Maintenance of profound deaf model mouse and functional analysis of it's auditory system
| Project/Area Number |
13035045
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
WATANABE Michiko Jikei University School of Medicine, Medical department, Research Assistant, 医学部, 助手 (10158660)
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| Co-Investigator(Kenkyū-buntansha) |
HASEGAWA Noriko Toita women's college, Department of Hygiene, Lecturer, 食物栄養, 講師 (30056717)
MANOME Yoshinobu Jikei University School of Medicine, Medical department, Lecturer, 医学部, 講師 (30219539)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 2002: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | hearing loss, / auditory system / congenital, / abnormal behavior / mouse-model, / 内耳神経系 |
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| Research Abstract |
We isolated a spontaneous mutant animal with abnormal behaviors when we encountered epileptic mice exhibiting circling movement in our closed colony of ICR Ascites mice. The mutant mice, designated to kuru2, did not respond to sounds. In order to elucidate their hearing ability, we measured the auditory brain stem response (ABR) of the mice. ABR demonstrated that the mice were profoundly impaired acuity. Abnormal behaviors including circling, ataxic gait, and hyperirritability of the mouse were demonstrated.
The genetic mode of the mouse was autosomal recessive. This result came from an exploration of the pedigree and backcross examinations. Either male or female mutants were mated with wild type animals. The F1 mice were backcrossed to the mutant mice. Behavior of 100 offspring were analyzed. None of the offspring F1 demonstrated hearing impairment or abnormal behaviors. Normal versus deaf mice was one to one. The result was same in the both sexes. We presumed that the phenotype might be from a single gene mutation. Since the animal has a wide variety of symptoms, a large-scale study will be required to elucidate the underlying genetics.
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Report
(3 results)
Research Products
(3 results)
