Opposing expression gradients of calcitonin-related polypeptide alpha (Calca/Cgrpα) and tyrosine hydroxylase (Th) in type II afferent neurons of the mouse cochlea.

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Opposing expression gradients of calcitonin-related polypeptide alpha (Calca/Cgrpα) and tyrosine hydroxylase (Th) in type II afferent neurons of the mouse cochlea.

J Comp Neurol. 2017 Oct 21;:

Authors: Wu JS, Vyas P, Glowatzki E, Fuchs PA

Abstract
Type II spiral ganglion neurons (SGNs) are small caliber, unmyelinated afferents that extend dendritic arbors hundreds of microns along the cochlear spiral, contacting many outer hair cells (OHCs). Despite these many contacts, type II afferents are insensitive to sound and only weakly depolarized by glutamate release from OHCs. Recent studies suggest that type II afferents may be cochlear nociceptors, and can be excited by ATP released during tissue damage, by analogy to somatic pain-sensing C-fibers. The present work compares the expression patterns among cochlear type II afferents of two genes found in C-fibers: calcitonin-related polypeptide alpha (Calca/Cgrpα), specific to pain-sensing C-fibers, and tyrosine hydroxylase (Th), specific to low-threshold mechanoreceptive C-fibers, which was shown previously to be a selective biomarker of type II versus type I cochlear afferents (Vyas et al, 2016). Whole-mount cochlear preparations from 3-week to 2-month-old CGRPα-EGFP (GENSAT) mice showed expression of Cgrpα in a subset of SGNs with type II-like peripheral dendrites extending beneath OHCs. Double labeling with other molecular markers confirmed that the labeled SGNs were neither type I SGNs nor olivocochlear efferents. Cgrpα starts to express in type II SGNs before hearing onset, but the expression level declines in the adult. The expression patterns of Cgrpα and Th formed opposing gradients, with Th being preferentially expressed in apical and Cgrpα in basal type II afferent neurons, indicating heterogeneity among type II afferent neurons. The expression of Th and Cgrpα was not mutually exclusive and co-expression could be observed, most abundantly in the middle cochlear turn. This article is protected by copyright. All rights reserved.

PMID: 29055051 [PubMed - as supplied by publisher]

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Opposing expression gradients of calcitonin-related polypeptide alpha (Calca/Cgrpα) and tyrosine hydroxylase (Th) in type II afferent neurons of the mouse cochlea.

Related Articles

Opposing expression gradients of calcitonin-related polypeptide alpha (Calca/Cgrpα) and tyrosine hydroxylase (Th) in type II afferent neurons of the mouse cochlea.

J Comp Neurol. 2017 Oct 21;:

Authors: Wu JS, Vyas P, Glowatzki E, Fuchs PA

Abstract
Type II spiral ganglion neurons (SGNs) are small caliber, unmyelinated afferents that extend dendritic arbors hundreds of microns along the cochlear spiral, contacting many outer hair cells (OHCs). Despite these many contacts, type II afferents are insensitive to sound and only weakly depolarized by glutamate release from OHCs. Recent studies suggest that type II afferents may be cochlear nociceptors, and can be excited by ATP released during tissue damage, by analogy to somatic pain-sensing C-fibers. The present work compares the expression patterns among cochlear type II afferents of two genes found in C-fibers: calcitonin-related polypeptide alpha (Calca/Cgrpα), specific to pain-sensing C-fibers, and tyrosine hydroxylase (Th), specific to low-threshold mechanoreceptive C-fibers, which was shown previously to be a selective biomarker of type II versus type I cochlear afferents (Vyas et al, 2016). Whole-mount cochlear preparations from 3-week to 2-month-old CGRPα-EGFP (GENSAT) mice showed expression of Cgrpα in a subset of SGNs with type II-like peripheral dendrites extending beneath OHCs. Double labeling with other molecular markers confirmed that the labeled SGNs were neither type I SGNs nor olivocochlear efferents. Cgrpα starts to express in type II SGNs before hearing onset, but the expression level declines in the adult. The expression patterns of Cgrpα and Th formed opposing gradients, with Th being preferentially expressed in apical and Cgrpα in basal type II afferent neurons, indicating heterogeneity among type II afferent neurons. The expression of Th and Cgrpα was not mutually exclusive and co-expression could be observed, most abundantly in the middle cochlear turn. This article is protected by copyright. All rights reserved.

PMID: 29055051 [PubMed - as supplied by publisher]

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Expression pattern of EYA4 in the common marmoset (Callithrix jacchus) cochlea.

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Expression pattern of EYA4 in the common marmoset (Callithrix jacchus) cochlea.

Neurosci Lett. 2017 Oct 17;:

Authors: Matsuzaki S, Hosoya M, Okano H, Fujioka M, Ogawa K

Abstract
The eyes absent (EYA)-like genes are essential for the formation of sensory organs among fly (Drosophila melanogaster) and mammals. EYA4, one of the vertebrate genes of Eya family, is reported to be causative for late-onset mid-frequency sensorineural hearing loss in humans, while Eya4-deficient mice exhibited congenital profound deafness and otitis media with effusion due to the eustachian tube dysmorphology. Because of the species difference in the phenotype, the pathophysiology of EYA4 in the human cochlea has yet to be elucidated. Here, we examine the expression pattern of EYA4 in the cochlea of common marmoset (Callithrix jacchus), a non-human primate. The results indicated a distinct expression pattern of EYA4 in the adult marmoset cochleae, especially strong in all supporting cells, while in mouse their expressions were diminished. Interestingly, EYA4 expression in the hair cells, supporting cells and neurons was co-localized with sine oculis homeobox-SIX1, a transcription factor essential for the transcriptional activity of EYA4. The results revealed inter-species differences in the expression pattern of EYA4 gene in supporting cells between primates and rodents. The results also indicated a fundamental role of EYA4 in the primate auditory cells. Experiments with primate models such as marmosets or with human cochlear cells may provide cues about the unknown pathogenesis of EYA4-related hearing loss.

PMID: 29054432 [PubMed - as supplied by publisher]

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Researchers Discover New Genes Critical for Understanding Hearing Loss

A study has identified new genes linked to hearing loss in mice, which will provide insights into the causes of hearing loss in humans (Nat Commun. 2017;8[1]:886). Scientists from Medical Research Council Hartwell who led the research found 67 genes that were associated with hearing loss, of which 52 had not been previously connected to hearing loss, by testing 3,006 strains of mice for signs of hearing loss. They assessed the hearing thresholds of these mice with rising volumes of sounds at different frequencies. Mice were considered hearing impaired if they could not hear the quieter sounds for two or more frequencies. The genes identified varied in how they affect hearing, with effects ranging from mild to severe hearing loss or hearing difficulties at lower or higher frequencies.

​​Steve Brown, PhD, senior author of this paper, said the results of the study increased the knowledge of the many genes and molecular mechanisms required for hearing and provide a short list of new genes to investigate to discover the genetic basis of many human hearing loss syndrome. "Further investigation of these hearing loss mouse models will increase understanding of how the auditory system develops, is maintained, and the pathological processes involved with its decline," Brown said. "In particular, we need to establish whether the genes impact on known hearing loss pathways or if they implicate new processes in the auditory system. A longer term benefit that could arise from studying these models might be the identification of critical cellular functions, which can then be targets for therapies."

 

 

Published: 10/20/2017 9:44:00 AM

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Researchers Discover New Genes Critical for Understanding Hearing Loss

A study has identified new genes linked to hearing loss in mice, which will provide insights into the causes of hearing loss in humans (Nat Commun. 2017;8[1]:886). Scientists from Medical Research Council Hartwell who led the research found 67 genes that were associated with hearing loss, of which 52 had not been previously connected to hearing loss, by testing 3,006 strains of mice for signs of hearing loss. They assessed the hearing thresholds of these mice with rising volumes of sounds at different frequencies. Mice were considered hearing impaired if they could not hear the quieter sounds for two or more frequencies. The genes identified varied in how they affect hearing, with effects ranging from mild to severe hearing loss or hearing difficulties at lower or higher frequencies.

​​Steve Brown, PhD, senior author of this paper, said the results of the study increased the knowledge of the many genes and molecular mechanisms required for hearing and provide a short list of new genes to investigate to discover the genetic basis of many human hearing loss syndrome. "Further investigation of these hearing loss mouse models will increase understanding of how the auditory system develops, is maintained, and the pathological processes involved with its decline," Brown said. "In particular, we need to establish whether the genes impact on known hearing loss pathways or if they implicate new processes in the auditory system. A longer term benefit that could arise from studying these models might be the identification of critical cellular functions, which can then be targets for therapies."

 

 

Published: 10/20/2017 9:44:00 AM

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Researchers Discover New Genes Critical for Understanding Hearing Loss

A study has identified new genes linked to hearing loss in mice, which will provide insights into the causes of hearing loss in humans (Nat Commun. 2017;8[1]:886). Scientists from Medical Research Council Hartwell who led the research found 67 genes that were associated with hearing loss, of which 52 had not been previously connected to hearing loss, by testing 3,006 strains of mice for signs of hearing loss. They assessed the hearing thresholds of these mice with rising volumes of sounds at different frequencies. Mice were considered hearing impaired if they could not hear the quieter sounds for two or more frequencies. The genes identified varied in how they affect hearing, with effects ranging from mild to severe hearing loss or hearing difficulties at lower or higher frequencies.

​​Steve Brown, PhD, senior author of this paper, said the results of the study increased the knowledge of the many genes and molecular mechanisms required for hearing and provide a short list of new genes to investigate to discover the genetic basis of many human hearing loss syndrome. "Further investigation of these hearing loss mouse models will increase understanding of how the auditory system develops, is maintained, and the pathological processes involved with its decline," Brown said. "In particular, we need to establish whether the genes impact on known hearing loss pathways or if they implicate new processes in the auditory system. A longer term benefit that could arise from studying these models might be the identification of critical cellular functions, which can then be targets for therapies."

 

 

Published: 10/20/2017 9:44:00 AM

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Stimulus Characteristics of Single-Word Tests of Children's Speech Sound Production

Purpose

This clinical focus article provides readers with a description of the stimulus characteristics of 12 popular tests of speech sound production.

Method

Using significance testing and descriptive analyses, stimulus items were compared in terms of the number of opportunities for production of all consonant singletons, clusters, and rhotic and nonrhotic vowels of Standard American English; phonetic/phonological and structural complexity; and the presence of bound morphemes.

Results

The tests varied widely in terms of the number of opportunities for production of consonant singletons, clusters, and rhotic and nonrhotic vowels. Most of the tests included only 1 opportunity, scored or unscored, to produce a majority of the consonant singletons in each word position. Only 3 of the tests included stimulus items with 3-element clusters. The majority contained limited opportunities to produce 3- or 4-syllable stimulus items. The tests provided sufficient opportunities for production of most vowels, although most did not score vowels. The tests differed significantly in the complexity of their stimulus items. Most, however, contained a negligible number of items that, with the addition of a bound morpheme, resulted in a word-final cluster.

Conclusion

Most of the tests elicit an inadequate sample with which to conduct a comprehensive phonological analysis.

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