PERINATAL HYPOXIA-ISCHEMIA DISRUPTS STRIATAL HIGH-AFFINITY [H-3] GLUTAMATE UPTAKE INTO SYNAPTOSOMES

[1] AMINO-ACIDS AS CENTRAL NERVOUS TRANSMITTERS - INFLUENCE OF IONS, AMINO-ACID ANALOGS, AND ONTOGENY ON TRANSPORT-SYSTEMS FOR L-GLUTAMIC AND L-ASPARTIC ACIDS AND GLYCINE INTO CENTRAL NERVOUS SYNAPTOSOMES OF RAT [J]. JOURNAL OF NEUROCHEMISTRY, 1973, 21 (06) : 1533 - 1550

[2] ELEVATION OF THE EXTRACELLULAR CONCENTRATIONS OF GLUTAMATE AND ASPARTATE IN RAT HIPPOCAMPUS DURING TRANSIENT CEREBRAL-ISCHEMIA MONITORED BY INTRACEREBRAL MICRODIALYSIS [J]. JOURNAL OF NEUROCHEMISTRY, 1984, 43 (05) : 1369 - 1374

[3] BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3

[4] ONTOGENETIC DEVELOPMENT OF KAINATE NEUROTOXICITY - CORRELATES WITH GLUTAMATERGIC INNERVATION [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1978, 75 (04) : 2025 - 2029

[5] Coyle J T, 1977, Int Rev Neurobiol, V20, P65, DOI 10.1016/S0074-7742(08)60651-0

[6] CELLULAR-ORIGIN OF ISCHEMIA-INDUCED GLUTAMATE RELEASE FROM BRAIN-TISSUE INVIVO AND INVITRO [J]. JOURNAL OF NEUROCHEMISTRY, 1985, 45 (01) : 145 - 151

[7] GLUTAMATE - A NEUROTRANSMITTER IN MAMMALIAN BRAIN [J]. JOURNAL OF NEUROCHEMISTRY, 1984, 42 (01) : 1 - 11

[8] GREENAMYRE J T, 1984, Society for Neuroscience Abstracts, V10, P225

[9] ISCHEMIA-INDUCED SHIFT OF INHIBITORY AND EXCITATORY AMINO-ACIDS FROM INTRACELLULAR TO EXTRACELLULAR COMPARTMENTS [J]. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1985, 5 (03) : 413 - 419

[10] NEUROTRANSMITTER AMINO-ACIDS IN THE CNS .2. SOME CHANGES IN AMINO-ACID LEVELS IN RAT-BRAIN SYNAPTOSOMES DURING AND AFTER INVITRO ANOXIA AND SIMULATED ISCHEMIA [J]. BRAIN RESEARCH, 1984, 304 (01) : 23 - 35

[1] AMINO-ACIDS AS CENTRAL NERVOUS TRANSMITTERS - INFLUENCE OF IONS, AMINO-ACID ANALOGS, AND ONTOGENY ON TRANSPORT-SYSTEMS FOR L-GLUTAMIC AND L-ASPARTIC ACIDS AND GLYCINE INTO CENTRAL NERVOUS SYNAPTOSOMES OF RAT [J]. JOURNAL OF NEUROCHEMISTRY, 1973, 21 (06) : 1533 - 1550

[2] ELEVATION OF THE EXTRACELLULAR CONCENTRATIONS OF GLUTAMATE AND ASPARTATE IN RAT HIPPOCAMPUS DURING TRANSIENT CEREBRAL-ISCHEMIA MONITORED BY INTRACEREBRAL MICRODIALYSIS [J]. JOURNAL OF NEUROCHEMISTRY, 1984, 43 (05) : 1369 - 1374

[3] BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3

[4] ONTOGENETIC DEVELOPMENT OF KAINATE NEUROTOXICITY - CORRELATES WITH GLUTAMATERGIC INNERVATION [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1978, 75 (04) : 2025 - 2029

[5] Coyle J T, 1977, Int Rev Neurobiol, V20, P65, DOI 10.1016/S0074-7742(08)60651-0

[6] CELLULAR-ORIGIN OF ISCHEMIA-INDUCED GLUTAMATE RELEASE FROM BRAIN-TISSUE INVIVO AND INVITRO [J]. JOURNAL OF NEUROCHEMISTRY, 1985, 45 (01) : 145 - 151

[7] GLUTAMATE - A NEUROTRANSMITTER IN MAMMALIAN BRAIN [J]. JOURNAL OF NEUROCHEMISTRY, 1984, 42 (01) : 1 - 11

[8] GREENAMYRE J T, 1984, Society for Neuroscience Abstracts, V10, P225

[9] ISCHEMIA-INDUCED SHIFT OF INHIBITORY AND EXCITATORY AMINO-ACIDS FROM INTRACELLULAR TO EXTRACELLULAR COMPARTMENTS [J]. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1985, 5 (03) : 413 - 419

[10] NEUROTRANSMITTER AMINO-ACIDS IN THE CNS .2. SOME CHANGES IN AMINO-ACID LEVELS IN RAT-BRAIN SYNAPTOSOMES DURING AND AFTER INVITRO ANOXIA AND SIMULATED ISCHEMIA [J]. BRAIN RESEARCH, 1984, 304 (01) : 23 - 35