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Blockley, A.

Publications and source records attributed to Blockley, A..

2 recordsLinked to original sources

Metabolism is correlative not causative for age-related auditory decline in an insect model

Aging is due to a complex decline of multiple biological processes. Some of the causes include oxidative damage, mitochondrial and proteostatic dysfunction, and DNA damage. The result is that as biological systems age their performance deteriorates. This age-related decline is well quantified, and experienced, for human hearing and is presumed to be due to a decrease in the ears metabolism - specifically a decrease in ability to maintain an electrochemical gradient, the endocochlear potential. However, direct measurements of metabolism across a lifespan in an auditory system are lacking. Even if metabolism does decrease with age, the question remains is it a cause of age-related auditory decline or simply correlative? All auditory systems across the animal kingdom share functional principles including ion pumping cells, auditory receptors, spiking auditory nerves and multiple supporting cells. Therefore, we used an insect, the desert locust, Schistocerca gregaria, as a physiologically versatile model to understand how cellular metabolism correlates with age and impacts on age-related auditory decline. We found that although metabolism correlates with age-related auditory decline it is not causative.

neuroscience↗

Physiological changes throughout the ear due to age and noise - a longitudinal study

Biological and mechanical systems, whether by their overuse or their aging, will inevitably fail. Hearing provides a poignant example of this with noise-induced and age-related hearing loss. Hearing loss is not unique to humans, however, and is experienced by all animals in the face of wild and eclectic differences in ear morphology and operation. Here we exploited the high throughput and accessible tympanal ear of the desert locust, Schistocerca gregaria (mixed sex) to rigorously quantify changes in the auditory system due to noise exposure (3 kHz pure tone at 126 dB SPL) and age. We analysed tympanal dispalcements, morphology of the auditory Mullers organ and measured activity of the auditory nerve, the transduction current and electrophysiological properties of individual auditory receptors. We found that noise mildly and transiently changes tympanal displacements, decreases both the width of the auditory nerve and the transduction current recorded from individual auditory neurons. Whereas age - but not noise - decreases the number of auditory neurons and increases their resting potential. Multiple other properties of Mullers organ were unaffected by either age or noise including: the number of supporting cells in Mullers organ or the nerve, membrane resistance and capacitance of the auditory neurons. The sound-evoked activity of the auditory nerve decreased as a function of age and this decrease was exacerbated by noise, with the largest difference during the middle of their life span. This middle-aged deafness pattern of hearing loss mirrors that found for humans exposed to noise early in their life. Key point summaryO_LIAge and noise lead to hearing loss. C_LIO_LITympanal displacements have a transient and delayed reduction after noise. C_LIO_LIThe number of auditory neurons decreases with age. The width of the auditory nerve is reduced with noise exposure. C_LIO_LILocusts repeatedly exposed to noise lost their hearing compared to silent controls, but their hearing became similar to old silent control locusts due to age-related hearing loss dominating. C_LIO_LIThe electrophysiological properties of the auditory neurons and the transduction current remained unchanged for aged locusts but repeated noise exposure led to a cumulative decrease in the transduction current. C_LI

physiology↗