It also protects nerve cells from the excitotoxic effects of glutamate, aids in energy production within the cells, and helps with glucose metabolism.18 ❋ M.D. Henry Emmons (2010)
The most widely used food ingredients that have excitotoxic activity are monosodium glutamate, aspartame, hydrolyzed vegetable protein, and other additives that stimulate the taste buds and mask the flavor of many processed foods, Fresh, natural foods don't require this form of flavor enhancement. ❋ Unknown (2009)
The artificial sweetener, aspartame, marketed as NutraSweet, Equal, and under several other brand names, is one of most widely consumed of the food additives with excitotoxic activity. ❋ Unknown (2009)
As to artificial sweeteners, they all have their drawbacks: bitter aftertaste, bloating and gas, excitotoxic potential for the brain and nervous system, allergic reactions, etc. ❋ Unknown (2007)
The characteristic punctate distribution of GAD65 along neurites of differentiated cultured hippocampal neurons was significantly reduced after excitotoxic injury, and the total GAD activity measured in extracts from the cerebellum or cerebral cortex at 24h postmortem (when there is a partial cleavage of GADs) was also decreased. ❋ PLoS ONE (2010)
Since calpains, a group of calcium activated proteases, play a key role in GAD65/67 cleavage under excitotoxic conditions the results suggest that GADs are cleaved after ubiquitination and degradation of an unknown binding partner by the proteasome. ❋ PLoS ONE (2010)
We found that excitotoxic stimulation of cultured hippocampal neurons with glutamate leads to a time-dependent cleavage of GAD65 and GAD67 in the N-terminal region of the proteins, and decrease the corresponding mRNAs. ❋ PLoS ONE (2010)
Over 500 products have been investigated for neuroprotective effects including those from the categories of free radical scavengers, anti-excitotoxic agents, apoptosis (programmed cell death) inhibitors, anti-inflammatory agents, neurotrophic factors, metal ion chelators, ion channel modulators and gene therapy. ❋ Unknown (2010)
He testified that he was not attributing the loss of Purkinje cells directly to mercury poisoning, but rather to the excitotoxic effects of mercury. ❋ Kathleen (2010)
Dr. Kinsbourne's hypothesis was based on Dr. Aposhian's opinions about the amount of mercury required to cause the excitotoxic process he proposed. ❋ Kathleen (2010)
The enzyme is cleaved under excitotoxic conditions, but the mechanisms involved and the functional consequences are not fully elucidated. ❋ PLoS ONE (2010)
ASD, the excitotoxic state Dr. Kinsbourne's hypothesis envisioned would produce neuronal death, followed by patient death. ❋ Kathleen (2010)
The new science readily predicts that such drugs are extremely harmful, due to their excitotoxic side effects on glial cell and brain structure, regardless of any learning problems they improve in the short term. ❋ Unknown (2010)
The results show a role of the UPS in the cleavage of GAD65/67 and point out the deregulation of GADs under excitotoxic conditions, which is likely to affect GABAergic neurotransmission. ❋ PLoS ONE (2010)
Primary cultures of cortical neurons do not become sensitized to excitotoxic insult until they have expressed at least a threshold level of NMDA receptors, about 14 DIV ❋ Unknown (2009)
The NO result is especially interesting given that over-stimulation of NMDA receptors via excitotoxic insult has been shown in cortical neurons to increase (via calcium-mediated activation of neuronal nitric oxide synthase (nNOS)) intracellular levels of NO-derived reactive nitrogen species, which potentially can play a role in subsequent cellular damage and death Over-expressed ZEB1 protects primary cortical neurons from a subset of pro-death insults. ❋ Unknown (2009)
All primary cortical cultures were used from 4 to 6 DIV (days in vitro), with the exception of neurons used for excitotoxicity studies, which were cultured for 14-18 DIV before excitotoxic challenge. ❋ Unknown (2009)
"In fact, we chemically blocked inhibitory circuits that unmasked the purely excitotoxic properties of PCB170." ❋ Unknown (2009)
We found that rats with extensive excitotoxic lesions of the hippocampal formation showed a dramatic deficit in acquisition of this task, whereas intact rats were able to learn this task in a few days. ❋ Unknown (2009)
Putkonen N, Mudo G, Pryazhnikov E, Reijonen S, et al. (2007) Endoplasmic reticulum stress inhibition protects against excitotoxic neuronal injury in the rat brain. ❋ Krzysztof Kucharz Et Al. (2009)
