L-glutamate can affect the release of [3H]DA by absorbing glutamate at the presynaptic level. Even with 0.5 μM of tetrodotoxin present, 50 μM of L-glutamic acid can still induce the release of [3H]DA [1].

Absorption, Distribution and Excretion
Absorbed from the lumen of the small intestine into the enterocytes.Absorption is efficient and occurs by an active transport mechanism.
/MILK/ Previous short observational studies on the free amino acid (FAA) content of human milk have shown that glutamine and glutamic acid increase in the first 4 to 6 weeks of life. Changes in human milk content of free amino acids (FAAs) was determined at colostrum, 1 month, and 3 months of lactation in 16 healthy lactating women after delivery of full-term infants. Milk was collected at the end of each feeding (hindmilk) during 24 hours. Glutamic acid and taurine were the most abundant FAAs at colostrum. Although taurine remained stable throughout lactation, glutamic acid (the prevalent FAA) and glutamine increased approximately 2.5 and 20 times, respectively, with progressing lactation representing more than 50% of total FAA at 3 months. The content of essential FAA was also stable, so the change in total FAA content was almost entirely due to the changes in glutamic acid and glutamine. Breast-fed infants are supplied with progressively increasing amounts of glutamine and glutamic acid throughout lactation. The increasing intake of glutamic acid and glutamine could benefit breast-fed infants with molecules that are likely to protect the enteral mucosa and act as neurotransmitters and as a source of nitrogen.
In this report, (13)N -labeled L-glutamine and L-glutamic acid was synthesized by an enzymatic method ... . Organ distribution studies and whole body scans in mongrel dogs demonstrated low myocardial uptake of glutamine and glutamic acid and that the liver demonstrated a greater uptake of glutamine than glutamic acid or ammonia.
The measurement of the intestinal metabolism of the nitrogen moiety of glutamic acid has been investigated by oral ingestion of l-[(15)N]glutamic acid and sampling of arterialized blood. Measurements have been made in six normal adults weighing an average of 72.8 kg ingesting 100 mg of l-[(15)N]glutamic acid after an overnight fast. Measurement of the enrichment of arterial glutamic acid, glutamine and alanine was by gas chromatography-mass spectrometry. Isotopic enrichment of the amino acids was followed for 150 min after the ingestion of the amino acid. Arterialized venous blood amino acid concentrations, measured by HPLC, demonstrated no significant changes during the course of the experiment. From the observed appearance of label in arterialized glutamic acid, alanine and glutamine, little luminal glutamic acid reaches the extracellular pool. The majority of the administered nitrogen label appears in the arterial alanine and glutamine components.

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Metabolism / Metabolites
Hepatic
Cortical excitability reflects a balance between excitation and inhibition. Glutamate is the main excitatory and GABA the main inhibitory neurotransmitter in the mammalian cortex. Changes in glutamate and GABA metabolism may play important roles in the control of cortical excitability. Glutamate is the metabolic precursor of GABA, which can be recycled through the tricarboxylic acid cycle to synthesize glutamate. GABA synthesis is unique among neurotransmitters, having two separate isoforms of the rate-controlling enzyme, glutamic acid decarboxylase. The need for two separate genes on two chromosomes to control GABA synthesis is unexplained. Two metabolites of GABA are present in uniquely high concentrations in the human brain. Homocarnosine and pyrrolidinone have a major impact on GABA metabolism in the human brain. Both of these GABA metabolites have anticonvulsant properties and can have a major impact on cortical excitability. /Glutamate, GABA/
The measurement of the intestinal metabolism of the nitrogen moiety of glutamic acid has been investigated by oral ingestion of l-[(15)N]glutamic acid and sampling of arterialized blood. Measurements have been made in six normal adults weighing an average of 72.8 kg ingesting 100 mg of l-[(15)N]glutamic acid after an overnight fast. Measurement of the enrichment of arterial glutamic acid, glutamine and alanine was by gas chromatography-mass spectrometry. Isotopic enrichment of the amino acids was followed for 150 min after the ingestion of the amino acid. Arterialized venous blood amino acid concentrations, measured by HPLC, demonstrated no significant changes during the course of the experiment. From the observed appearance of label in arterialized glutamic acid, alanine and glutamine, little luminal glutamic acid reaches the extracellular pool. The majority of the administered nitrogen label appears in the arterial alanine and glutamine components.
Hepatic

[1]. Giorguieff MF, et al. Presynaptic effect of L-glutamic acid on the release of dopamine in rat striatal slices. Neurosci Lett. 1977 Oct;6(1):73-7.

L-glutamic acid is an optically active form of glutamic acid having L-configuration. It has a role as a nutraceutical, a micronutrient, an Escherichia coli metabolite, a mouse metabolite, a ferroptosis inducer and a neurotransmitter. It is a glutamine family amino acid, a proteinogenic amino acid, a glutamic acid and a L-alpha-amino acid. It is a conjugate acid of a L-glutamate(1-). It is an enantiomer of a D-glutamic acid.
A peptide that is a homopolymer of glutamic acid.
L-Glutamate is a metabolite found in or produced by Escherichia coli (strain K12, MG1655).
L-Glutamic acid is a metabolite found in or produced by Escherichia coli (strain K12, MG1655).
Glutamic Acid has been reported in Streptomyces akiyoshiensis, Pinus densiflora, and other organisms with data available.
Glutamic Acid is a non-essential alpha-amino acid and excitatory neurotransmitter. Glutamic acid can serve as a precursor for the synthesis of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA).
Glutamic acid (Glu), also referred to as glutamate (the anion), is one of the 20 proteinogenic amino acids. It is not among the essential amino acids. Glutamate is a key molecule in cellular metabolism. In humans, dietary proteins are broken down by digestion into amino acids, which serves as metabolic fuel or other functional roles in the body. Glutamate is the most abundant fast excitatory neurotransmitter in the mammalian nervous system. At chemical synapses, glutamate is stored in vesicles. Nerve impulses trigger release of glutamate from the pre-synaptic cell. In the opposing post-synaptic cell, glutamate receptors, such as the NMDA receptor, bind glutamate and are activated. Because of its role in synaptic plasticity, it is believed that glutamic acid is involved in cognitive functions like learning and memory in the brain. Glutamate transporters are found in neuronal and glial membranes. They rapidly remove glutamate from the extracellular space. In brain injury or disease, they can work in reverse and excess glutamate can accumulate outside cells. This process causes calcium ions to enter cells via NMDA receptor channels, leading to neuronal damage and eventual cell death, and is called excitotoxicity. The mechanisms of cell death include: * Damage to mitochondria from excessively high intracellular Ca2+. * Glu/Ca2+-mediated promotion of transcription factors for pro-apoptotic genes, or downregulation of transcription factors for anti-apoptotic genes. Excitotoxicity due to glutamate occurs as part of the ischemic cascade and is associated with stroke and diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease. glutamic acid has been implicated in epileptic seizures. Microinjection of glutamic acid into neurons produces spontaneous depolarization around one second apart, and this firing pattern is similar to what is known as paroxysmal depolarizing shift in epileptic attacks. This change in the resting membrane potential at seizure foci could cause spontaneous opening of voltage activated calcium channels, leading to glutamic acid release and further depolarization.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
See also: Monosodium Glutamate (active moiety of); Glutamic Acid Hydrochloride (has salt form); Glatiramer Acetate (monomer of) ... View More ...

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Drug Indication
Considered to be nature's "Brain food" by improving mental capacities; helps speed the healing of ulcers; gives a "lift" from fatigue; helps control alcoholism, schizophrenia and the craving for sugar.

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Mechanism of Action
Glutamate activates both ionotropic and metabotropic glutamate receptors. The ionotropic ones being non-NMDA (AMPA and kainate) and NMDA receptors. Free glutamic acid cannot cross the blood-brain barrier in appreciable quantities; instead it is converted into L-glutamine, which the brain uses for fuel and protein synthesis. It is conjectured that glutamate is involved in cognitive functions like learning and memory in the brain, though excessive amounts may cause neuronal damage associated in diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease. Also, the drug phencyclidine (more commonly known as PCP) antagonizes glutamate at the NMDA receptor, causing behavior reminiscent of schizophrenia. Glutamate in action is extremely difficult to study due to its transient nature.

C5H9NO4

147.1293

147.053

56-86-0

L-Glutamic acid monosodium salt;142-47-2;L-Glutamic acid-1-13C;81201-99-2;L-Glutamic acid-15N;21160-87-2;L-Glutamic acid-13C5,15N;202468-31-3;L-Glutamic acid-13C5;55443-55-5;L-Glutamic acid-d5;2784-50-1;L-Glutamic acid-d3;203805-84-9;L-Glutamic acid-13C;115473-51-3;L-Glutamic acid-13C2;115473-56-8;L-Glutamic acid-13C5,15N,d5;1420815-74-2;L-Glutamic acid-5-13C;81202-00-8;L-Glutamic acid-15N,d5

33032

White to off-white solid powder

1.4±0.1 g/cm3

333.8±32.0 °C at 760 mmHg

205 °C (dec.)(lit.)

155.7±25.1 °C

0.0±1.5 mmHg at 25°C

1.522

-1.43

3

5

4

10

145

1

C(CC(=O)O)[C@@H](C(=O)O)N

WHUUTDBJXJRKMK-VKHMYHEASA-N

InChI=1S/C5H9NO4/c6-3(5(9)10)1-2-4(7)8/h3H,1-2,6H2,(H,7,8)(H,9,10)/t3-/m0/s1

(2S)-2-aminopentanedioic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~6.25 mg/mL (~42.48 mM)
DMSO :< 1 mg/mL

Solubility in Formulation 1: 9.09 mg/mL (61.78 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication (<60°C).

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 (Please use freshly prepared in vivo formulations for optimal results.)