Up-regulation of GLT1 expression increases glutamate uptake and attenuates the Huntington's disease phenotype in the R6/2 mouse
Open accessAbstract
The striatum, which processes cortical information for behavioral output, is a key target of Huntington's disease (HD), an autosomal dominant condition characterized by cognitive decline and progressive loss of motor control. Increasing evidence implicates deficient glutamate uptake caused by a down-regulation of GLT1, the primary astroglial glutamate transporter. To test this hypothesis, we administered ceftriaxone, a beta-lactam antibiotic known to elevate GLT1 expression (200 mg/kg, i.p., for 5 days), to symptomatic R6/2 mice, a widely studied transgenic model of HD. Relative to vehicle, ceftriaxone attenuated several HD behavioral signs: paw clasping and twitching were reduced, while motor flexibility, as measured in a plus maze, and open-field climbing were increased. Assessment of GLT1 expression in striatum confirmed a ceftriaxone-induced increase relative to vehicle. To determine if the change in behavior and GLT1 expression represented a change in striatal glutamate handling, separate groups of behaving mice were evaluated with no-net-flux microdialysis. Vehicle treatment revealed a glutamate uptake deficit in R6/2 mice relative to wild-type controls that was reversed by ceftriaxone. Vehicle-treated animals, however, did not differ in GLT1 expression, suggesting that the glutamate uptake deficit in R6/2 mice reflects dysfunctional rather than missing GLT1. Our results indicate that impaired glutamate uptake is a major factor underlying HD pathophysiology and symptomology. The glutamate uptake deficit, moreover, is present in symptomatic HD mice and reversal of this deficit by up-regulating the functional expression of GLT1 with ceftriaxone attenuates the HD phenotype.
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GLT-1 shows dysfunction or decreased expression in patients with neurodegenerative diseases such as PD, AD, or ALS.
“GLT-1 shows dysfunction or decreased expression in patients with neurodegenerative diseases such as PD [26], AD [27], or ALS [17]”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [17]
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- Authors
- Miller, B. R., Dorner, J. L., Shou, M., Sari, Y., Barton, S. J., Sengelaub, D. R., Kennedy, R. T., & Rebec, G. V.
- Affiliations
- Indiana University Bloomington (US)
- University of Michigan (US)
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2008-04
- Volume
- 153
- Issue
- 1
- Pages
- 329-337
- ISSN
- 0306-4522 (ISSN-L)
- PMC
- PMC2424273
- OpenAlex
- W1978723069
- Cited by
- 280
- References
- 55
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 5 · 2023: 5 · 2022: 9 · 2021: 12 · 2020: 15 · 2019: 13 · 2018: 16 · 2017: 23 · 2016: 19 · 2015: 23 · 2014: 24 · 2013: 22 · 2012: 23
- FWCI
- 8.94
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS035663, R01 NS-35663)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- Huntington's disease, GLT-1, glutamate transporters, glutamate uptake, ceftriaxone, R6/2 mice, striatum, astrocytes, motor impairment, behavioral phenotypes, gene upregulation
- MeSH terms
- Animals, Ceftriaxone, Corpus Striatum, Disease Models, Animal, Huntington Disease, Male, Mice, Transgenic, Synaptic Transmission, Phenotype, Up-Regulation, Glutamic Acid, Maze Learning, Excitatory Amino Acid Transporter 2, Extracellular Fluid, Mice
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