Chapter 39, Objective 1; “What is an essential amino acid?

T1 - Glutamate and GABA synthesis, release, transport and metabolism as targets for seizure control

T1 - Glutamate synthase and the synthesis of glutamate in plants.

On the instigation of glutamate synthesis by NH+4 addition a significant NAD(P)H oxidation occurs with liver mitochondria but no detectable change occurs with brain mitochondria.

Chapter 39, Objective 8; “What are the products of the catabolism of cysteine?”

How does glutamate acquire the amino groups for this purpose?

The neurotransmitter is formed from glutamate by the action of glutamate decarboxylase. It appears that glutamine serves as the precursor for glutamate, making phosphate-activated glutaminase, an important enzyme for synthesis.

T1 - Anaplerosis for Glutamate Synthesis in the Neonate and in Adulthood

Glutamate is toxic, not in spite of its importance, but because of it . Glutamate mediate a lot of information, included information that regulates brain development and information which determines cellular survival, differentiation and elimination as well as formation and elimination of nerve contacts (synapses). From this ,it follows that glutamate has to be present in the right concentrations in the right places for the right time. Both too much and too little glutamate is harmful. This implies that glutamate is both essential and highly toxic at the same time.

Glutamate is important in the synthesis of urea.


Ammonia and glutamic acid metabolism in brain and liver

Glutamic acid is also implicated in epileptic seizures. Microinjection of glutamic acid into neurons produces spontaneous depolarizations 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.

Glutamate Overload is Slowly Destroying The Minds of …

Chapter 39, Objective 13; “Concerning Homer Sistine...If he had an inborn error in cystathionine synthase, what would happen to his concentrations of methionine, homocysteine, and cysteine?

How to Increase GABA and Balance Glutamate - Holistic Help

If his problem had been a deficiency of folate or vitamin B12 , what would you expect to happen to the concentrations of methionine, homocysteine, and cysteine?

29/12/2017 · Synthesis of Glutama..

Glutamate is of particular interest to neurologists because of its possible involvement in acute or chronic neurodegenerative processes. It is useful to consider three distinct possible mechanisms. One is the possibility that exogenous glutamate, or related compounds acting on glutamate receptors, can be consumed in the diet and damage the brain. Second, there is the possibility that endogenous glutamate released from neurons can contribute to acute neurodegeneration occurring in relation to cerebral ischemia or traumatic brain injury. Third, there is the possibility that activation of glutamate receptors contributes to the process of cell death in chronic neurodegenerative disorders, such as motor neuron disease (MND) or amyotrophic lateral sclerosis (ALS), Huntington’s disease, Parkinson’s disease and Alzheimer’s disease.

Synthesis of glutamate – uphinapsimaticonmafogena

Transporters found in neuronal and glial membranes rapidly remove glutamate from 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 receptor channels, leading to neuronal damage and eventual cell death, and is called . The mechanisms of cell death include damage to mitochondria from excessively high intracellular Ca2+ and 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, autism, some forms of mental retardation, and Alzheimer's disease.