Ceftriaxone increases glutamate uptake and reduces striatal tyrosine hydroxylase loss in 6-OHDA Parkinson's model
Open accessAbstract
Excess glutamatergic neurotransmission may contribute to excitotoxic loss of nigrostriatal neurons in Parkinson's disease (PD). Here, we determined if increasing glutamate uptake could reduce the extent of tyrosine hydroxylase (TH) loss in PD progression. The beta-lactam antibiotic, ceftriaxone, increases the expression of glutamate transporter 1 (GLT-1), a glutamate transporter that plays a major role in glutamate clearance in central nervous system and may attenuate adverse behavioral or neurobiological function in other neurodegenerative disease models. In association with >80% TH loss, we observed a significant decrease in glutamate uptake in the established 6-hydroxydopamine (6-OHDA) PD model. Ceftriaxone (200 mg/kg, i.p.) increased striatal glutamate uptake with >5 consecutive days of injection in nonlesioned rats and lasted out to 14 days postinjection, a time beyond that required for 6-OHDA to produce >70% TH loss (∼9 days). When ceftriaxone was given at the time of 6-OHDA, TH loss was ∼57% compared to ∼85% in temporally matched vehicle-injected controls and amphetamine-induced rotation was reduced about 2-fold. This attenuation of TH loss was associated with increased glutamate uptake, increased GLT-1 expression, and reduced Serine 19 TH phosphorylation, a calcium-dependent target specific for nigrostriatal neurons. These results reveal that glutamate uptake can be targeted in a PD model, decrease the rate of TH loss in a calcium-dependent manner, and attenuate locomotor behavior associated with 6-OHDA lesion. Given that detection of reliable PD markers will eventually be employed in susceptible populations, our results give credence to the possibility that increasing glutamate uptake may prolong the time period before locomotor impairment occurs.
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The dopaminergic and glutamatergic systems in the brain work together to regulate motor and cognitive functions.
“The dopaminergic and glutamatergic systems in the brain work together to regulate motor and cognitive functions [23].”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [23]
Ceftriaxone reportedly reduced the loss of dopaminergic neurons in PD patients by increasing GLT-1 expression.
“Ceftriaxone reportedly reduced the loss of dopaminergic neurons in PD patients by increasing GLT-1 expression [23]”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [23]
CTX promotes neurogenesis at SN and hippocampal dentate gyrus in rat PD models.
“At the neuronal level, pre- or post- treatment with CTX prevented the loss of TH-positive neurons, reduced glutamatergic hyperactivity, and promoted neurogenesis at the level of SN and hippocampal dentate gyrus in different rat models of the disease [233,237,238,239,240,241,242].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [240]
CTX administration reverts memory loss in PD models.
“As a consequence, dyskinesia, motor impairment and memory loss were all reverted upon CTX administration [233,234,237,238,239,240,242,243,244], although conflicting evidence still remains about its ability to improve learning outcomes [245].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [240]
CTX administration reverts motor impairment in PD models.
“As a consequence, dyskinesia, motor impairment and memory loss were all reverted upon CTX administration [233,234,237,238,239,240,242,243,244], although conflicting evidence still remains about its ability to improve learning outcomes [245].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [240]
CTX prevents loss of TH-positive neurons in rat PD models.
“At the neuronal level, pre- or post- treatment with CTX prevented the loss of TH-positive neurons, reduced glutamatergic hyperactivity, and promoted neurogenesis at the level of SN and hippocampal dentate gyrus in different rat models of the disease [233,237,238,239,240,241,242].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [240]
CTX reduces glutamatergic hyperactivity in rat PD models.
“At the neuronal level, pre- or post- treatment with CTX prevented the loss of TH-positive neurons, reduced glutamatergic hyperactivity, and promoted neurogenesis at the level of SN and hippocampal dentate gyrus in different rat models of the disease [233,237,238,239,240,241,242].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [240]
CTX administration reverts dyskinesia in PD models.
“As a consequence, dyskinesia, motor impairment and memory loss were all reverted upon CTX administration [233,234,237,238,239,240,242,243,244], although conflicting evidence still remains about its ability to improve learning outcomes [245].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [240]
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- Authors
- Chotibut, T., Davis, R. W., Arnold, J. C., Frenchek, Z., Gurwara, S., Bondada, V., Geddes, J. W., & Salvatore, M. F.
- Affiliations
- Louisiana State University Health Sciences Center Shreveport (US)
- University of Kentucky (US)
- Louisiana State University (US)
- Corresponding author
- Salvatore, Michael F.
- Venue
- Molecular Neurobiology
- Published
- 2013-12-03
- Volume
- 49
- Issue
- 3
- Pages
- 1282-1292
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- PMC
- PMC4618839
- OpenAlex
- W2007282493
- Cited by
- 86
- References
- 93
- Citations by year
- 2026: 7 · 2025: 2 · 2024: 7 · 2023: 7 · 2022: 8 · 2021: 14 · 2020: 6 · 2019: 8 · 2018: 3 · 2017: 6 · 2016: 7 · 2015: 5 · 2014: 6
- FWCI
- 3.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG040261)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- ceftriaxone, glutamate uptake, GLT-1, tyrosine hydroxylase, Parkinson's disease, 6-hydroxydopamine, striatum, nigrostriatal neurons, excitotoxicity, locomotor behavior, beta-lactam antibiotics
- MeSH terms
- Animals, Ceftriaxone, Corpus Striatum, Male, Parkinson Disease, Secondary, Tyrosine 3-Monooxygenase, Oxidopamine, Rats, Sprague-Dawley, Glutamic Acid, Rats
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