N‐Acetyl‐Aspartyl‐Glutamate: Regional Levels in Rat Brain and the Effects of Brain Lesions as Determined by a New HPLC Method

@article{Koller1984NAcetylAspartylGlutamateRL,
  title={N‐Acetyl‐Aspartyl‐Glutamate: Regional Levels in Rat Brain and the Effects of Brain Lesions as Determined by a New HPLC Method},
  author={Kerry J. Koller and Robert C. Zaczek and Joseph T. Coyle},
  journal={Journal of Neurochemistry},
  year={1984},
  volume={43}
}
Abstract: An isocratic HPLC method to measure endogenous N‐acetyl‐aspartyl‐glutamate (NAAG) and N‐acetyl‐aspartate (NAA) is described. After removal of primary amines by passage of tissue extracts over AG‐50 resin, the eluate was subject to HPLC anion‐exchange analysis and eluted with phosphate buffer with absorbance monitored at 214 nm. The retention time for NAA was 5.6 min and for NAAG 11.4 min with a limit sensitivity of 0.1 nmol. The levels of NAA and NAAG were measured in 16 regions of… 
Hydrolysis of the Brain Dipeptide N‐Acetyl‐l‐Aspartyl‐l‐Glutamate: Subcellular and Regional Distribution, Ontogeny, and the Effect of Lesions on N‐Acetylated‐α‐Linked Acidic Dipeptidase Activity
TLDR
Certain discrepancies in the regional and ontogenetic profiles of NAAG and NAALADase suggest that this relationship is not an exclusive one and may reflect a role for NAALadase on additional N‐acetylated acidic peptides in vivo.
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Endogenous NAAG or [3H]NAAG added to CSF samples were not significantly degraded when the CSF was incubated at 37°C during one hour, suggesting that the peptide is a highly stable metabolite in the subarachnoid space.
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It is suggested strongly that NAA is not a neurotransmitter and the increase of NAA in the ECF immediately after K+ stimulation may reflect an involvement in brain osmoregulation and/or acid‐base homeostasis.
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TLDR
Data suggest the presence in brain of a specific peptidase targeting carboxy‐terminal glutamate‐containing dipeptides that may be coupled to the Na+‐dependent glutamate transporter, which provides a possible mechanism for NAAG inactivation subsequent to its release from nerve endings.
N‐Acetylation of L‐Aspartate in the Nervous System: Differential Distribution of a Specific Enzyme
TLDR
L‐Aspartate N‐ acetyltransferase, a nervous system enzyme that mediates the synthesis of N‐acetyl‐L‐aspartic acid, has been characterized and found to be membrane‐associated and was solubilized by treatment with Triton X‐100.
Neurochemical and Immunocytochemical Studies on the Distribution of N‐Acetyl‐Aspartylglutamate and N‐Acetyl‐Aspartate in Rat Spinal Cord and Some Peripheral Nervous Tissues
TLDR
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The Regional Distribution of N‐Acetylaspartylglutamate (NAAG) and Peptidase Activity Against NAAG in the Rat Nervous System
TLDR
The hypothesis that hydrolysis of NAAG to glutamate and N‐acetylaspartate is a consistent aspect of the physiology and metabolism of this peptide after synaptic release is supported.
Postmortem Degradation of N-Acetyl Aspartate and N-Acetyl Aspartylglutamate: An HPLC Analysis of Different Rat CNS Regions
TLDR
The data show a significant postmortem degradation of NAA and NAAG that needs to be considered when these compounds are studied ex-vivo.
Ontogenesis of N-acetyl-aspartate and N-acetyl-aspartyl-glutamate in rat brain.
TLDR
The results of this study suggest that NAAG is localized in a cell system that matures early and rises steadily from 15 DG to adulthood with a 30-fold increase in whole brain concentration.
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References

SHOWING 1-10 OF 24 REFERENCES
A Gas Chromatographic Method for the Determination of N‐Acetyl‐l‐Aspartic Acid, N‐Acetyl‐α‐ Aspartylglutamic Acid and β‐Citryl‐l‐Glutamic Acid and Their Distributions in the Brain and Other Organs of Various Species of Animals
TLDR
A simple and sensitive gas‐chromatographic method for the determination of N‐acetyl‐l‐aspartic acid (NA‐Asp), N‐ acetyl‐α‐ aspartylglutamic acid ( NA‐AsP‐Glu) and β‐citryl‐ l‐glutamate (β‐CG) was developed and showed a reciprocal relationship in their regional distribution in mature brains.
Characterization of Two [3H]Glutamate Binding Sites in Rat Hippocampal Membranes
TLDR
The relative potencies of a wide range of compounds, with known pharmacological activities, to inhibit [3H]glutamate binding were very different for the Na+‐independent and Na-dependent binding and suggested that the former sites were related to postsynaptic glutamate receptors, whereas the latter wererelated to high‐affinity uptake sites.
Characterization of the interactions of N-acetyl-aspartyl-glutamate with [3H]L-glutamate receptors.
TLDR
The results suggest that N-acetyl-aspartyl-glutamate may play a role as an endogenous excitatory peptide in the mammalian central nervous system and raise the question whether endogenous brain peptides enriched in acidic amino acids may serve as exciteatory transmitters.
N-acetylaspartylglutamate: an endogenous peptide with high affinity for a brain "glutamate" receptor.
TLDR
The peptide exhibits potent convulsant properties when injected into the rat hippocampus, similar to those produced by the glutamate receptor agonist, quisqualic acid, raising the question whether endogenous brain peptides enriched in acidic amino acids may serve as excitatory neurotransmitters.
HIGH AFFINITY l‐[3H]GLUTAMATE BINDING TO POSTSYNAPTIC RECEPTOR SITES ON RAT CEREBELLAR MEMBRANES
TLDR
Comparison of the potencies of a wide range of compounds with known pharmacological activities, demonstrated that their ability to displace specific glutamate binding was consistent with specific interactions with glutamate receptors.
Microinjection of kainic acid into the rat hippocampus.
TLDR
Intrahippocampal injection of kainate may be a useful rodent model for temporal lobe seizure disorders and the synaptosomal high affinity uptake process for [3H]choline and [ 3H]norepinephrine are significantly reduced at 10 days after injection.
Excitatory amino acid analogues: Neurotoxicity and seizures
TLDR
A poor correlation between the neurotoxic and convulsant potencies of these excitatory amino acid analogues is demonstrated and it is suggested that receptor-specific interactions may account for these disparities.
Effects of cortical ablation on the neurotoxicity and receptor binding of kainic acid in striatum
TLDR
The results suggest that afferent input exerts a permissive effect on the neurotoxic action of kainic acid and that neurotoxicity may involve a cooperative interaction between kaini acid at specific receptors on vulnerable neurons and synaptically released endogenous neurotransmitters, in particular L‐glutamic acid.
SUBCELLULAR LOCALIZATION OF N‐ACETYL‐ASPARTYL‐GLUTAMATE, N‐ACETYL‐GLUTAMATE AND GLUTATHIONE IN BRAIN
TLDR
The subcellular distribution of N‐acetyl‐aspartate, N-acetyl-aspartyl‐glutamate, N‐ acetyl‐ glutamate and glutathione (reduced) was investigated in mitochondria and synaptosomal compartments of the cytoplasmatic compartments.
CONTENTS OF SEVERAL AMINO ACIDS IN THE CEREBELLUM, BRAIN STEM AND CEREBRUM OF THE ‘STAGGERER’, ‘WEAVER’ AND ‘NERVOUS’ NEUROLOGICALLY MUTANT MICE 1
TLDR
A possible role for glutamate functioning as an excitatory transmitter when released from the cerebellar granule cells is discussed in terms of a possible roles for GABA and alanine in the cerebrum of the nervous mutants.
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