By Hyman M., Ed. Schipper
256 pages, sixty seven figures, 6 tables, hardcover This monograph is the 1st of its type to concentration particularly at the position 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 scientific neuroscience literature. The chapters are grouped into 3 sections: I. Biology of Astrocytes. The chapters during this part will represent a finished dialogue of the identified services of astroglia within the mammalian CNS and the jobs those cells may well play within the pathophysiology of neurological issues. II. Astrocytes in Human mind Senescence and Neurodegenerative issues. during this part, the pathology of astrocytes and their putative roles in human CNS senescence and diverse neurodegenerative stipulations are coated in significant aspect. III. Experimental versions of Astrocyte Senescence: Implications for Neurodegenerative ! disorder. during this ultimate part, experimental ways to the delineation of the function of astroglia in mind getting older and degeneration are defined. This publication may still allure largely to easy neuroscientists drawn to a variety of elements of the biology of those cells in addition to to clinically-oriented investigators excited by the pathogenesis of the main human neurodegenerative issues.
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Additional info for Astrocytes in Brain Aging and Neurodegeneration (Neuroscience Intelligence Unit 3)
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. The calcium responses to iGluR agonists (KA, AMPA, NMDA) found in astrocytes in hippocampal slices, but not in our acutely isolated hippocampal astrocytes, could be due to the depolarization of astrocytes by K+ released from excited neurons, which then activate voltage-activated Ca2+ channels leading to [Ca2+]i increases in astrocytes.
Thus, with a [K+]o of around 3 mM there will only be a small amount of activation between 3 and 10 mM K+, the saturation level for K+ activation of the Na+/K+ pump, while with a Km for Na+i of ~ 10 mM and [Na+]i ≅ 10 mM14 the pump is poised to be maximally activated by increases or decreases in [Na+]i from its normal levels. Sontheimer et al52,25 found that some astrocytes have a high density of TTX-sensitive Na+ channels, and suggested that these channels are responsible for maintaining the intracellular Na+ levels required for the functioning of the Na+/K+ pump.
Zalc B, Collet A, Monge M et al. Tamm-Horsfall protein, a kidney marker is expressed on brain sulfogalactosylceramide-positive astroglial structures. Brain Res 1984; 291:182-187. Functions of Astrocytes 33 45. Kettenmann H, Bormann J. Patch-clamp study of gamma-aminobutyric acid receptor Cl– channels in cultured astrocytes. Proc Natl Acad Sci U S A 1988; 85:9336-9340. 46. Kimelberg HK, Frangakis MV. Furosemide- and bumetanide-sensitive ion transport and volume control in primary astrocyte cultures from rat brain.