Aspartate and glutamate induced reductions in extracellular free calcium and sodium concentration in area CA1 of 'in vitro' hippocampal slices of rats.
Extracellular Ca2+ and Na+ were simultaneously measured with ion selective electrodes in the CA1 pyramidal cell layer of rat hippocampal slices. Repetitive stimulation of the Schaffer collateral/commissural fiber system led to decreases in [Ca2+] omicron and [Na+] omicron (delta Ca, delta Na) by up to 0.5 mM and 13 mM, respectively. Iontophoretic application of glutamate or aspartate caused dose-dependent delta Ca of more than 1 mM and delta Na of more than 45 mM. Such ionic alterations were smaller in the presence of GABA or of the Ca2+ antagonists Ni2+ and Mg2+. Ca2+ signals were diminished when evoked in low-Na+ bathing medium and Na+ signals were reduced in Ca2+-free solutions. Thus glutamate- and aspartate-dependent decreases in [Na+] omicron and [Ca2+] omicron appear to be caused by 3 different mechanisms: Na+ movement through amino acid-activated ionophores; Ca2+ movement through selective channels, and Ca2+-dependent Na+ movement.
D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology*; D002118:Calcium / Q000032:analysis*; D005110:Extracellular Space / Q000032:analysis*; D005971:Glutamates / Q000494:pharmacology*; D006624:Hippocampus / Q000032:analysis; D066298:In Vitro Techniques; D051381:Rats / Q000502:physiology*; D012964:Sodium / Q000032:analysis*; D013779:Tetrodotoxin / Q000494:pharmacology
D005971:Glutamates; D001224:Aspartic Acid; D013779:Tetrodotoxin; D012964:Sodium; D002118:Calcium