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Gait disturbances in BIO 14.6 and BIO TO‐2 dystrophic hamsters
Author(s) -
Hampton Thomas G,
Kale Ajit,
Amende Ivo,
McCue Scott,
Bhagavan Hemmi N,
VanDongen Case G
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a399
Subject(s) - hamster , mesocricetus , gait , muscular dystrophy , treadmill , anatomy , biology , medicine , physical medicine and rehabilitation
The myopathic hamster strains BIO 14.6 and BIO TO‐2 are deficient in delta sarcoglycan and serve as excellent animal models for cardiomyopathy and muscular dystrophy. Gait disturbances that are important clinically have not been described in these hamsters. We therefore performed gait analysis of 3 mo and 9 mo old male BIO 14.6 & BIO TO‐2 and BIO F1B control hamsters using ventral plane videography based on ~10 consecutive strides for each of the 4 limbs on a transparent treadmill belt. In one experiment, 1 mo old BIO TO‐2 and F1B hamsters were also studied. BIO 14.6 & TO‐2 hamsters showed kinematic and postural disturbances including shorter swing, stride, and stance durations. Propulsion duration of the hind limbs, an indicator of muscle strength, was shorter in 9 mo old BIO 14.6 & TO‐2 hamsters as compared with F1B (P<0.01). Braking duration, reflecting generation of ground reaction forces, was delayed in 9 mo old BIO 14.6 & TO‐2 hamsters compared with F1B (P<0.01). Hind paw eversion, evidence of muscle weakness, was greater in 9 mo old TO‐2 than in F1B hamsters (P<0.01). The propulsive deficits were evident in both dystrophic strains at 3 mo, and in TO‐2 at 1 mo. This is the first quantitative analysis of gait in dystrophic hamsters demonstrating gait disturbances as early as 1 mo. Our findings show that these BIO hamsters recapitulate the functional features of human muscular dystrophy and therefore they are appropriate animal models for this disease. Early detection of gait disturbances is expected to facilitate the development of therapeutic modalities for muscular dystrophy.