PlumX Metrics
Embed PlumX Metrics

Anoxia-induced hippocampal LTP is regeneratively produced by glutamate and nitric oxide from the neuro-glial-endothelial axis

iScience, ISSN: 2589-0042, Vol: 27, Issue: 4, Page: 109515
2024
  • 2
    Citations
  • 0
    Usage
  • 7
    Captures
  • 15
    Mentions
  • 0
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

Most Recent News

How does Oxygen Depletion Disrupt Memory Formation in the Brain?

Scientists identify a positive molecular feedback loop which could explain stroke-induced memory loss. Ischaemic and haemorrhagic stroke. Credit: Scientific Animations CC4.0 In learning, neurons communicate

Article Description

Transient anoxia causes amnesia and neuronal death. This is attributed to enhanced glutamate release and modeled as anoxia-induced long-term potentiation (aLTP). aLTP is mediated by glutamate receptors and nitric oxide (·NO) and occludes stimulation-induced LTP. We identified a signaling cascade downstream of ·NO leading to glutamate release and a glutamate-·NO loop regeneratively boosting aLTP. aLTP in entothelial ·NO synthase (eNOS)-knockout mice and blocking neuronal NOS (nNOS) activity suggested that both nNOS and eNOS contribute to aLTP. Immunostaining result showed that eNOS is predominantly expressed in vascular endothelia. Transient anoxia induced a long-lasting Ca 2+ elevation in astrocytes that mirrored aLTP. Blocking astrocyte metabolism or depletion of the NMDA receptor ligand D-serine abolished eNOS-dependent aLTP, suggesting that astrocytic Ca 2+ elevation stimulates D-serine release from endfeet to endothelia, thereby releasing ·NO synthesized by eNOS. Thus, the neuro-glial-endothelial axis is involved in long-term enhancement of glutamate release after transient anoxia.

Provide Feedback

Have ideas for a new metric? Would you like to see something else here?Let us know