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Gene Transfer of Calbindin D 28k cDNA via Herpes Simplex Virus Amplicon Vector Decreases Cytoplasmic Calcium Ion Response and Enhances Neuronal Survival Following Glutamatergic Challenge but Not Following Cyanide
Author(s) -
Meier Timothy J.,
Ho Dora Y.,
Park Travis S.,
Sapolsky Robert M.
Publication year - 1998
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1998.71031013.x
Subject(s) - herpes simplex virus , glutamatergic , calbindin , amplicon , calcium , complementary dna , biology , cyanide , virology , chemistry , microbiology and biotechnology , gene , virus , biochemistry , glutamate receptor , polymerase chain reaction , receptor , inorganic chemistry , organic chemistry
Excitatory amino acid overstimulation of neurons can lead to a marked rise in cytoplasmic Ca 2+ concentration ([Ca 2+ ]) i ) and be followed by neuron death from hours to days later. If the rise in [Ca 2+ ] i is prevented, either by removing Ca 2+ from the extracellular environment or by placing Ca 2+ chelators in the cytosol of the stimulated cells, the neurotoxicity associated with excitotoxins can be ameliorated. We have recently shown that neurons infected with a herpes simplex virus amplicon vector expressing cDNA for calbindin D 28k responded to hypoglycemia with decreased [Ca 2+ ] i and increased survival relative to controls. We now report that vector‐infected neurons respond to glutamatergic insults with lower [Ca 2+ ] i than controls and with increased survival. Infected neurons exposed to sodium cyanide did not respond with lower [Ca 2+ ] i than controls, nor did they demonstrate increased survival postinsult. We examine these results in light of our earlier report and in the context of the potential of vectors like this for neuronal gene therapy.