems and experimental types of CNS senescence and degeneration. As such, this quantity within the Neuroscience Intelligence Unit sequence represents a singular and critical contribution to the elemental and medical neuroscience literature. The chapters are grouped into 3 sections: I. Biology of Astrocytes. The chapters during this part will represent a entire dialogue of the recognized features of astroglia within the mammalian CNS and the jobs those cells may possibly play within the pathophysiology of neurological issues. II. Astrocytes in Human mind Senescence and Neurodegenerative problems. during this part, the pathology of astrocytes and their putative roles in human CNS senescence and numerous neurodegenerative stipulations are coated in substantial aspect. III. Experimental versions of Astrocyte Senescence: Implications for Neurodegenerative ! disorder. during this ultimate part, experimental ways to the delineation of the position of astroglia in mind getting older and degeneration are defined. This booklet should still allure generally to uncomplicated neuroscientists drawn to a number of features of the biology of those cells in addition to to clinically-oriented investigators inquisitive about the pathogenesis of the most important human neurodegenerative issues.
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Additional resources for Astrocytes in Brain Aging and Neurodegeneration
Uptake of the EAAs is likely to be slower than needed to alter synaptic transmission and therefore is more likely to serve for long term control. 71 This increase in steady state glutamate levels could be due to a decreased conversion to glutamine within astrocytes, leading to a large increase in glutamate which more than offsets the increased release. 72-75 The GLT-1 is the major form in rat brain. GLT-1 and GLAST coexist on the same astrocyte membranes, but do not form complexes with each other.
A novel ATP-dependent inward rectifier potassium channel expressed predominantly in glial cells. J Biol Chem 1995; 270:16339-16346. 32 Astrocytes in Brain Aging and Neurodegeneration 17. Newman EA. High potassium conductance in astrocyte endfeet. Science 1986; 233:453-454. 18. Roy ML, Sontheimer H. β-adrenergic modulation of glial inwardly rectifying potassium channels. J Neurochem 1995; 64:1576-1584. 19. Robert A, Magistretti PJ. AMPA/kainate receptor activation blocks K+ currents via internal Na+ increase in mouse cultured stellate astrocytes.
Techniques used to measure these responses have been mainly electrophysiological, or calcium imaging with confocal microscopy. 108 However, slice studies do present several difficulties. An important one is secondary effects on astrocytes due to the release of neurotransmitters or K+ from neurons stimulated by the applied transmitters. TTX used in slice studies can only block action potential-induced terminal release of neurotransmitters and not transmitter release induced by TTXinsensitive action potentials or extrasynaptic release from dendrites or axons.