Calcium-dependent release of glutamate from human cerebral cortex.
The release of the excitatory amino acids glutamate and aspartate from human neocortex was investigated in vitro by utilizing brain tissue removed during anterior temporal lobectomies for tumor or epilepsy. Depolarization (50 mM K+) increased the glutamate release to 291% of control (809 pmol/mg/min) during blocked synaptic transmission and to 669% (1859 pmol/mg/min) when synaptic transmission was not blocked. Aspartate release increased to 141% (326 pmol/mg/min) and 178% (412 pmol/mg/min) respectively. The difference between release with and without blocked synaptic transmission was statistically significant only for glutamate (P less than 0.01). These data provides evidence for a Ca(2+)-dependent release of glutamate, supporting a possible role of this amino acid as a neurotransmitter in human neocortex.
Hegstad
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Institute for Surgical Research, Rikshospitalet, National Hospital, University of Oslo, Norway.
Haugstad
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Hauglie-Hanssen
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Langmoen
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D001224:Aspartic Acid / Q000378:metabolism; D002118:Calcium / Q000502:physiology*; D002540:Cerebral Cortex / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D006801:Humans; D066298:In Vitro Techniques; D009407:Nerve Block; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission
D005971:Glutamates; D001224:Aspartic Acid; D018698:Glutamic Acid; D002118:Calcium