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Calbindin-D28K is a constitutive Ca2(+)-binding protein expressed in hippocampal neurons that are resistant to various forms of excitotoxic injury. However, the local factors controlling calbindin-D28K expression within the central nervous system are unknown. We report that neuronal excitation via the perforant path leads to an increased expression of calbindin-D28K mRNA within dentate granule cells. This response is related specifically to stimulation that induces prolonged periods of bursting afterdischarges and precedes cellular injury. The up regulation of calbindin-D28K mRNA occurs during the type of neuronal activation associated with elevated cytosolic Ca2+ and suggests that the maintenance of Ca2+ homeostasis includes a system of feedback control at the level of gene expression.
D H Lowenstein, and
M F Miles, and
F Hatam, and
T McCabe
June 1990,
The Journal of biological chemistry,
D H Lowenstein, and
M F Miles, and
F Hatam, and
T McCabe
January 2002,
Neuroscience,
D H Lowenstein, and
M F Miles, and
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T McCabe
September 1991,
Brain research,
D H Lowenstein, and
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T McCabe
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Annals of the New York Academy of Sciences,
D H Lowenstein, and
M F Miles, and
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October 1991,
Brain research,
D H Lowenstein, and
M F Miles, and
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T McCabe
January 1992,
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D H Lowenstein, and
M F Miles, and
F Hatam, and
T McCabe
October 1995,
Brain research,
D H Lowenstein, and
M F Miles, and
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T McCabe
January 2000,
Pharmacology & toxicology,
D H Lowenstein, and
M F Miles, and
F Hatam, and
T McCabe
January 2001,
Neuroscience,
D H Lowenstein, and
M F Miles, and
F Hatam, and
T McCabe
August 1995,
Journal of neurochemistry,
