bp(GO:"GO:0051935")

Entity

Name

GO:0051935

Namespace

go

Namespace Version

20180828

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/go.belns

Synaptic glutamate concentration is promptly restored to normal levels, however, through the rapid uptake of unbound glutamate molecules by nearby glial cells, which subsequently convert these glutamate molecules to glutamine. The resulting glutamine molecules are then recycled to the neurons, and the cycle of glutamatergic signaling begins anew PubMed:16273023

In patients with Alzheimer's disease, available evidence points to a disruption in the glutamatergic neurotransmission cycle at the point of glial cell reuptake of free glutamate from the synapse. Neuropathologic studies have documented reduced levels of glutamate reuptake in the frontal and temporal cortices of patients with Alzheimer's disease,10 possibly due to oxidative modification of the glutamate transporter 1 molecule. Furthermore, diminished uptake by vesicular glutamate transporter has been reported in patients with Alzheimer's disease PubMed:16273023

Synaptic glutamate concentration is promptly restored to normal levels, however, through the rapid uptake of unbound glutamate molecules by nearby glial cells, which subsequently convert these glutamate molecules to glutamine. The resulting glutamine molecules are then recycled to the neurons, and the cycle of glutamatergic signaling begins anew PubMed:16273023