Abstract：
:Hippocampal slices prepared from adult rats were loaded with fura-2 and the intracellular free Ca2+ concentration ([Ca2+]i) in the CA1 pyramidal cell layer was measured. Hypoxia (oxygen-glucose deprivation) elicited a gradual increase in [Ca2+]i in normal Krebs solution. At high extracellular sodium concentrations ([Na+]o), the hypoxia-induced response was attenuated. In contrast, hypoxia in low [Na+]o elicited a significantly enhanced response. This exaggerated response to hypoxia at a low [Na+]o was reversed by pre-incubation of the slice at a low [Na+]o prior to the hypoxic insult. The attenuation of the response to hypoxia by high [Na+]o was no longer observed in the presence of antagonist to glutamate transporter. However, antagonist to Na+-Ca2+ exchanger only slightly influenced the effects of high [Na+]o. These observations suggest that disturbance of the transmembrane gradient of Na+ concentrations is an important factor in hypoxia-induced neuronal damage and corroborates the participation of the glutamate transporter in hypoxia-induced neuronal injury. In addition, the excess release of glutamate during hypoxia is due to a reversal of Na+-dependent glutamate transporter rather than an exocytotic process.
journal_name
Brain Resjournal_title
Brain researchauthors
Yamaguchi S,Endo K,Kitajima T,Ogata H,Hori Ydoi
10.1016/s0006-8993(98)01037-3subject
Has Abstractpub_date
1998-12-07 00:00:00pages
351-8issue
2eissn
0006-8993issn
1872-6240pii
S0006-8993(98)01037-3journal_volume
813pub_type
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