Home cage activity and behavioral performance in inbred and hybrid mice

Tang, Xiangdong; Orchard, Stuart M.; Sanford, Larry D.

doi:10.1016/s0166-4328(02)00228-0

Cited by 131 publications

(101 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the HA and OF tests conducted in this study, both sexes of the B6 mice exhibited higher values than the D2 and DBF 1 mice for all activity-related parameters; the DBF 1 mice showed values higher or similar to those of the D2 mice. These results are consistent with published strain comparisons: [26] for the HA test, and [3,13,24,26] for the OF test. For PA performance, D2 mice were the worst learners among the groups at both shock intensities for males and at 0.3 mA for females, whereas B6 mice were the worst learners at 0.15 mA for females in this study.…”

Section: Discussionsupporting

confidence: 91%

ENU Mutagenesis Screening for Dominant Behavioral Mutations Based on Normal Control Data Obtained in Home-Cage Activity, Open-Field, and Passive Avoidance Tests

et al. 2010

View full text Add to dashboard Cite

Abstract:To establish the cutoff values for screening ENU-induced behavioral mutations, normal variations in mouse behavioral data were examined in home-cage activity (HA), openfield (OF), and passive-avoidance (PA) tests. We defined the normal range as one that included more than 95% of the normal control values. The cutoffs were defined to identify outliers yielding values that deviated from the normal by less than 5% for C57BL/6J, DBA/2J, DBF 1 , and N 2 (DXDB) progenies. Cutoff values for G1-phenodeviant (DBF 1 ) identification were defined based on values over ±3.0 SD from the mean of DBF 1 for all parameters assessed in the HA and OF tests. For the PA test, the cutoff values were defined based on whether the mice met the learning criterion during the 2nd (at a shock intensity of 0.3 mA) or the 3rd (at a shock intensity of 0.15 mA) retention test. For several parameters, the lower outliers were undetectable as the calculated cutoffs were negative values. Based on the cutoff criteria, we identified 275 behavioral phenodeviants among 2,646 G1 progeny. Of these, 64 were crossed with wild-type DBA/2J individuals, and the phenotype transmission was examined in the G2 progeny using the cutoffs defined for N 2 mice. In the G2 mice, we identified 15 novel dominant mutants exhibiting behavioral abnormalities, including hyperactivity in the HA or OF tests, hypoactivity in the OF test, and PA deficits. Genetic and detailed behavioral analysis of these ENU-induced mutants will provide novel insights into the molecular mechanisms underlying behavior.

show abstract

Section: Discussionsupporting

confidence: 91%

ENU Mutagenesis Screening for Dominant Behavioral Mutations Based on Normal Control Data Obtained in Home-Cage Activity, Open-Field, and Passive Avoidance Tests

et al. 2010

View full text Add to dashboard Cite

show abstract

“…The greater effects of CRH and AST on wakefulness and sleep in BALB/cJ mice compared to C57BL/6J mice are consistent with findings that BALB/cJ mice are more reactive in behavioral tests of anxiety (Belzung and Griebel, 2001;Tang et al, 2002b) and also show greater alterations in sleep in response to a number of stressors (Wurbel et al, 1998;Sanford et al, 2003a;2003b;2003d). Thus, strain differences in the effects of CRH and AST may be linked to underlying differences in the CRH system that may also be involved in the relative responsiveness to stressors in C57BL/6J and BALB/cJ mice.…”

Section: Discussionsupporting

confidence: 84%

Mouse strain differences in the effects of corticotropin releasing hormone (CRH) on sleep and wakefulness

et al. 2008

View full text Add to dashboard Cite

Corticotropin releasing hormone (CRH) plays a major role in central nervous system responses to stressors and has been implicated in stress-induced alterations in sleep. In the absence of stressors, CRH contributes to the regulation of spontaneous waking. We examined the effects of CRH and astressin (AST), a non-specific CRH antagonist, on wakefulness and sleep in two mouse strains with differential responsiveness to stress to determine whether CRH might also differentially affect undisturbed sleep and activity. Less reactive C57BL/6J (n=7) and high reactive BALB/cJ (n=7) male mice were implanted with a transmitter for determining sleep via telemetry and with a guide cannula aimed into a lateral ventricle. After recovery from surgery and habituation to handling, ICV microinjections of CRH (0.04, 0.2, and 0.4 μg), AST (0.1, 0.4, and 1.0 μg) or vehicle alone (pyrogenfree saline, 0.2 μl) were administered during the fourth h after lights on and sleep was recorded for the subsequent 8 h. Comparisons of wakefulness and sleep were conducted across conditions and across strains. In C57BL/6J mice, REM was significantly decreased after microinjections of CRH (0.2 μg) and CRH (0.4 μg), and NREM and total sleep were decreased after microinjections of CRH (0.4 μg ). CRH (0.4 μg) and AST did not significantly change wakefulness or sleep. In BALB/cJ mice, CRH (0.4 μg) increased wakefulness and decreased NREM, REM and total sleep. AST decreased active wakefulness and significantly increased REM at the low and high dosages. These findings demonstrate that CRH produces changes in arousal when given to otherwise undisturbed mice. Strain differences in the effects of CRH and AST may be linked to the relative responsiveness of C57BL/6J and BALB/cJ mice to stressors and to underlying differences in the CRH system.

show abstract

“…LRS thresholds: 9.5 (suggestive), 16.5 (significant), and 26.4 (highly significant). Bouwknecht and Paylor, 2002), free-exploration tests (Kopp et al, 1999;Tang et al, 2002;Yilmazer-Hanke et al, 2003), the novel object test (Tang et al, 2002), and the elevated plus maze (Kim et al, 2002). The A/J mouse strain was selected because these mice: (1) were relatively nonresponsive to citalopram in the TST , (2) showing high levels of anxiety and defecation (Crawley et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Pharmacogenomic Evaluation of the Antidepressant Citalopram in the Mouse Tail Suspension Test

Crowley

Brodkin

Blendy

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

The identification of genetic variants regulating antidepressant response in human patients would allow for more individualized, rational, and successful drug treatments. We have previously identified the BALB/cJ inbred mouse strain as highly responsive to the selective serotonin reuptake inhibitor (SSRI) citalopram in the tail suspension test (TST), a widely used and well-established screening paradigm for detecting compounds with antidepressant activity. In contrast, A/J mice did not show a significant response to citalopram in this test despite exposure to equivalent plasma levels of the drug. To identify genetic determinants of this differential response, 506 F 2 mice from an intercross between BALB/cJ and A/J mice were phenotyped. Composite interval mapping of 92 mice from the phenotypic extremes revealed three loci on chromosomes 7, 12, and 19 affecting citalopram response in the TST. The quantitative trait locus (QTL) at the telomeric end of chromosome 19 showed the greatest level of significance. Three candidate genes residing in this locus include those for vesicular monoamine transporter 2 (VMAT2, slc18a2), alpha 2A adrenergic receptor (adra2a), and beta 1 adrenergic receptor (adrb1). The protein coding regions of these three genes in BALB/cJ and A/J mice were sequenced and two polymorphisms were found in VMAT2 (Leu117Pro and Ser505Pro), while the transcribed regions of adra2a and adrb1 were of identical sequence between strains. Follow-up studies are needed to determine if the VMAT2 polymorphisms are functional and if they could explain the chromosome 19 QTL. The present quantitative trait study suggests possible candidate genes for human pharmacogenetic studies of therapeutic responses to SSRIs such as citalopram.

show abstract

Home cage activity and behavioral performance in inbred and hybrid mice

Cited by 131 publications

References 37 publications

ENU Mutagenesis Screening for Dominant Behavioral Mutations Based on Normal Control Data Obtained in Home-Cage Activity, Open-Field, and Passive Avoidance Tests

ENU Mutagenesis Screening for Dominant Behavioral Mutations Based on Normal Control Data Obtained in Home-Cage Activity, Open-Field, and Passive Avoidance Tests

Mouse strain differences in the effects of corticotropin releasing hormone (CRH) on sleep and wakefulness

Pharmacogenomic Evaluation of the Antidepressant Citalopram in the Mouse Tail Suspension Test

Contact Info

Product

Resources

About