The BALB/c mouse as an animal model for progressive sensorineural hearing loss

Willott, James F.; Turner, Jeremy G.; Carlson, Stephanie; Ding, Dalian; Bross, Lori S.; Falls, William A.

doi:10.1016/s0378-5955(97)00189-5

Cited by 105 publications

(81 citation statements)

References 40 publications

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“…BALB/cJ and MRL/ MpJ) of 10 strains used in the present study exhibit AHL at later ages (Jimenez et al, 1999;Ralls, 1967;Willott et al, 1998;Zheng et al, 1999). When evaluated by click-and tone-pip-elicited ABR threshold, for example, BALB/cJ and MRL/MpJ mice exhibited late onset hearing loss at an age of 30 weeks or older .…”

Section: Discussionmentioning

confidence: 68%

Auditory brainstem responses in 10 inbred strains of mice

et al. 2006

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The auditory brainstem response (ABR) is an evoked potential response of auditory activity in the auditory nerve and subsequent fiber tracts and nuclei within the auditory brainstem pathways. The threshold, amplitude, and latency analysis of the ABR provides information on the peripheral hearing status and the integrity of brainstem pathways. In this study, we compared the threshold, amplitude, and latency of ABRs recorded from 149 mice of 10 commonly used inbred strains (BALB/cJ, C3HeB/FeJ, C3H/HeJ, CAST/EiJ, CBA/CaJ, CBA/J, FVB/ NJ, MRL/MpJ, NZB/BlNJ, and SJL/J) using clicks of different intensities. The ABR thresholds of these strains ranged from 32 to 43 dB SPL. The amplitude of both waves I and IV of ABRs, which increased monotonically with click intensity in most strains, differed significantly among different strains at each intensity tested. Moreover, the amplitude of both waves was inversely correlated with the body weight of each strain at most intensities tested. In general, the amplitude of wave IV was smaller than that of wave I resulting in the IV/I amplitude ratio of <1.0 in all strains. The peak latency of both waves I and IV decreased significantly with click intensity in each strain. However, this intensitydependent decrease was greater for wave IV than for wave I such that the wave I-IV inter-peak latency also decreased significantly with increasing intensity. I-IV inter-peak latencies for MRL/ MpJ, C3HeB/FeJ, NZB/BlNJ, and C3H/HeJ strains are longer than FVB/NJ, SJL/J, or CAST/EiJ. This work is the first step to study the genetic basis underlying strain-related differences in auditory pathway.

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Section: Discussionmentioning

confidence: 68%

Auditory brainstem responses in 10 inbred strains of mice

et al. 2006

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“…In addition, BALB/cJ generally showed less conditioned fear than C57BL/6J (as evidenced by lesser freezing either during conditioning or the first trial block of extinction), as previously reported (Bolivar et al 2001;Bothe et al 2005). Although BALB/c show slightly more age-related hearing loss than C57BL/6, this is unlikely to be a factor at the age tested (Willott et al 1998) and therefore, the lesser fear conditioning appears to a genuine dissociation from the increased anxiety-like behavior in this strain.…”

Section: Discussionmentioning

confidence: 89%

Effects of adolescent fluoxetine treatment on fear-, anxiety-or stress-related behaviors in C57BL/6J or BALB/cJ mice

et al. 2008

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Rationale-5-Hydroxytryptamine (5-HT, serotonin) plays a major role in brain ontogeny. Disruption of 5-HT during early postnatal development produces lasting changes in rodent 'emotionrelated' behaviors. Adverse effects of treatment with serotonin reuptake inhibitor (SRI) antidepressants have been reported in human adolescents. However, the long-term effects of chronic SRI treatment during adolescence in rodents remain unclear.Objectives-The objectives of the study are to assess the effects of fluoxetine treatment throughout the adolescent period in measures of fear-, anxiety-and stress-related endpoints in drug-free adults and to examine these effects in two genetic strains of mice differing in baseline stress-and anxietyrelated behaviors and sensitivity to SRIs. Materials and methods-C57BL/6Jand BALB/cJ mice received one of two fluoxetine doses for 4 weeks during adolescence (3-7 weeks old). A separate group of C57BL/6J and BALB/cJ mice received fluoxetine for 4 weeks during adulthood (8-12 weeks old). After a 3-week washout period, mice were tested for anxiety-like behaviors (novel open field, elevated plus-maze), fear conditioning and extinction, and stress-related responses to forced swim, as well as serotonin brain levels.Results-Adolescent fluoxetine treatment did not increase adult measures of anxiety-, fear-or stress-related behaviors, or brain serotonin levels. The same duration of treatment in adulthood also had no effects on these measures when tested after a 3-week washout period.Conclusions-In clear contrast with emotion-related abnormalities caused by preadolescent fluoxetine treatment or genetic inactivation of fluoxetine's pharmacological target, the 5-HT transporter, fluoxetine treatment throughout mouse adolescence did not produce detectable, lasting abnormalities in either "high" or "low anxiety" inbred mouse strains.

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“…Several inbred strains of mice, such as C57BL/6J, DBA/2J, and BALB/cByJ, exhibit agerelated hearing loss (AHL) and provide valuable models for human presbycusis [6][7][8][9][10]. By backcross linkage analysis of F1 hybrids between CAST/Ei and strains that exhibit AHL, we previously mapped a locus (symbol Ahl) on mouse chromosome (Chr) 10 and showed that it is a major contributor to AHL susceptibility in all 10 inbred strains examined [11,12].…”

Section: Introductionmentioning

confidence: 99%

“…One approach for unraveling the complex genetic basis of human presbycusis is to use inbred strains of the laboratory mouse as models. Mice offer a promising approach because of their short lifespan and ease of experimental manipulation, and because of the anatomical and functional similarities between the human and mouse cochlea [4,5].Several inbred strains of mice, such as C57BL/6J, DBA/2J, and BALB/cByJ, exhibit agerelated hearing loss (AHL) and provide valuable models for human presbycusis [6][7][8][9][10]. By backcross linkage analysis of F1 hybrids between CAST/Ei and strains that exhibit AHL, we previously mapped a locus (symbol Ahl) on mouse chromosome (Chr) 10 and showed that it is a major contributor to AHL susceptibility in all 10 inbred strains examined [11,12].…”

mentioning

confidence: 99%

Ahl2, a Second Locus Affecting Age-Related Hearing Loss in Mice

Johnson

Zheng

2002

Genomics

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Inbred mouse strains with age-related hearing loss (AHL) provide valuable models for studying the genetic basis of human presbycusis. Here we report the genetic mapping of a second AHL locus in mice (designated Ahl2) that is a major contributor to the 8-to 10-month difference in hearing loss onset times between NOD/LtJ and C57BL/6J mice. A whole-genome linkage scan of 110 progeny from a (C57BL/6J × NOD/LtJ) × NOD/LtJ backcross revealed statistically significant associations of ABR thresholds with markers on chromosome 5, with a peak lod score of 5.5 for D5Mit309. At 6 months of age, backcross progeny that inherited two copies of the recessive NOD/LtJ-derived allele at this locus (genotype ahl2/ahl2) exhibited ABR thresholds that were on average 26 decibels above those of heterozygous mice. Analysis of a (CAST/Ei × NOD/LtJ) × NOD/LtJ backcross, which segregates strain-specific alleles at both Ahl2 and the Ahl locus on chromosome 10, showed that the hearing loss attributable to Ahl2 is dependent on a predisposing Ahl genotype. The statistically significant effect of Ahl2 observed in crosses with NOD/LtJ was not seen in crosses involving three other strains with early onset AHL: A/J, BUB/BnJ, and SKH2/J. Age-related hearing loss (or presbycusis) is the most common form of sensory impairment in human populations [1,2] and adversely affects the quality of life of many elderly individuals [3]. The genetic basis of presbycusis is poorly understood because of the extreme difficulty in studying such a late-onset, complex disease. The cumulative effects of non-genetic factors such as noise trauma, disease, or ototoxic drugs vary greatly among individuals over the course of their lifetimes, confounding estimates of genetic components. One approach for unraveling the complex genetic basis of human presbycusis is to use inbred strains of the laboratory mouse as models. Mice offer a promising approach because of their short lifespan and ease of experimental manipulation, and because of the anatomical and functional similarities between the human and mouse cochlea [4,5].Several inbred strains of mice, such as C57BL/6J, DBA/2J, and BALB/cByJ, exhibit agerelated hearing loss (AHL) and provide valuable models for human presbycusis [6][7][8][9][10]. By backcross linkage analysis of F1 hybrids between CAST/Ei and strains that exhibit AHL, we previously mapped a locus (symbol Ahl) on mouse chromosome (Chr) 10 and showed that it is a major contributor to AHL susceptibility in all 10 inbred strains examined [11,12]. Although all 10 strains exhibit AHL, severity and onset times vary greatly. For example, C57BL/6J mice do not exhibit hearing loss until 10 months of age or older, whereas NOD/LtJ mice exhibit a much earlier onset-before 3 months. Analysis of progeny from crosses between C57BL/6J and NOD/LtJ mice showed that variation in AHL onset time was not associated with the Chr 10 Ahl locus [12], indicating that other genes must be responsible.Here we report the genetic mapping of a second AHL locus (Ahl2) on Chr 5 that is a ...

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The BALB/c mouse as an animal model for progressive sensorineural hearing loss

Cited by 105 publications

References 40 publications

Auditory brainstem responses in 10 inbred strains of mice

Auditory brainstem responses in 10 inbred strains of mice

Effects of adolescent fluoxetine treatment on fear-, anxiety-or stress-related behaviors in C57BL/6J or BALB/cJ mice

Ahl2, a Second Locus Affecting Age-Related Hearing Loss in Mice

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