Different effects of removing extracellular Ca2+ on cytosolic Ca2+ response to anoxia of sensory neurons and carotid chemoreceptor cells from newborn rabbits.
Jpn J Physiol
; 45(2): 279-89, 1995.
Article
en En
| MEDLINE
| ID: mdl-7563964
ABSTRACT
To study the mechanism of the increases in cytosolic Ca2+ ([Ca2+]i) induced by anoxia, the author examined the effect of removing extracellular Ca2+ on the [Ca2+]i response in cultured nodose ganglion neurons (control) and carotid body glomus cells prepared from newborn rabbits using a fura-2 microfluorimetry. The sensory neurons showed a small increase in [Ca2+]i during anoxia which was not affected by the removal of extracellular Ca2+ or D600. On the other hand, in the chemoreceptor glomus cells, Ca2+ removal eliminated the anoxia-induced large [Ca2+]i increase in 85% of the tested cells (n = 67), and depressed it in the rest. Interestingly, recovery from exposure to an anoxic Ca(2+)-free solution reversibly produced a large and transient rise in [Ca2+]i. The magnitude of this post-anoxic/Ca(2+)-free [Ca2+]i transient correlated with the intensity of the suppression of the [Ca2+]i response to anoxia in Ca(2+)-free solution. Also the [Ca2+]i transient was mostly inhibited by L-type Ca2+ channel blockers (nifedipine and D600), but was not affected by tetrodotoxin. These results suggest that the anoxia-induced large increase in [Ca2+]i were, in most glomus cells, coming from extracellular sources and, in a few cells, from both extracellular sources and from intracellular pools, whereas the slight increase in [Ca2+]i in sensory neurons was probably produced by releasing Ca2+ from intracellular stores. The post-anoxic/Ca(2+)-free [Ca2+]i transient, seen in the chemoreceptor cells alone, may have resulted from modification of the anoxic [Ca2+]i response by Ca2+ removal and involves mostly L-type Ca2+ channels and a few other Ca2+ entry pathways.
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Banco de datos:
MEDLINE
Asunto principal:
Oxígeno
/
Cuerpo Carotídeo
/
Calcio
/
Citosol
/
Neuronas Aferentes
Límite:
Animals
Idioma:
En
Año:
1995
Tipo del documento:
Article