Hyper stimulated, Exhausted, Death
<neuroexcitotoxicity>
Like a race horse running until it drops dead.
Toxic nerves from hyper-stimulation:
- Stroke
- tremors
- ALS, Parkinson's
- age related; speech, swallowing, walking problems
Caused by:
- taste enhanced foods, low fat, low sugar
- food additives (glutamates, aspartates), lacking nutrients
- vitamin D supplements (lipid accumulation - LDL-C)
- Eating whole grains, ergotism (alkaloids)
- Excess calcium (TRP - Transient Receptor Potential)
- Corona Virus attachment to vitamin D receptors (ACE2)
Why does Corona Virus want to stimulate the cell?
Viruses cannot replicate on their own
How does Corona virus work?
- Attaches to the lipid vitamin D receptor, sticky oil
- Enslaves the cell
- Stimulates cellular replication through calcium channels for viral gain
- The cell exhausts from over stimulation, dies and the membrane bleeds
<Technical section>
--- Archived from Wikipedia, the free encyclopedia plus [ comments ]
Excitotoxicity
Low Ca2+ buffering and excitotoxicity under physiological stress and pathophysiological conditions in motor neuron (MNs).
[ Motor Neuron, the nerves that operate muscles lose the ability to 'control' calcium. Why? Calcium, one of the nerve and mitochondria simulators, becomes excess and the cell cannot slow down to normal speed; perpetual hyper-stimulation. The cell exhausts while metabolic toxins accumulate. Seen with taste enhanced foods (low fat, low sugar "zero" sugar), loud music, party drugs. Temporary stimulants, in normal food are sodium and potassium (salt) can rinse away but the hard calcium remains with residual stimulation. Further reading: Transient Receptor Potential (TRPs) ]
[ Initally the cell does not die but becomes 'sluggish' and then we constantly 'want' to revisit the stimulation, addiction-like, and crave bread, sugar and soy-like sauces (glutamate rich foods) ]
Low Ca2+ buffering in amyotrophic lateral sclerosis (ALS) vulnerable hypoglossal MNs exposes mitochondria to higher Ca2+ loads compared to highly buffered cells.
[ Mitochondria are regulated by calcium levels. Age related decline can be measured in mitochondria dysfunction ]
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Calcium, ATP, and ROS: a mitochondrial love-hate triangle.
[ ROS - Reactive Oxygen Species; see: Nitric Oxide - NO- ]
Brookes PS1, Yoon Y, Robotham JL, Anders MW, Sheu SS.
Abstract
The mitochondrion is at the core of cellular energy metabolism, being the site of most ATP generation. Calcium is a key regulator of mitochondrial function and acts at several levels within the organelle to stimulate ATP synthesis. However, the dysregulation of mitochondrial Ca(2+) homeostasis is now recognized to play a key role in several pathologies. For example, mitochondrial matrix Ca(2+) overload can lead to enhanced generation of reactive oxygen species, triggering of the permeability transition pore, and cytochrome c release, leading to apoptosis. Despite progress regarding the independent roles of both Ca(2+) and mitochondrial dysfunction in disease, the molecular mechanisms by which Ca(2+) can elicit mitochondrial dysfunction remain elusive. This review highlights the delicate balance between the positive and negative effects of Ca(2+) and the signaling events that perturb this balance. Overall, a "two-hit" hypothesis is developed, in which Ca(2+) plus another pathological stimulus can bring about mitochondrial dysfunction.
- PMID:15355853
- DOI:10.1152/ajpcell.00139.2004
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Under normal physiological conditions, the neurotransmitter opens glutamate, NMDA and AMPA receptor channels, and voltage dependent Ca2+ channels (VDCC) with high glutamate release, which is taken up again by EAAT1 and EAAT2.
This results in a small rise in intracellular calcium that can be buffered in the cell.
In ALS, a disorder in the glutamate receptor channels leads to high calcium conductivity, resulting in high Ca2+ loads and increased risk for mitochondrial damage. [ low fat foods have additional amounts of glutamates to give the 'savory' or 'meat' taste by stimulation the tongue nerves. The Liver attempts to remove excess glutamates with the SGOT/AST enzyme, but when it fails to keep up we have uncontrolable nerve stimulation and nerve death - ALS ]
This triggers the mitochondrial production of reactive oxygen species (ROS), which then inhibit glial EAAT2 function. This leads to further increases in the glutamate concentration at the synapse and further rises in postsynaptic calcium levels, contributing to the selective vulnerability of MNs in ALS. Jaiswal et al., 2009.[1]
Excitotoxicity is the pathological process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This occurs when receptors for the excitatory neurotransmitter glutamate (glutamate receptors) such as the NMDA receptor and AMPA receptor are overactivated by glutamatergic storm. Excitotoxins like NMDA and kainic acid which bind to these receptors, as well as pathologically high levels of glutamate, can cause excitotoxicity by allowing high levels of calcium ions (Ca2+) to enter the cell.[1][2] Ca2+ influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA.
Excitotoxicity may be involved in spinal cord injury, stroke, traumatic brain injury, hearing loss (through noise overexposure or ototoxicity), and in neurodegenerative diseases of the central nervous system (CNS) such as multiple sclerosis, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Parkinson's disease, alcoholism, alcohol withdrawal or hyperammonemia and especially over-rapid benzodiazepine withdrawal, and also Huntington's disease.[3][4] Other common conditions that cause excessive glutamate concentrations around neurons are hypoglycemia. Blood sugars are the primary glutamate removal method from inter-synaptic spaces at the NMDA and AMPA receptor site. Persons in excitotoxic shock must never fall into hypoglycemia. Patients should be given 5% glucose (dextrose) IV drip during excitotoxic shock to avoid a dangerous build up of glutamate around NMDA and AMPA neurons[citation needed]. When 5% glucose (dextrose) IV drip is not available high levels of fructose are given orally. Treatment is administered during the acute stages of excitotoxic shock along with glutamate antagonists. Dehydration should be avoided as this also contributes to the concentrations of glutamate in the inter-synaptic cleft[5] and "status epilepticus can also be triggered by a build up of glutamate around inter-synaptic neurons."[6]