# Second messenger regulation of mammalian hair cell mechanotransduction

> **NIH NIH F31** · UNIVERSITY OF COLORADO DENVER · 2021 · $9,023

## Abstract

Project Summary
Cochlear amplification is a critical feature of the mammalian auditory system and underlies our incredible
sound sensitivity, dynamic range, and frequency selectivity. This process arises from the ability of sensory
receptors in the cochlea, called hair cells, to dynamically amplify and tune their response to incoming sound.
Hair cells are specialized mechanoreceptors which convert mechanical information from sound waves into an
electrical potential through a process termed mechano-electrical transduction (MET). MET is a necessary
component of cochlear amplification, since mutations that abolish MET result in a loss of the cochlear amplifier
and produce hearing loss.
Current models of the MET process arose from decades of experiments performed in the hair cells of lower
vertebrates or the mammalian vestibular system, which are systems that respond primarily to low frequencies.
Given the evolutionary divergence of mammals from lower vertebrates, it is likely that new mechanisms in the
MET process had to arise to account for the expanded frequency range and faster kinetics of the mammalian
auditory system. Previously, it has been assumed that these same mechanisms translate directly to
mammalian MET, but our lab has provided the first evidence that there are fundamental differences in the
underlying mechanisms between mammalian and non-mammals. Thus, there is a critical need to determine
the mammalian-specific mechanisms of MET regulation which forms the basis for the high hearing sensitivity
unique to mammals.
The cyclic adenosine monophosphate (cAMP) second messenger is one signaling pathway that has been
suggested to regulate mammalian MET and is implicated in human hearing loss. However, the precise function
of cAMP and it's downstream effectors in MET mechanisms and hearing function has not been explicitly tested
in mammals. In this study, I will combine electrophysiology and in-vivo assays of auditory function to determine
the physiological significance of cAMP signaling in MET mechanisms and hearing function in the mammalian
system.

## Key facts

- **NIH application ID:** 10085993
- **Project number:** 5F31DC018457-02
- **Recipient organization:** UNIVERSITY OF COLORADO DENVER
- **Principal Investigator:** Andrew Allan Mecca
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $9,023
- **Award type:** 5
- **Project period:** 2020-01-01 → 2021-02-14

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10085993

## Citation

> US National Institutes of Health, RePORTER application 10085993, Second messenger regulation of mammalian hair cell mechanotransduction (5F31DC018457-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10085993. Licensed CC0.

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