ISSN:
1432-1106
Keywords:
Intracellular free Ca2+
;
Quin2
;
Brain cells
;
Ca2+ channels
;
Excitatory amino acids
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Dispersed brain cells from 12–14 day old mouse embryos were loaded with the Ca2+-sensitive fluorescent probe, quin2 and shown to have a resting intracellular Ca2+ concentration ([Ca2+]i) of 158 nM (SE ± 5) in the presence of 1 mM [Ca2+]o. When external [Ca2+] was raised from 0 to 1 mM there was an increase of [Ca2+]i of 70 nM; with further additions of Ca to 〉10 mM [Ca2+]o the level of [Ca2+]i increased by 〈25 nM. Releasable intracellular Ca2+ stores, estimated from the increase in [Ca2+] produced by 4Br A23187 in the absence of extracellular Ca2+, were 24 fmol/106 cells. A small increase in [Ca2+]i could be produced by the mitochondrial inhibitor, carbonyl cyanide m-chlorophenylhydrazone (CCCP). When extracellular K+ was raised by 10–20 mM, intracellular Ca2+ levels increased from 152 (SE ± 7) to 204 nM (SE ± 10). These K+-induced increases in [Ca2+]i were blocked by verapamil, did not occur in the absence of extracellular Ca2+, and presumably reflect the activation of voltage-dependent Ca2+ channels. N-methyl-D-aspartic acid (NMDA) evoked an increase in [Ca2+]i, while the kainate-like lathyrus sativus neurotoxin, L-3-oxalyl-amino-2aminopropionic acid (L-3,2-OAP) did not; this is consistent with previous observations of different and respectively Ca2+-dependent and -independent mechanisms of action of these excitatory amino acids.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00235975
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