Neuroprotective effect of ketamine/xylazine on two rat models of Parkinson's disease

Ferro, M.M.; Angelucci, M.E.M.; Anselmo-Franci, J.A.; Canteras, N.S.; Cunha, Cláudio Da

doi:10.1590/s0100-879x2006005000053

Cited by 15 publications

(8 citation statements)

References 17 publications

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“…40) 6-OHDA has been reported to cause a more severe depletion of DA than 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in a previous study. 41) Hence, it seems that 6-OHDA is the most useful neurotoxin to evaluate the neuroprotective efficacy of TCA. TH catalyzes the conversion of L-tyrosine to L-dihydroxyphenylalanine (L-DOPA), which is the rate-limiting first step in the biosynthesis of DA.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Pyo

Jeong

Yeo

et al. 2013

Biological & Pharmaceutical Bulletin

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The anti-inflammatory and neuroprotective effects of trans-cinnamaldehyde (TCA) were investigated on the inflammatory cells and the dopaminergic degeneration in mice. TCA inhibited the up-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the lipopolysaccharide (LPS)-induced inflammatory BV2 microglial cells. To investigate the TCA efficacy on the 6-hydroxydopamine (6-OHDA)-induced dopaminergic degeneration in mice, an intracerebroventricular injection of 6-OHDA was given to the mice, and TCA (30 mg/kg) was intraperitoneally administered. At 7 d after the 6-OHDA injection, 6-OHDA led to a severe loss of tyrosine hydroxylase (TH)-positive dopaminergic neurons in the striatum and substantia nigra (SN). On the other hand, TCA dramatically maintained the number of TH-positive dopaminergic neurons in the striatum and SN regions of the 6-OHDA-treated mice, which indicates that TCA is able to inhibit the 6-OHDA-induced reduction of TH expression in the dopaminergic neurons in the striatum and SN regions. TCA also inhibited the induction of iNOS and COX-2 in the 6-OHDA model, similarly as shown in the LPS-induced inflammatory BV2 microglial cells. These results indicate that TCA has a neuroprotective effect on dopaminergic neurons and that this effect may be associated with the inhibition of inflammatory responses. These findings suggest that TCA may be a therapeutic candidate for the prevention of inflammationmediated neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Pyo

Jeong

Yeo

et al. 2013

Biological & Pharmaceutical Bulletin

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“…Unfortunately, the conclusions that can be drawn from this study are limited. No behavioral assessments were performed and it is now known that the anesthetic they used, ketamine, is neuroprotective against MPTP-related degeneration of dopaminergic cells (Ferro et al 2007). Compared to mice, few studies have used MPTPlesioned rats.…”

Section: Mptpmentioning

confidence: 99%

Intranasal Administration of Neurotoxicants in Animals: Support for the Olfactory Vector Hypothesis of Parkinson’s Disease

et al. 2011

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The causes of Parkinson's disease (PD) are unknown, but there is evidence that exposure to environmental agents, including a number of viruses, toxins, agricultural chemicals, dietary nutrients, and metals, is associated with its development in some cases. The presence of smell loss and the pathological involvement of the olfactory pathways in the early stages of PD are in accord with the tenants of the olfactory vector hypothesis. This hypothesis postulates that some forms of PD may be caused or catalyzed by environmental agents that enter the brain via the olfactory mucosa. In this article, we provide an overview of evidence implicating xenobiotics agents in the etiology of PD and review animal, mostly rodent, studies in which toxicants have been introduced into the nose in an attempt to induce behavioral or neurochemical changes similar to those seen in PD. The available data suggest that this route of exposure results in highly variable outcomes, depending upon the involved xenobiotic, exposure history, and the age and species of the animals tested. Some compounds, such as rotenone, paraquat, and 6-hydroxydopamine, have limited capacity to reach and damage the nigrostriatal dopaminergic system via the intranasal route. Others, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), readily enter the brain via this route in some species and influence the function of the nigrostriatal pathway. Intranasal infusion of MPTP in some rodents elicits a developmental sequence of behavioral and neurochemical changes that closely mimics that seen in PD. For this reason, such an MPTP rodent model appears to be an ecologically valid means for assessing novel palliative treatments for both the motor and non-motor symptoms of PD. More research is needed, however, on this and other ecologically valid models.

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“…One point needs to be explained; since ketamine was used in this study, and it is known to be an N-methyl-Daspartate antagonist, it may have had a protective effect on the MPTP-induced neurotoxic lesion [55,56] and hence might have slightly ameliorated the evolution of parkinsonian symptoms. But a systemic influence was avoided by using the same protocol in each monkey and so did not influence the overall profile of the results.…”

Section: Discussionmentioning

confidence: 99%

MPTP Induces Systemic Parkinsonism in Middle-Aged Cynomolgus Monkeys: Clinical Evolution and Outcomes

Yue

Zeng

Tang³

et al. 2016

Neurosci. Bull.

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In this study, we developed a systemic PD model in middle-aged cynomolgus monkeys using individualized low-dose MPTP, to explore effective indicators for the early prediction of clinical outcomes. MPTP was not stopped until the animals showed typical PD motor symptoms on days 10 to 13 after MPTP administration when the Kurlan score reached 10; this abrogated the differences in individual susceptibility to MPTP. The clinical symptoms persisted, peaking on days 3 to 12 after MPTP withdrawal (rapid progress stage), and then the Kurlan score plateaued. A Kurlan score at the end of the rapid progress stage [15 reflected stable or slowly-progressive PD, while a score\15 indicated spontaneous recovery. The entire clinical evolution and outcome of the systemic PD model was characterized in this study, thus providing options for therapeutic and translational research.

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Neuroprotective effect of ketamine/xylazine on two rat models of Parkinson's disease

Cited by 15 publications

References 17 publications

Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Intranasal Administration of Neurotoxicants in Animals: Support for the Olfactory Vector Hypothesis of Parkinson’s Disease

MPTP Induces Systemic Parkinsonism in Middle-Aged Cynomolgus Monkeys: Clinical Evolution and Outcomes

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