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Brain Res. 1990 Jan 29;508(1):1-6.

Aging-related prolongation of calcium spike duration in rat hippocampal slice neurons.

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Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27103.


Calcium (Ca) spike potentials were investigated in cesium-loaded, tetrodotoxin (TTX)-treated CA1 pyramidal cells in hippocampal slices from young-mature and aged rats. The duration of single Ca spike potentials was prolonged in cells from aged rats, indicating that previously observed age-related changes in Ca-dependent mechanisms (e.g. in the K-mediated afterhyperpolarization and in frequency potentiation) may result from an age-related increase of voltage-dependent Ca conductance. Since we recently found that Ca spike duration in hippocampus can be modulated strongly by a form of Ca-dependent inactivation of Ca current, spike inactivation paradigms also were examined. However, following 5- or 10-s-long depolarizing pulses, or during a 2-Hz train of elicited Ca spikes, there were no age differences in percent inactivation. These results do not support (but do not fully rule out) the possibility that impaired Ca-dependent inactivation underlies the increase in the Ca spike with aging. Conceivably, this prolongation of voltage-dependent Ca influx could have implications for our understanding of normal and abnormal brain aging.

[Indexed for MEDLINE]

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