Age-related changes in the motricity of the inbred mice strains 129/sv and C57BL/6j

Serradj, Najet; Jamon, Marc

doi:10.1016/j.bbr.2006.11.001

Cited by 39 publications

(29 citation statements)

References 60 publications

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“…Rather, motor responses were similar for MPTPp-treated and untreated mice. Moreover, at this late stage, vehicle-treated mice displayed a decline in motor performance as compared to earlier time-points, a phenomenon which might be age-related, in accordance with previous reports (Fleming et al 2004;Serradj et al 2007). In MPTPp treated-mice an age-related decline in motor performance was not detectable, likely due to the partial restoration of dopamine neurotransmission observed at the 2 months time-point (see following section), that may account for the similar motor performance displayed by treated and control mice.…”

Section: Chronic Mptpp-induced Behavioral Impairmentssupporting

confidence: 86%

Progressive Dopaminergic Degeneration in the Chronic MPTPp Mouse Model of Parkinson’s Disease

et al. 2009

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Parkinson's disease (PD) is characterized by a progressive degeneration of dopamine (DA) neurons and gradual worsening of motor symptoms. The investigation of progressive degenerative mechanisms and potential neuroprotective strategies relies on experimental models of the chronic neuropathology observed in human. The present study investigated the progressive nature of neurodegeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid (MPTPp) chronic mouse model of PD. MPTP (25 mg/kg) plus probenecid (250 mg/kg) were administered twice a week for 5 weeks. We evaluated behavioral deficits (olfactory and motor impairment), neurodegeneration (loss of tyrosine hydroxylase (TH)-positive cells in the substantia nigra pars compacta, SNc), biochemical markers of functional impairment in the caudate-putamen (CPu) (striatal enkephalin mRNA, DA and DOPAC levels), and glial reactivity (CD11b and GFAP immunoreactivity in the SNc and CPu) at progressive time-points (after 1, 3, 7, and 10 administrations of MPTPp). Olfactory dysfunction already appeared after the 1st MPTPp injection, whereas motor dysfunction appeared after the 3rd and worsened upon subsequent administrations. Moreover, starting after three MPTPp injections, we observed a gradual decline of TH-positive cells in the SNc, and a gradual raise of enkephalin mRNA in the CPu. Striatal DA levels reduction was not different among all time-points evaluated, whereas DOPAC levels were similarly reduced after 1-7 MPTP injections, but were further decreased after the 10th injection. Reactive microglia and astroglia were observed in both the SNc and CPu from the 1st MPTPp administration. In the SNc, gliosis displayed a gradual increase over the treatment. After 2 months, TH, DA, DOPAC, and reactive glia in the SNc were still altered in MPTPp-treated mice as compared to controls. By showing a progressive development of behavioral deficits and nigral neurodegeneration, together with impairment of biochemical parameters and gradual increase of glial response, results suggest that the chronic MPTPp protocol is a model of progressive PD, which may be suitable to investigate chronic pathological processes and neuroprotective strategies in PD.

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Section: Chronic Mptpp-induced Behavioral Impairmentssupporting

confidence: 86%

Progressive Dopaminergic Degeneration in the Chronic MPTPp Mouse Model of Parkinson’s Disease

et al. 2009

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“…Despite the general finding that age-related deficits are observed on this test, there remains considerable disagreement about the age at which deficits become apparent. A number of studies have reported that deficits appear around 12–13 months in C57BL/6 mice (Thouvarecq et al, 2001; Vogel et al, 2002), though deficits have been reported as early as 7 months (Fetsko et al, 2005; Serradj and Jamon, 2007). Depending on the study, paradigm, and species, deficits become progressively worse with older age, though this is not reported in all cases.…”

Section: Behavioral Tests and Age Sensitivitymentioning

confidence: 99%

“…For example, C57BL/6 mice outperformed 129/Sv mice at multiple ages tested and showed a significant decrease in motor learning beginning at 7 months, which declined further at 13 months (Serradj and Jamon, 2007). 129/Sv mice showed no real improvements in motor learning from 1 to 3 months and showed a slight (but non-significant) decrease at the older ages.…”

Section: Behavioral Tests and Age Sensitivitymentioning

confidence: 99%

Age sensitivity of behavioral tests and brain substrates of normal aging in mice

Kennard

Woodruff-Pak

2011

Front. Ag. Neurosci.

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Knowledge of age sensitivity, the capacity of a behavioral test to reliably detect age-related changes, has utility in the design of experiments to elucidate processes of normal aging. We review the application of these tests in studies of normal aging and compare and contrast the age sensitivity of the Barnes maze, eyeblink classical conditioning, fear conditioning, Morris water maze, and rotorod. These tests have all been implemented to assess normal age-related changes in learning and memory in rodents, which generalize in many cases to age-related changes in learning and memory in all mammals, including humans. Behavioral assessments are a valuable means to measure functional outcomes of neuroscientific studies of aging. Highlighted in this review are the attributes and limitations of these measures in mice in the context of age sensitivity and processes of brain aging. Attributes of these tests include reliability and validity as assessments of learning and memory, well-defined neural substrates, and sensitivity to neural and pharmacological manipulations and disruptions. These tests engage the hippocampus and/or the cerebellum, two structures centrally involved in learning and memory that undergo functional and anatomical changes in normal aging. A test that is less well represented in studies of normal aging, the context pre-exposure facilitation effect (CPFE) in fear conditioning, is described as a method to increase sensitivity of contextual fear conditioning to changes in the hippocampus. Recommendations for increasing the age sensitivity of all measures of normal aging in mice are included, as well as a discussion of the potential of the under-studied CPFE to advance understanding of subtle hippocampus-mediated phenomena.

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“…Between the C57BL/6J (B6) and the 129X1/SvJ (129) strains of mice, the former exhibits greater motor ability in several measures of coordinated movement, yet shows greater age-related declines in coordination and motor fatigue than their 129 counterparts (Serradj and Jamon, 2007; 2009) Furthermore, work from others has indicated difference endogenous motor ability across various strains of mice (Hoit et al, 2002; Kale et al, 2004) as well as difference between strains in response to EtOH (Crabbe et al, 2008). …”

Section: Introductionmentioning

confidence: 99%

Response to ethanol induced ataxia between C57BL/6J and 129X1/SvJ mouse strains using a treadmill based assay

Hansen

Pulst

2013

Pharmacology Biochemistry and Behavior

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More sensitive assays of mouse motor ataxia may provide a better understanding of the pathological profile. Treadmill gait analysis using ventral imaging allows for unhindered access to the ambulating mouse. In contrast to genetic mutations or exogenous brain injury, ethanol (EtOH) allows for the detection of dose dependent changes in motor behavior, which can be used to assess an assay’s detection sensitivity. EtOH induced ataxia was assessed in C57BL/6J (B6) and 129X1/SvJ (129) mice using the DigiGait imaging system. Gait was analyzed across EtOH dosage (1.75, 2.25 and 2.75 g/kg) in each strain using a linear mixed effects model. Overall, 129 mice displayed greater susceptibility to EtOH ataxia than their B6 counterparts. In both strains, hind paws exhibited greater sensitivity to EtOH dosage than fore paws. Across most variables analyzed, only a modest EtOH-induced change in motor behavior was observed in each strain with the 1.75g/kg EtOH doses failing to elicit significant change. These data indicate the ability to detect motor differences between strains, yet only moderate ability to detect change across EtOH dosage using the automated treadmill. Rotarod assays, however, were able to detect motor impairment at lower doses of EtOH. The significant, but opposite changes in paw placement with increasing EtOH doses highlight strain-specific differences in biophysical adaptations in response to acute EtOH intoxication.

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Age-related changes in the motricity of the inbred mice strains 129/sv and C57BL/6j

Cited by 39 publications

References 60 publications

Progressive Dopaminergic Degeneration in the Chronic MPTPp Mouse Model of Parkinson’s Disease

Progressive Dopaminergic Degeneration in the Chronic MPTPp Mouse Model of Parkinson’s Disease

Age sensitivity of behavioral tests and brain substrates of normal aging in mice

Response to ethanol induced ataxia between C57BL/6J and 129X1/SvJ mouse strains using a treadmill based assay

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