Related Experiment Video
Updated: Aug 13, 2026
15:08
Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
Published on: October 21, 2017
Trigeminal Nerve Electrical Stimulation Attenuates Hypoxic-Ischemic Brain Injury by Regulating GLT-1-mediated
1Department of Intensive Care Medicine, Xi'an No. 3 Hospital, the Affiliated Hospital of Northwest University, Xi'an, Shaanxi, 710018, China.
Brain Research Bulletin
|August 11, 2026
Summary
Trigeminal nerve stimulation (TNS) offers neuroprotection against neonatal hypoxic-ischemic brain injury (HIBD). TNS enhances glutamate transporter-1 (GLT-1) expression, reducing endoplasmic reticulum stress (ERS) and neuronal damage.
Area of Science:
- Neuroscience
- Neonatal Medicine
- Neurology
Background:
- Neonatal hypoxic-ischemic encephalopathy (HIBD) is a leading cause of infant mortality and disability.
- Understanding the mechanisms of HIBD is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the neuroprotective effects of trigeminal nerve stimulation (TNS) in neonatal HIBD.
- To elucidate the role of glutamate transporter-1 (GLT-1) and endoplasmic reticulum stress (ERS) in TNS-mediated neuroprotection.
Main Methods:
- Rats with induced HIBD were treated with TNS, with or without GLT-1 or PERK inhibitors.
- Cerebral infarct volume and histopathology were assessed.
- Expression of GLT-1 and ERS-related proteins was analyzed via qPCR and Western blotting.
Main Results:
- TNS significantly reduced infarct volume and brain injury in HIBD rats.
- TNS increased hippocampal GLT-1 expression and decreased ERS markers (GRP78, ATF4, CHOP).
- Inhibiting GLT-1 or PERK partially reversed TNS's neuroprotective effects.
Conclusions:
- TNS demonstrates significant neuroprotection in neonatal HIBD.
- The mechanism involves enhanced GLT-1 expression and suppressed ERS.
- TNS represents a potential therapeutic strategy for neonatal HIBD.
