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Título : | The Activity of the Na+/Ca2+ Exchanger Largely Modulates the Ca2+i Signal Induced by Hypo-Osmotic Stress in Rat Cerebellar Astrocytes. The Effect of Osmolarity on Exchange Activity |
Autor : | Rojas, H Ramos, M Benaím, Gustavo Caputo, C DiPolo, R |
Palabras clave : | Na+/Ca2+ exchange hypo-osmotic stress [Ca2+]i release ryanodine receptors cerebellar astrocytes |
Fecha de publicación : | 2008 |
Editorial : | J. Physiol. Sci |
Citación : | Vol. 58, No. 4; |
Resumen : | We recently demonstrated that rat cerebellar Type-1
astrocytes express a very active Na+/Ca2+ exchanger highly colocalized
with ryanodine receptors (RyRs), which in turn play a
key role in glutamate-induced Ca2+ signaling through a calciuminduced
calcium release (CICR) mechanism. In this work we
have explored whether the Na+/Ca2+ exchanger has any role in
the Ca2+
i signal induced by hypo-osmotic stress in these cells,
using microspectrofluorometric measurements with Fura-2,
pharmacological tools, and confocal microscopy image analysis.
We present evidence for the first time that the increase in
[Ca2+]i in rat cerebellar Type-1 astrocytes, resulting from moderate
hypotonic shock, is mediated by Ca2+
release from ryanodine-
operated Ca2+
i stores, and that the magnitude of the intracellular
Ca2+ signal induced by hypotonicity in the short term (up
to 240 s) is small and controlled by the activity of the Na+/Ca2+
exchanger operating in its extrusion mode. With longer times in
the hypotonic medium, intracellular Ca2+ store depletion leads
to Ca2+ entry through store-operated Ca2+ channels. We found it
interesting that the activity of the Na+/Ca2+ exchanger measured
during this reverse mode operation (Ca2+ entry in exchange for
internal Na+) was found to be greatly increased in hypotonic
solutions and decreased in hypertonic ones. The buffering of
the [Ca2+] i rise induced by hypo-osmotic stress may prevent
excessive increases in [Ca2+]i, which otherwise might impair the
normal function of this glial cell. |
URI : | http://hdl.handle.net/10872/4633 |
ISSN : | doi:10.2170/physiolsci.RP009208 |
Aparece en las colecciones: | Artículos Publicados
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