• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Age-Dependent Astroglial Vulnerability to Hypoxia and Glutamate: The Role for Erythropoietin

Violeta

Senior Member
Messages
2,976
I đź’™ this study.

https://pubmed.ncbi.nlm.nih.gov/24124607/

How many of my symptoms are caused by glutamate and hypoxia.
And what came first, the glutamate or the hypoxia?

1712943370652.png
 
Last edited:

Violeta

Senior Member
Messages
2,976

Activation of the gut-brain axis by dietary glutamate and physiologic significance in energy homeostasis


https://pubmed.ncbi.nlm.nih.gov/19587084/#:~:text=l-Glutamate receptors and their,indirectly by these vagal inputs.

l-Glutamate receptors and their cellular transduction molecules have recently been identified in gut epithelial cells. Stimulation of such l-glutamate receptors by luminal l-glutamate activates vagal afferent nerve fibers and then parts of the brain that are targeted directly or indirectly by these vagal inputs.

l-Glutamate is a multifunctional amino acid involved in taste perception, intermediary metabolism, and excitatory neurotransmission. In addition, recent studies have uncovered new roles for l-glutamate in gut-brain axis activation and energy homeostasis.

l-Glutamate receptors and their cellular transduction molecules have recently been identified in gut epithelial cells. Stimulation of such l-glutamate receptors by luminal l-glutamate activates vagal afferent nerve fibers and then parts of the brain that are targeted directly or indirectly by these vagal inputs.

Notably, 3 areas of the brain—the medial preoptic area, the hypothalamic dorsomedial nucleus, and the habenular nucleus—are activated by intragastric l-glutamate but not by glucose or sodium chloride. Furthermore, the chronic, ad libitum ingestion of a palatable solution of monosodium l-glutamate (1% wt:vol) by rats has also been found to reduce weight gain, fat deposition, and plasma leptin concentrations compared with rats that ingest water alone. No difference in food intake was observed. Such effects may also be vagally mediated.

Together, such findings contribute to the growing knowledge base that indicates that l-glutamate signaling via taste and gut l-glutamate receptors may influence multiple physiologic functions, such as thermoregulation and energy homeostasis.

The study focuses on l-glutamate in the diet, not on correct usage in the brain.
 
Last edited:

Violeta

Senior Member
Messages
2,976
Molecular Mechanisms of Glutamate Toxicity in Parkinson’s Disease

https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2020.585584/full

Under pathological conditions, when excessive glutamate is released from the presynaptic membrane or the reuptake function of glutamate is impaired, the extracellular glutamate concentration increases. Activated microglia and reactive astrocytes release large amounts of glutamate (Takeuchi et al., 2006; Wetherington et al., 2008). Too much glutamate induces excessive stimulation of glutamate receptors and increases the concentration of Na+ and Ca2+ in the cell, which may directly cause neuronal damage and cell death. In this way, increased extracellular glutamate concentration is the basis for the effects of glutamate excitotoxicity.

The term “excitatory toxicity” was first proposed in 1986 to describe the ability of excessive extracellular glutamate to kill neurons by activating NMDARs.


This part amazes me.
Although the mechanisms of excitotoxicity have long been studied, there is still a lack of understanding of the intracellular mechanisms of excitotoxicity leading to neuronal death.

This is what I was wondering about: is the glutamate cycle, or whatever you would call it, involved with dopamine.

In PD, dopaminergic information transmitted by dopaminergic neurons decreases,
 

Violeta

Senior Member
Messages
2,976

Glutamatergic Signaling Along The Microbiota-Gut-Brain Axis


https://www.mdpi.com/1422-0067/20/6/1482

Just one thing from this study tonight:

Research in this area opens the possibility to target glutamatergic neurotransmission, either pharmacologically or by the use of probiotics producing neuroactive molecules, as a therapeutic approach for the treatment of gastrointestinal and related psychiatric disorders.