ArticleFrontiers in neuroscience2022
Ceftriaxone Suppresses Group II Metabotropic Glutamate Receptor Expression Contributing to Reversal of Recognition Memory Deficits of Amyloid Precursor Protein/Presenilin 1 AD Mice.
Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- Impairment of hippocampal long-term potentiation by soluble amyloid-β oligomers is mediated by glutamate transporter 1 expressed in neurons.Neural regeneration research · 2026Article
- Harnessing electroacupuncture: a promising strategy against sleep deprivation-exacerbated post-cardiac arrest brain injury.Scientific reports · 2025Article
- Sulbactam protects neurons against double neurotoxicity of amyloid beta and glutamate load by upregulating glial glutamate transporter 1.Cell death discovery · 2024Article
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6 authors at 1 institution in 1 country.
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Abstract
Group II metabotropic glutamate receptors (Group II mGluRs) are the peri-synaptic receptor of glutamatergic neurons and negatively regulate glutamate release from presynaptic neurons. Glutamate in the synaptic cleft is mainly taken into astrocytes by glutamate transporter-1 (GLT-1), which is primarily expressed in astrocytes. Increasing evidence showed that inhibiting or suppressing the activation of Group II mGluRs would contribute to the improvement of learning and memory deficits in Alzheimer's disease (AD) animal models. Ceftriaxone (Cef) has been reported to alleviate the spatial memory deficits in AD model mice by improving GLT-1-related clearance and metabolism of glutamate. Therefore, the present study further investigates the improving effect of Cef on recognition memory deficits and the involvement of Group II mGluRs in the process using the APP/PS1 AD mouse model. Novel object recognition tests showed that the Cef treatment significantly improved the recognition memory deficits of the AD mice. The Western blot and immunohistochemistry analysis showed that the Cef treatment significantly suppressed the upregulation of Group II mGluRs expression in APP/PS1 AD mice. The above suppression effect of Cef was blocked by dihydrokainic acid, an inhibitor of GLT-1 uptake activity. Furthermore, the Cef treatment significantly restored the downregulation in the downstream molecules of Group II mGluRs activation, including the expression of PKA and phosphorylated SNAP-25 in the APP/PS1 AD mice. The Cef treatment had no effect on the content of Aβ
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