Changes in cytosolic sodium caused by a toxic glutamate treatment of cultured hippocampal neurons.
Changes in cytosolic Na+ ([Na+]i) caused by a toxic glutamate (GLU) or NMDA treatment of cultured hippocampal neurons were monitored by using SBFI fluorescent probe and imaging microscopy. Both GLU and NMDA (50 or 100 microM in Mg(2+)-free solution, 15 min) induced a marked increase in [Na+]i (from 6-8 to 30-45 mM) which persisted after the termination of a treatment. The competitive NMDA antagonist, APV (100 microM) when applied in the post-NMDA period failed to decrease the elevated [Na+]i. The results obtained strongly suggest that the main reason for an impairment of Na+/Ca2+ exchange in the post-glutamate period (see Febs Letters 1993, 324, 271-273) is a reduction of the transmembrane Na+ gradient caused apparently by inhibition of Na(+)-K+ pump.
Pinelis
V G
VG
Institute of Pediatrics, Moscow, Russia.
Segal
M
M
Greenberger
V
V
Khodorov
B I
BI
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D046508:Culture Techniques / Q000379:methods; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D005971:Glutamates / Q000633:toxicity*; D018698:Glutamic Acid; D006624:Hippocampus / Q000378:metabolism*; D007700:Kinetics; D008274:Magnesium / Q000494:pharmacology; D008856:Microscopy, Fluorescence / Q000379:methods; D016202:N-Methylaspartate / Q000633:toxicity; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D009498:Neurotoxins / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism*; D013997:Time Factors; D014701:Veratridine / Q000494:pharmacology
D005971:Glutamates; D009498:Neurotoxins; D018698:Glutamic Acid; D016202:N-Methylaspartate; D014701:Veratridine; D015763:2-Amino-5-phosphonovalerate; D012964:Sodium; D008274:Magnesium; D002118:Calcium