Ceftriaxone mediated rescue of nigral oxidative damage and motor deficits in MPTP model of Parkinson's disease in rats

Bisht, Rohit; Kaur, Baninder; Gupta, H.; Prakash, Atish

doi:10.1016/j.neuro.2014.05.009

Cited by 47 publications

(43 citation statements)

References 49 publications

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“…The cellular source of increased GLT-1 expression by ceftriaxone is likely astocytes, 57 although a neuronal GLT-1 component may not be ruled out. 71 Ceftriaxone also can activate other potentially protective signaling pathways, 58,72 which were not evaluated in our study. The regimen of ceftriaxone used herein decreased dyskinesia rating scores by approximately 70%.…”

Section: Discussionmentioning

confidence: 93%

“…11,[53][54][55] When initiated at the time of 6-OHDA, thereby increasing GLT-1 expression during the progression of TH loss, ceftriaxone can attenuate TH loss 9 days after 6-OHDA lesions in association with the increased uptake of glutamate and reduced Ca 21dependent phosphorylation of TH. 11 Increased GLT-1 expression by ceftriaxone may also reduce DA neuron loss when initiated prior to 56 or after 11,57,58 the experimental DA lesion. We reasoned that ceftriaxone may reduce LID by augmenting glutamate uptake or reducing the rate of TH loss using an established model of LID.…”

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confidence: 99%

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Ceftriaxone reduces L‐dopa–induced dyskinesia severity in 6‐hydroxydopamine parkinson's disease model

et al. 2017

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Background Increased extracellular glutamate may contribute to L-DOPA induced dyskinesia, a debilitating side effect faced by Parkinson’s disease patients 5–10 years after L-DOPA treatment. Therapeutic strategies targeting post-synaptic glutamate receptors to mitigate dyskinesia may have limited success due to significant side effects. Increasing glutamate uptake may be another approach to attenuate excess glutamatergic neurotransmission to mitigate dyskinesia severity or prolong the time prior to onset. Initiation of a ceftriaxone regimen at time of nigrostriatal lesion, can attenuate tyrosine hydroxylase loss in conjunction with increased glutamate uptake and glutamate transporter GLT-1 expression in a rat 6-hydroxydopamine model. Here, we examined if a ceftriaxone regimen initiated 1 week after nigrostriatal lesion, but prior to L-DOPA, could reduce L-DOPA-induced dyskinesia in an established dyskinesia model. Methods Ceftriaxone (200 mg/kg, i.p., once daily, 7 consecutive days) was initiated 7 days post-6-hydroxydopamine lesion (days 7–13) and continued every other week (days 21–27, 35–39) until the end of the study (day 39 post-lesion, 20 days of L-DOPA). Results Ceftriaxone significantly reduced abnormal involuntary movements at 5 time points examined during chronic L-DOPA treatment. Partial recovery of motor impairment from nigrostriatal lesion by L-DOPA was unaffected by ceftriaxone. The ceftriaxone-treated L-DOPA group had significantly increased striatal GLT-1 expression and glutamate uptake. Striatal tyrosine hydroxylase loss in this group was not significantly different compared to the L-DOPA alone group. Conclusions Initiation of ceftriaxone after nigrostriatal lesion, but prior to and during L-DOPA, may reduce dyskinesia severity without affecting L-DOPA efficacy or reduction of striatal tyrosine hydroxylase loss.

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Section: Discussionmentioning

confidence: 93%

mentioning

confidence: 99%

Ceftriaxone reduces L‐dopa–induced dyskinesia severity in 6‐hydroxydopamine parkinson's disease model

et al. 2017

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“…Rats have been used to model PD using MPTP toxin in previous studies (15)(16)(17). Although studies using primate models of PD have a higher evidence level compared to those using rat models, to our knowledge, no study has shown that results of studies in rat models cannot be extended to human.…”

Section: Methodsmentioning

confidence: 99%

Investigation of the Effect of Cycloserine on Motor Function in a Rat Model of Parkinson’s disease

Taherian

Arabahmadi

Taherian

2017

Caspian.J.Neurol.Sci

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Background:Previous studies have shown cycloserine to be neuroprotective in some neurodegenerative disorders. Objectives:To investigate the effect of cycloserine on motor function in Parkinson's disease in a rat model. Materials and Methods:Fifty-six healthy male wistar rats were used in this study and were divided into seven groups according to receiving saline, low dose (i.e. 100 mg/kg) and high dose (i.e. 200 mg/kg) of cycloserine for a short period (i.e. 8 days) (groups A-C, respectively) or long period (i.e. 16 days) (groups D-F, respectively) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-rat model of Parkinson. Also, a healthy group not receiving MPTP or any other drug was considered as the control group (group G). Apomorphine-induced rotational test (AIRT), elevated body swing test (EBST) and rotarod performance test (RPT) were done to examine behavioral performances.Results: Long-period treatment with cycloserine reduced MPTP-induced behavioral disturbances, i.e. net number of rotations in AIRT, net biased swing in EBST and reduced rotarod performance time in RPT, more than short period treatment. Although high dose of cycloserine was more effective than its low dose in reducing motor disturbance in initial trials of each test, long period treatment with low dose of cycloserine was similar to long period treatment with a high dose of it in reducing MPTP-induced Parkinsonism in EBST and RPT in latent trials. Conclusion:Long-period treatment with low-dose cycloserine seems to be the best option to obtain a sufficient neuroprotective effect for lowering motor disturbance in Parkinson's disease.

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“…Ropinirole, a secondgeneration, non-ergoline dopamine receptor agonist with D2-like receptor selectivity and a chemical structure similar to that of dopamine was found to enhance GSH levels and CAT [182] activity and to diminish nitrate levels [182] in the striatum in MPTP-lesioned animals.…”

Section: Anti-parkinsonian Drugs That Modulate Oxidative Balancementioning

confidence: 98%

Oxidative Stress in Neurodegenerative Diseases

Xueping¹,

Chen²,

Chunyan³

et al. 2013

Metal‐based Neurodegeneration

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Ceftriaxone mediated rescue of nigral oxidative damage and motor deficits in MPTP model of Parkinson's disease in rats

Cited by 47 publications

References 49 publications

Ceftriaxone reduces L‐dopa–induced dyskinesia severity in 6‐hydroxydopamine parkinson's disease model

Ceftriaxone reduces L‐dopa–induced dyskinesia severity in 6‐hydroxydopamine parkinson's disease model

Investigation of the Effect of Cycloserine on Motor Function in a Rat Model of Parkinson’s disease

Oxidative Stress in Neurodegenerative Diseases

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