Baseline striatal and nigral interneuronal protein levels in two distinct mice strains differ in accordance with their MPTP susceptibility

Bhaduri, Bidisha; Abhilash, P.L.; Alladi, Phalguni Anand

doi:10.1016/j.jchemneu.2018.04.005

Cited by 12 publications

(12 citation statements)

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“…MPTP-induced mouse model of Parkinson's disease has been widely used and accepted for studying molecular mechanisms correlated with behavioral changes (Dawson and Dawson, 2003;Meredith and Rademacher, 2011) and initial screening of new treatments (Perry et al, 1985;Tatton and Greenwood, 1991;Meredith and Rademacher, 2011). In this context, the C57BL/6 mouse strain that is most sensitive to MPTP has been employed to study pre-and post-treatment (Przedborski et al, 2000;Sedelis et al, 2000;Bhaduri et al, 2018). The dosage and time of MPTP regimen had been applied as a subacute MPTP mouse PD model (Serra et al, 2008;Shi et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective and Neurorestorative Effects of Holothuria scabra Extract in the MPTP/MPP+-Induced Mouse and Cellular Models of Parkinson’s Disease

et al. 2020

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Extracts from Holothuria scabra (HS) have been shown to possess anti-inflammation, anti-oxidant and anti-cancer activities. More recently, it was shown to have neuroprotective potential in Caenorhabditis elegans PD model. Here, we assessed whether HS has neuroprotective and neurorestorative effects on dopaminergic neurons in both mouse and cellular models of PD. We found that both pre-treatment and post-treatment with HS improved motor deficits in PD mouse model induced with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) as determined by grid walk test. This was likely mediated by HS protective and restorative effects on maintaining the numbers of dopaminergic neurons and fibers in both substantia nigra pars compacta (SNpc) and striatum. In a cellular model of PD, HS significantly attenuated 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis of DAergic-like neurons differentiated from SH-SY5Y cells by enhancing the expression of Bcl-2, suppressing the expression of cleaved Caspase 3 and preventing depolarization of mitochondrial membrane. In addition, HS could stimulate the expression of tyrosine hydroxylase (TH) and suppressed the formation of α-synuclein protein. Taken together, our in vivo and in vitro findings suggested that HS is an attractive candidate for the neuroprotection rather than neurorestoration in PD.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective and Neurorestorative Effects of Holothuria scabra Extract in the MPTP/MPP+-Induced Mouse and Cellular Models of Parkinson’s Disease

et al. 2020

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“…The C57BL/6 J mice, which possessed fewer DA neurons, were more vulnerable to MPTP, in comparison to CD-1. The other differentiating features that could determine vulnerability or resistance to MPTP include nigral DA neuronal size, expression of tyrosine hydroxylase (TH), Nurr1, PitX3, caspase-3,calbindin D28k, and glial-derived neurotrophic factor, along with mitochondrial and interneuron-related proteins (Vidyadhara et al 2016(Vidyadhara et al , 2017(Vidyadhara et al , 2019bBhaduri et al 2018;Seshadri and Alladi 2019). Monoamine oxidase-B (MAO-B) is a key enzyme that forms toxic methyl-4-phenylpyridinium (MPP +) from the MPTP in astroglia.…”

Section: Introductionmentioning

confidence: 99%

Differences in Neuronal Numbers, Morphology, and Developmental Apoptosis in Mice Nigra Provide Experimental Evidence of Ontogenic Origin of Vulnerability to Parkinson’s Disease

et al. 2021

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Parkinson disease (PD) prevalence varies by ethnicity. In an earlier study, we replicated the reduced vulnerability to PD in an admixed population, using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-susceptible C57BL/6 J, MPTP-resistant CD-1 and their F1 crossbreds. In the present study, we investigated if the differences have a developmental origin. Substantia nigra was evaluated at postnatal days 2 (P2), P6, P10, P14, P18, and P22. C57BL/6 J mice had smaller nigra and fewer dopaminergic neurons than the CD-1 and crossbreds at P2, which persisted through development. A significant increase in numbers and nigral volume was observed across strains until P14. A drastic decline thereafter was specific to C57BL/6 J. CD-1 and crossbreds retained their numbers from P14 to stabilize with supernumerary neurons at adulthood. The neuronal size increased gradually to attain adult morphology at P10 in the resistant strains, vis-à-vis at P22 in C57BL/6 J. Accordingly, in comparison to C57BL/6 J, the nigra of CD-1 and reciprocal crossbreds possessed cytomorphological features of resilience, since birth. The considerably lesser dopaminergic neuronal loss in the CD-1 and crossbreds was seen at P2 and P14 and thereafter was complemented by attenuated developmental cell death. The differences in programmed cell death were confirmed by reduced TUNEL labelling, AIF, and caspase-3 expression. GDNF expression aligned with the cell death pattern at P2 and P14 in both nigra and striatum. Earlier maturity of nigra and its neurons appears to be better features that reflect as MPTP resistance at adulthood. Thus, variable MPTP vulnerability in mice and also differential susceptibility to PD in humans may arise early during nigral development.

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“…Amongst the mice, different strain or same strain from another source shows strikingly different sensitivity to the MPTP concerning the loss of DA neurons in SNpc and striatum [10]. The most sensitive of the mouse strain to MPTP intoxication is the C57BL/6, followed by CD-1 and BALB, with the least being the Swiss Webster [26,27]. Therefore, to get the best reproducible PD results from one experiment to another, a male mouse of at least 8 weeks of age, the average weight of 22 g and same mouse strain must be obtained from the same source [28].…”

Section: Introductionmentioning

confidence: 99%

MPTP-induced mouse model of Parkinson’s disease: A promising direction of therapeutic strategies

Mustapha

Taib

2020

Bosn J of Basic Med Sci

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Amongst the popular animal models of Parkinson’s disease (PD) commonly used in researches are those that employ neurotoxins, especially the 1-methyl- 4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP). MPTP neurotoxin exerts its neurotoxicity by causing a barrage of insults such as oxidative stress, mitochondrial apoptosis, inflammation, excitotoxicity, and formation of inclusion bodies acting singly and in concert. All of this ultimately leads to dopaminergic neuron damage in substantia nigra pars compacta and striatum. The selective neurotoxicity induced by MPTP in the nigrostriatal dopaminergic neuron of the mouse brain brought a new dawn in our perspectives about PD. For decades now MPTP-induced mouse model of PD has become the gold standard in PD research despite its shortcoming in fully recapitulating PD symptomatology. It has the advantage of easy practicability, affordability, less ethical consideration, and more clinical correlation over the other toxin models of PD. The model has rejuvenated researches in PD and has also opened new frontiers in the quest for more novel therapeutic and adjuvant agents for PD. Hence, this review summarizes the MPTP’s role in producing Parkinson-like symptoms in mice, the MPTP-induced mouse model’s experimental role, and the recent development in PD therapeutics using this model to enrich our existing knowledge on this neurotoxin. Furthermore, our review promotes the use of this model by researchers for developing more promising therapeutic strategies.

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Baseline striatal and nigral interneuronal protein levels in two distinct mice strains differ in accordance with their MPTP susceptibility

Cited by 12 publications

References 65 publications

Neuroprotective and Neurorestorative Effects of Holothuria scabra Extract in the MPTP/MPP+-Induced Mouse and Cellular Models of Parkinson’s Disease

Neuroprotective and Neurorestorative Effects of Holothuria scabra Extract in the MPTP/MPP+-Induced Mouse and Cellular Models of Parkinson’s Disease

Differences in Neuronal Numbers, Morphology, and Developmental Apoptosis in Mice Nigra Provide Experimental Evidence of Ontogenic Origin of Vulnerability to Parkinson’s Disease

MPTP-induced mouse model of Parkinson’s disease: A promising direction of therapeutic strategies

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