The functional age of hearing loss in a mouse model of presbycusis. II. Neuroanatomical correlates

Francis, Howard W.; Ryugo, David K.; Gorelikow, Melissa J; Prosen, Cynthia A.; May, Bradford J.

doi:10.1016/s0378-5955(03)00212-0

Cited by 32 publications

(34 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is now well established that loss of radial fibers can exceed the loss of spiral ganglion cell bodies in human cases of presbycusis (Chen et al, 2006;Nadol, 1979;Pauler et al, 1986;Schrott, 1988, 1990). A distal-to-proximal gradient of radial fiber loss has also been observed in C57BL/6J mice (White et al, 2000), a laboratory animal model that exhibits patterns of hearing loss and cochlear degeneration comparable to human presbycusis (Francis et al, 2003;Henry and Chole, 1980;Hequembourg and Liberman, 2001;Li and Borg, 1991). Alterations in sensory-neural synaptic structure that precede or follow denervation may hold the key to understanding the mechanisms of afferent cochlear pathology.…”

Section: Introductionmentioning

confidence: 88%

See 1 more Smart Citation

Synaptic alterations at inner hair cells precede spiral ganglion cell loss in aging C57BL/6J mice

Stamataki¹,

Francis²,

Lehar³

et al. 2006

Hearing Research

136

129

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 88%

“…Intracochlear perfusion of fixatives was performed while the animal was deeply anesthetized after ABR measurements (Francis et al, 2004(Francis et al, , 2003. The middle ear was entered through a post-auricular incision and visualized using an operating microscope.…”

Section: Cochlear Tissue Processingmentioning

confidence: 99%

Synaptic alterations at inner hair cells precede spiral ganglion cell loss in aging C57BL/6J mice

Stamataki¹,

Francis²,

Lehar³

et al. 2006

Hearing Research

136

129

View full text Add to dashboard Cite

“…It has been reported that some strains of mice, particularly C57 mice, experience some loss of hearing as they age (Zheng et al 1999;Johnson et al 2000;Davis et al 2001;Francis et al 2003). This loss is typically restricted to frequencies above 16 kHz starting at 6 mo of age (White et al 2000;Prosen et al 2003).…”

Section: Modification Of Experimental Parameters Reduced Nonassociatimentioning

confidence: 99%

Genetic background differences and nonassociative effects in mouse trace fear conditioning

Smith¹,

Gallagher²,

Stanton³

2007

Learn. Mem.

View full text Add to dashboard Cite

Fear conditioning, including variants such as delay and trace conditioning that depend on different neural systems, is widely used to behaviorally characterize genetically altered mice. We present data from three strains of mice, C57/BL6 (C57), 129/SvlmJ (129), and a hybrid strain of the two (F 1 hybrids), trained on various versions of a trace fear-conditioning protocol. The initial version was taken from the literature but included unpaired control groups to assess nonassociative effects on test performance. We observed high levels of nonassociative freezing in both contextual and cued test conditions. In particular, nonassociative freezing in unpaired control groups was equivalent to freezing shown by paired groups in the tests for trace conditioning. A number of pilot studies resulted in a new protocol that yielded strong context conditioning and low levels of nonassociative freezing in all mouse strains. During the trace-CS test in this protocol, freezing in unpaired controls remained low in all strains, and both the C57s and F 1 hybrids showed reliable associative trace fear conditioning. Trace conditioning, however, was not obtained in the 129 mice. Our findings indicate that caution is warranted in interpreting mouse fear-conditioning studies that lack control conditions to address nonassociative effects. They also reveal a final set of parameters that are important for minimizing such nonassociative effects and demonstrate strain differences across performance in mouse contextual and trace fear conditioning.

show abstract

“…Unlike in a number of vertebrate classes, including birds, amphibians and fishes, mammals are unable to regenerate these essential cells once they are lost (Edge and Chen, 2008). Hair cell damage and death are the predominant pathologies underlying many types of acquired hearing loss, including noise-induced, ototoxin-induced and age-related hearing loss (Francis et al, 2003;Rizzi and Hirose, 2007;Wang et al, 2002). Despite their clinical importance, the pathways regulating hair cell survival remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Caprin-1 is a target of the deafness genePou4f3and is recruited to stress granules in cochlear hair cells in response to ototoxic damage

Towers¹,

Kelly²,

Sud³

et al. 2011

Journal of Cell Science

View full text Add to dashboard Cite

The POU4 family of transcription factors are required for survival of specific cell types in different sensory systems. Pou4f3 is essential for the survival of auditory sensory hair cells and several mutations in human POU4F3 cause hearing loss. Thus, genes regulated by Pou4f3 are likely to be essential for hair cell survival. We performed a subtractive hybridisation screen in an inner-ear-derived cell line to find genes with differential expression in response to changes in Pou4f3 levels. The screen identified the stress-granule-associated protein Caprin-1 as being downregulated by Pou4f3. We demonstrated that this regulation occurs through the direct interaction of Pou4f3 with binding sites in the Caprin-1 5′ flanking sequence, and describe the expression pattern of Caprin-1 mRNA and protein in the cochlea. Moreover, we found Caprin-1-containing stress granules are induced in cochlear hair cells following aminoglycoside-induced damage. This is the first report of stress granule formation in mammalian hair cells and suggests that the formation of Caprin-1-containing stress granules is a key damage response to a clinically relevant ototoxic agent. Our results have implications for the understanding of aminoglycoside-induced hearing loss and provide further evidence that stress granule formation is a fundamental cellular stress response.

show abstract

The functional age of hearing loss in a mouse model of presbycusis. II. Neuroanatomical correlates

Cited by 32 publications

References 16 publications

Synaptic alterations at inner hair cells precede spiral ganglion cell loss in aging C57BL/6J mice

Synaptic alterations at inner hair cells precede spiral ganglion cell loss in aging C57BL/6J mice

Genetic background differences and nonassociative effects in mouse trace fear conditioning

Caprin-1 is a target of the deafness genePou4f3and is recruited to stress granules in cochlear hair cells in response to ototoxic damage

Contact Info

Product

Resources

About