Excitatory Amino Acid Receptors and Depolarization‐Induced Ca2+ Influx into Hippocampal Slices

@article{Crowder1987ExcitatoryAA,
  title={Excitatory Amino Acid Receptors and Depolarization‐Induced Ca2+ Influx into Hippocampal Slices},
  author={Janet M. Crowder and Martin J. Croucher and Henry F. Bradford and James F. Collins},
  journal={Journal of Neurochemistry},
  year={1987},
  volume={48}
}
Abstract: Hippocampal brain slices were incubated with depolarizing agents or excitatory amino acids either alone or in the presence of excitatory amino acid antagonists [ω‐phosphonic α‐aminocarboxylic acids—2‐amino‐4‐phosphonobutyric acid (AP4), 2‐amino‐5‐phosphonovaleric acid (AP5), or 2‐amino‐7‐phosphonoheptanoic acid (AP7)—or γ‐D‐glutamylaminomethylsulphonic acid (GAMS)] or a calcium‐channel blocker, (S)‐1‐(3‐methoxyphenyl)‐3‐methylaza‐7‐cyano‐7‐ (3,4‐dimethoxyphenyl)‐8‐methyl‐nonane… 
Autoreceptor Regulation of Glutamate and Aspartate Release from Slices of the Hippocampal CA1 Area
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TLDR
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TLDR
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TLDR
The results suggest that the anti‐excitotoxic action of 2‐chloroado is mediated primarily through a specific presynaptic receptor mechanism involving reduction of transmitter glutamate release, possibly occurring through an inhibition of Ca2+ influx.
Glutamate Neurotoxicity and the Inhibition of Protein Synthesis in the Hippocampal Slice
TLDR
It is observed with a brain slice preparation that only high concentrations of glutamate caused neurotoxicity in the presence of oxygen and glucose and that these effects were not reversed by glutamate receptor antagonists, suggesting that glutamate released during ischemia causes injury by activating NMDA receptors.
Glutamate receptor-induced 45Ca2+ accumulation in cortical cell culture correlates with subsequent neuronal degeneration
TLDR
With brief exposure, high concentrations of AMPA, kainate, or K+ produced much less death or 45Ca2+ accumulation than produced by glutamate, especially if 10 microM MK-801 was included in the exposure medium to block NMDA receptor activation.
Optical Imaging of Hippocampal Neurons with a Chloride‐Sensitive Dye: Early Effects of In Vitro Ischemia
TLDR
Mild ischemia induces the accumulation of [Cl−]i secondary to GABAA receptor activation, in the absence of cellular swelling or death, as indicated by the volume‐sensitive dye calcein.
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TLDR
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