Peer-reviewed veterinary case report
Glutamate buildup and low EAAT2 in dogs with necrotizing
By Pham, Ngoc-Thi et al.·Published in The Journal of veterinary medical science·2008·Department of Veterinary Medical Sciences, Japan·View original on PubMed →
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Original publication title: Impaired expression of excitatory amino acid transporter 2 (EAAT2) and glutamate homeostasis in canine necrotizing meningoencephalitis.
- Species:
- dog
Plain-English summary
A group of dogs with a serious brain condition called necrotizing meningoencephalitis (NME) showed high levels of certain chemicals in their spinal fluid, specifically glutamate and aspartate. These dogs had a problem with a transporter that helps regulate glutamate, which is important for brain function. This imbalance might be linked to the disease's development. Understanding these changes could help veterinarians find better ways to treat NME in dogs.
People also search for: dog brain disease symptoms · necrotizing meningoencephalitis treatment · high glutamate in dogs
Abstract
To clarify the involvement of excitatory and inhibitory amino acids in canine necrotizing meningoencephalitis (NME), glutamate, aspartate, taurine and gamma-aminobutylic acid (GABA) were determined in the cerebrospinal fluids (CSF) from eight NME cases and ten healthy controls. NME dogs exhibited significantly higher concentrations of glutamate and aspartate than those in controls (p<0.001 and p<0.001, respectively), while there was no difference in taurine or GABA between the two groups. When fetal canine astrocytes were cultured for 24 hr in the presence of NME-CSF, supernatant concentrations of glutamate, aspartate and taurine were significantly elevated. Simultaneously, expression of excitatory amino acid transporter 2 (EAAT2) mRNA was significantly reduced in the astrocytes without change in EAAT1 mRNA. Hence, reduced expression of EAAT2 and impaired glutamate homeostasis may contribute to the pathogenesis of NME.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/18981663/