Inorganic mercury modifies Ca2+ signals, triggers apoptosis and potentiates NMDA toxicity in cerebellar granule neurons
Articolo
Data di Pubblicazione:
1997
Citazione:
Inorganic mercury modifies Ca2+ signals, triggers apoptosis and potentiates NMDA toxicity in cerebellar granule neurons / A.D. Rossi, B. Viviani, B. Zhivotovsky, L. Manzo, S. Orrenius, M. Vahter, P. Nicotera. - In: CELL DEATH AND DIFFERENTIATION. - ISSN 1350-9047. - 4:4(1997), pp. 317-324.
Abstract:
Hg2+ (0.1 microM-0.5 microM) modified the Ca2+ signals elicited by either KCl or the glutamate-receptor agonist, N-methyl-D-aspartate (NMDA), in cerebellar granule cells (CGCs). Hg2+ enhanced the intracellular Ca2+ transient elicited by high K+ and prevented a complete recovery of the resting intracellular Ca2+ concentration ([Ca2+]i) after either KCl or NMDA stimulation. Higher Hg2+ concentrations (up to 1 microM) increased [Ca2+]i directly. Following the short-term exposure to Hg2+, CGCs underwent apoptosis, which was identified by the cleavage of DNA into large (700-50 kbp) and oligonucleosomal DNA fragments, and by the appearance of typical apoptotic nuclei. Combined treatment with 0.1-0.3 microM Hg2+ and a sublethal NMDA concentration (50 microM) potentiated DNA fragmentation and apoptotic cell death. When the exposure to Hg2+ was carried out in Ca2+-free media or in the presence of Ca2+ channel blockers (L-type or NMDA-R antagonists), the effects on signalling and apoptosis were prevented. Our results suggest that very low Hg2+ concentrations can trigger apoptosis in CGCs by facilitating Ca2+ entry through membrane channels.
Tipologia IRIS:
01 - Articolo su periodico
Keywords:
Apoptosis; Calcium; Excitotoxicity; L-type channels
Elenco autori:
A.D. Rossi, B. Viviani, B. Zhivotovsky, L. Manzo, S. Orrenius, M. Vahter, P. Nicotera
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