Hyperactivity in the Gunn rat model of neonatal jaundice: age-related attenuation and emergence of gait deficits

Stanford, John A.; Shuler, Jeffrey M.; Fowler, Stephen C.; Stanford, Kimberly G.; Ma, Daifu; Bittel, Douglas C.; Pichon, Jean-Baptiste Le; Shapiro, Steven M.

doi:10.1038/pr.2014.199

Cited by 9 publications

(7 citation statements)

References 39 publications

(45 reference statements)

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“…Mature Gunn rats experience reduced weight compared to wild‐type littermate . The current data regarding lower age‐dependent growth in Gunn rats is consistent with recent data for body weight in 3–20 months Gunn vs. wild‐type rats . Gunn animals commence at birth with normal body weights, yet diverge as control animals grow at a significantly faster rate (apparent from ~10 weeks of age), resulting in 25–30% lower body weight (~100 g) at 12 months (Fig.…”

Section: Discussionsupporting

confidence: 90%

Chronically elevated bilirubin protects from cardiac reperfusion injury in the male Gunn rat

et al. 2017

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Section: Discussionsupporting

confidence: 90%

Chronically elevated bilirubin protects from cardiac reperfusion injury in the male Gunn rat

et al. 2017

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“…These integrated power values were averaged across low mobility bouts to produce a single measure of integrated power per mouse. Additional measures of “long runs” and “crossings” were scored with the aid of a scrolling graphics program, written in Visual Basic to extract gait parameters that are not included in the commercial software (Fowler et al , 2017; Stanford et al , 2015). Long runs refers to the number of runs for which gait data were calculated (runs had to be long, fast, straight, and continuous with well-formed force-time waveforms), and crossings were counted on the basis of being long and straight (by visual inspection) but not necessarily fast and not having well-formed rhythmic waveforms.…”

Section: Methodsmentioning

confidence: 99%

Targeted deletion of GD3 synthase protects against MPTP‐induced neurodegeneration

Akkhawattanangkul

Maiti

Xue

et al. 2017

Genes Brain and Behavior

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Parkinson’s disease is a debilitating neurodegenerative condition for which there is no cure. Converging evidence implicates gangliosides in the pathogenesis of several neurodegenerative diseases, suggesting a potential new class of therapeutic targets. We have shown that interventions that simultaneously increase the neuroprotective GM1 ganglioside and decrease the pro-apoptotic GD3 ganglioside—such as inhibition of GD3 synthase (GD3S) or administration of sialidase—are neuroprotective in vitro and in a number of preclinical models. In the present study we investigated the effects of GD3S deletion on parkinsonism induced by 1-Methyl-4phenyl-1,2,3,6-tetrahydropyridine (MPTP). MPTP was administered to GD3S−/− mice or controls using a subchronic regimen consisting of three series of low-dose injections (11 mg/kg/day x 5 days each, 3 weeks apart), and motor function was assessed after each. The typical battery of tests used to assess parkinsonism failed to detect deficits in MPTP-treated mice. More sensitive measures—such as the force-plate actimeter and treadmill gait parameters—detected subtle effects of MPTP, some of which were absent in mice lacking GD3S. In wild-type mice MPTP destroyed 53% of the tyrosine-hydroxylase (TH)-positive neurons in the substantia nigra pars compacta (SNc) and reduced striatal dopamine 60.7%. In contrast, lesion size was only 22.5% in GD3S−/− mice and striatal dopamine was reduced by 37.2%. Stereological counts of Nissl-positive SNc neurons that did not express TH suggest that neuroprotection was complete but TH expression was suppressed in some cells. These results demonstrate that inhibition of GD3S has neuroprotective properties in the MPTP model may warrant further investigation as a therapeutic target.

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“…1; also see [16] for an example of these methods applied to rats). Temporally aligned on the same screen with the force data were the mouse's location coordinates, which allowed the program user to identify and record only rhythmic, long, straight, fast, continuous runs and their associated force time series.…”

Section: Methodsmentioning

confidence: 99%

Use of a force-sensing automated open field apparatus in a longitudinal study of multiple behavioral deficits in CAG140 Huntington’s disease model mice

Fowler

Muma

2015

Behavioural Brain Research

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Behavioral testing of mouse models of Huntington's disease (HD) is a key component of preclinical assessment for potential pharmacological intervention. An open field with a force plate floor was used to quantify numerous spontaneous behaviors in a slowly progressing model of HD. CAG140 (+/+, +/−, −/−) male and female mice were compared in a longitudinal study from 6 to 65 weeks of age. Distance traveled, wall rears, wall rear duration, number of low mobility bouts, in-place movements, number of high velocity runs, and gait parameters (stride rate, stride length, and velocity) were extracted from the ground reaction forces recorded in 20-min actometer sessions. Beginning at 11 weeks, HD mice (both +/− and +/+) were consistently hypoactive throughout testing. Robust hypoactivity at 39 weeks of age was not accompanied by gait disturbances. By 52 and 65 weeks of age the duration of wall rears increased and in-place tremor-like movements emerged at 65 weeks of age in the +/+, but not in the +/− HD mice. Taken together, these results suggest that hypoactivity preceding frank motor dysfunction is a characteristic of CAG140 mice that may correspond to low motivation to move seen clinically in the premanifest/prediagnostic stage in human HD. The results also show that the force plate method provides a means for tracking the progression of behavioral dysfunction in HD mice beyond the stage when locomotion is lost while enabling quantification of tremor-like and similar in-place behaviors without a change in instrumentation. Use of force plate actometry also minimizes testing-induced enrichment effects when batteries of different tests are carried out longitudinally.

show abstract

Hyperactivity in the Gunn rat model of neonatal jaundice: age-related attenuation and emergence of gait deficits

Cited by 9 publications

References 39 publications

Chronically elevated bilirubin protects from cardiac reperfusion injury in the male Gunn rat

Chronically elevated bilirubin protects from cardiac reperfusion injury in the male Gunn rat

Targeted deletion of GD3 synthase protects against MPTP‐induced neurodegeneration

Use of a force-sensing automated open field apparatus in a longitudinal study of multiple behavioral deficits in CAG140 Huntington’s disease model mice

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