Inner ear sensory afferent connections establish sensory maps between the inner ear hair cells and the vestibular and auditory nuclei to allow vestibular and sound information processing. While molecular guidance of sensory afferents to the periphery has been well studied, molecular guidance of central projections from the ear is only beginning to emerge. Disorganized central projections of spiral ganglion neurons in a Wnt/PCP pathway mutant, Prickle1, suggest the Wnt/PCP pathway plays a role in guiding cochlear afferents to the cochlear nuclei in the hindbrain, consistent with known expression of the Wnt receptor, Frizzled3 (Fzd3) in inner ear neurons. We therefore investigated the role of Wnt signaling in central pathfinding in Fzd3 mutant mice and Fzd3 morpholino treated frogs and found aberrant central projections of vestibular afferents in both cases. Ear transplantations from knockdown to control Xenopus showed that it is the Fzd3 expressed within the ear that mediates this guidance. Also, cochlear afferents of Fzd3 mutant mice lack the orderly topological organization observed in controls. Quantification of Fzd3 expression in spiral ganglion neurons show a gradient of expression with Fzd3 being higher in the apex than in the base. Together, these results suggest that a gradient of Fzd3 in inner ear afferents directs projections to the correct dorsoventral column within the hindbrain.
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http://dx.doi.org/10.1038/s41598-019-46553-6 | DOI Listing |
Alzheimers Dement
December 2024
University of Miami, Miami, FL, USA.
Background: Exposures to hazardous noise causes irreversible injury to the structures of the inner ear, leading to changes in hearing and balance function with strong links to age-related cognitive impairment. While the role of noise-induced hearing loss in long-term health consequences, such as progression or development of Alzheimer's Disease (AD) has been suggested, the underlying mechanisms and behavioral and cognitive outcomes or therapeutic solutions to mitigate these changes remain understudied. This study aimed to characterize the association between blast exposure, hearing loss, and the progression of AD pathology, and determine the underlying mechanisms.
View Article and Find Full Text PDFSci Rep
January 2025
Department of ENT/Audiology & School for Mental Health and NeuroScience (MHENS), Maastricht University Medical Centre, Maastricht, The Netherlands.
Traditionally, the place-pitch 'tonotopically' organized auditory neural pathway was considered to be hard-wired. Cochlear implants restore hearing by arbitrarily mapping frequency-amplitude information. This study shows that recipients, after a long period of sound deprivation, preserve a level of auditory plasticity, enabling them to swiftly and concurrently learn speech understanding with two alternating, distinct frequency maps.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Geosciences, Princeton University, Princeton, NJ, 08540, USA.
Hypoxia tolerance and its variation with temperature, activity, and body mass, are critical ecophysiological traits through which climate impacts marine ectotherms. To date, experimental determination of these traits is limited to a small subset of modern species. We leverage the close coupling of carbon and oxygen in animal metabolism to mechanistically relate these traits to the carbon isotopes in fish otoliths (δC).
View Article and Find Full Text PDFNat Commun
January 2025
School of Biosciences, University of Sheffield, Sheffield, S10 2TN, UK.
The refinement of neural circuits towards mature function is driven during development by patterned spontaneous calcium-dependent electrical activity. In the auditory system, this sensory-independent activity arises in the pre-hearing cochlea and regulates the survival and refinement of the auditory pathway. However, the origin and interplay of calcium signals during cochlear development is unknown in vivo.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
School of Biosciences, University of Sheffield, Sheffield S10 2TN, United Kingdom.
Myosin-VIIA (MYO7A) is an unconventional myosin responsible for syndromic (Usher 1B) or nonsyndromic forms of deafness in humans when mutated. In the cochlea, MYO7A is expressed in hair cells, where it is believed to act as the motor protein tensioning the mechanoelectrical transducer (MET) channels, thus setting their resting open probability (). However, direct evidence for this unique role for an unconventional myosin in mature hair cells is lacking.
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