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Volume 17, Number 14, Issue of July 15, 1997 pp. 5629-5639
Copyright ©1997 Society for NeuroscienceCalcium Channel Density and Hippocampal Cell Death with Age in Long-Term Culture
Received Jan. 9, 1997; revised May 2, 1997; accepted May 7, 1997.
Nada M. Porter, Olivier Thibault, Véronique Thibault, Kuey-Chu Chen, and Philip W. Landfield University of Kentucky, Department of Pharmacology, College of Medicine, Lexington, Kentucky 40536
The expression of voltage-gated calcium (Ca2+) channel activity in brain cells is known to be important for several aspects of neuronal development. In addition, excessive Ca2+ influx has been linked clearly to neurotoxicity both in vivo and in vitro; however, the temporal relationship between the development of Ca2+ channel activity and neuronal survival is not understood. Over a period spanning 28 d in vitro, progressive increases in high voltage-activated whole-cell Ca2+ current and L-type Ca2+ channel activity were observed in cultured hippocampal neurons. On the basis of single-channel analyses, these increases seem to arise in part from a greater density of functionally available L-type Ca2+ channels. An increase in mRNA for the
1 subunit of L-type Ca2+ channels occurred over a similar time course, which suggests that a change in gene expression may underlie the increased channel density. Parallel studies showed that hippocampal neuronal survival over 28 d was inversely related to increasing Ca2+ current density. Chronic treatment of hippocampal neurons with the L-type Ca2+ channel antagonist nimodipine significantly enhanced survival. Together, these results suggest that age-dependent increases in the density of Ca2+ channels might contribute significantly to declining viability of hippocampal neurons. The results also are analogous to patterns seen in neurons of aged animals and therefore raise the possibility that long-term primary neuronal culture could serve as a model for some aspects of aging changes in hippocampal Ca2+ channel function.
Key words: hippocampal neurons; calcium currents; cell death; cell culture; L-type calcium channels; aging
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