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Potassium-stimulated calcium uptake in astrocytes and its potent inhibition by nimodipine

โœ Scribed by Dr. L. Hertz; A. S. Bender; D. M. Woodbury; H. S. White


Book ID
102908432
Publisher
John Wiley and Sons
Year
1989
Tongue
English
Weight
627 KB
Volume
22
Category
Article
ISSN
0360-4012

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โœฆ Synopsis


Elevation of the extracellular potassium concentration above its "resting" level of 5.4 mM stimulated uptake of 45Ca2+ in primary cultures of astrocytes. This effect was only observed when cells were exposed to excess potassium shortly after their exposure to 45Ca2+ and was potently inhibited (IC5,, -3 nM) by the calcium channel blocker nimodipine. In contrast, nimodipine exerted little effect on unstimulated basal uptake of 45Ca2+. These findings suggest that the therapeutic benefit of calcium channel blockers in epilepsy may result in part from the ability of these drugs to prevent calcium entry into astrocytes during seizures when the extracellular potassium is elevated four-to fivefold above normal.

ing sites for these drugs have been observed in many different brain preparations (Ehlert et al.


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Uptake and release of glycine in cerebel
โœ Dr. I. Holopainen; P. Kontro ๐Ÿ“‚ Article ๐Ÿ“… 1989 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 884 KB

The properties of [3H]glycine uptake and release were studied with cerebellar granule cells, 7-9 days in vitro, (DIV) and astrocytes, 14-15 DIV, in primary cultures. The uptake of glycine in both cell types consisted of a saturable high-affinity transport and nonsaturable diffusion. The transport co