a(CHEBI:"glutamate(1-)")

Entity

Name

glutamate(1-)

Namespace

chebi

Namespace Version

20180828

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/chebi-names.belns

Tau Modifications Sections of NESTOR

In healthy individuals, the glutamatergic neurotransmission cycle begins in the mitochondria of hippocampal neurons, where the enzyme glutaminase catalyzes the conversion of glutamine to glutamate. Next, the vesicular glutamate transporter molecule mediates the packaging of these glutamate molecules into vesicles. Glutamate-containing vesicles are then released from the neuron, resulting in elevated synaptic concentrations of free glutamate, which can transmit neural signals by interacting with glutamatergic receptors on postsynaptic neurons PubMed:16273023

The capacity for thinking and remembering is derived from various input and output pathways between the hippocampus and the neocortex,9 and all such pathways rely on signaling mediated by the neurotransmitter glutamate. PubMed:16273023

The capacity for thinking and remembering is derived from various input and output pathways between the hippocampus and the neocortex,9 and all such pathways rely on signaling mediated by the neurotransmitter glutamate. PubMed:16273023

Primary cortical neurons exposed to the mitochondrial toxin NaN3 (0.1-3 mM) were submitted to oxidative stress with H2O2 (30-150 μM), to mimic conditions observed in neurodegenerative disorders. The effects of such treatment on a series of parameters useful in characterizing neuronal damage were investigated: (i) the basal release of glutamate, evaluated as (3)H-d-Aspartate efflux, was sharply, concentration-dependently, increased; (ii) the phosphorylation status of intracellular markers known to be involved in the neurodegenerative processes, in particular in Alzheimer disease: tau and GSK3β were increased, as well as the protein level of β-secretase (BACE1) and p35/25 evaluated by Western blotting, while (iii) the cell metabolic activity, measured with the MTT method, was reduced, in a concentration- and time-dependent manner. The latter effect, as well as tau hyperphosphorylation, was prevented both by a mixture of antioxidant drugs (100 μM ascorbic acid, 10 μM trolox, 100 μM glutathione) and by the anti-Alzheimer drug, memantine, 20 μM. PubMed:23722080

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

The capacity for thinking and remembering is derived from various input and output pathways between the hippocampus and the neocortex,9 and all such pathways rely on signaling mediated by the neurotransmitter glutamate. PubMed:16273023

The capacity for thinking and remembering is derived from various input and output pathways between the hippocampus and the neocortex,9 and all such pathways rely on signaling mediated by the neurotransmitter glutamate. PubMed:16273023

We demonstrated that the treatment of cultured hippocampal neurons with 125 µM glutamate for 20 min induced the cleavage of p35 to produce the p25 fragment 6 h after glutamate treatment, and the maximal levels of p25 were detected at 12 h (Fig. 1A), which is consistent with a peak in tau hyperphosphorylation (AT8). PubMed:27087442

Additionally, NF-κB activity is also actuated by glutamate- mediated excitatory neurotransmission in the hippocampus, cerebral cortex, and the cerebellar granule cells PubMed:28745240

Glutamate induced stimulation of cerebellar granule cells via the N-methyl-D-aspartate (NMDA) receptor activate p65:p50 dimers and enhance transactivation of pro-apoptotic factors PubMed:25652642

Glutamate induced stimulation of cerebellar granule cells via the N-methyl-D-aspartate (NMDA) receptor activate p65:p50 dimers and enhance transactivation of pro-apoptotic factors PubMed:25652642