Hearing Aid Delay Effects on Neural Phase Locking.

OBJECTIVES: This study was designed to examine the effects of hearing aid delay on the neural representation of the temporal envelope. It was hypothesized that the comb-filter effect would disrupt neural phase locking, and that shorter hearing aid delays would minimize this effect. DESIGN: Twenty-one participants, ages 50 years and older, with bilateral mild-to-moderate sensorineural hearing loss were recruited through print advertisements in local senior newspapers. They were fitted with three different sets of hearing aids with average processing delays that ranged from 0.5 to 7 msec. Envelope-following responses (EFRs) were recorded to a 50-msec /da/ syllable presented through a speaker placed 1 meter in front of the participants while they wore the three sets of hearing aids with open tips. Phase-locking factor (PLF) and stimulus-to-response (STR) correlations were calculated from these recordings. RESULTS: Recordings obtained while wearing hearing aids with a 0.5-msec processing delay showed higher PLF and STR correlations compared with those with either 5-msec or 7-msec delays. No differences were noted between recordings of hearing aids with 5-msec and 7-msec delays. The degree of difference between hearing aids was greater for individuals who had milder degrees of hearing loss. CONCLUSIONS: Hearing aid processing delays disrupt phase locking due to mixing of processed and unprocessed sounds in the ear canal when using open domes. Given previous work showing that better phase locking correlates with better speech-in-noise performance, consideration should be given to reducing hearing aid processing delay in the design of hearing aid algorithms.

Chronic social defeat stress broadly inhibits gene expression in the peripheral taste system and alters taste responses in mice.

Human studies have linked stress exposure to unhealthy eating behavior. However, the mechanisms that drive stress-associated changes in eating behavior remain incompletely understood. The sense of taste plays important roles in food preference and intake. In this study, we use a chronic social defeat stress (CSDS) model in mice to address whether chronic stress impacts taste sensation and gene expression in taste buds and the gut. Our results showed that CSDS significantly elevated circulating levels of corticosterone and acylated ghrelin while lowering levels of leptin, suggesting a change in metabolic hormones that promotes food consumption. Stressed mice substantially increased their intake of food and water 3-5 days after the stress onset and gradually gained more body weight than that of controls. Moreover, CSDS significantly decreased the expression of multiple taste receptors and signaling molecules in taste buds and reduced mRNA levels of several taste progenitor/stem cell markers and regulators. Stressed mice showed significantly reduced sensitivity and response to umami and sweet taste compounds in behavioral tests. In the small intestine, the mRNA levels of Gnat3 and Tas1r2 were elevated in CSDS mice. The increased Gnat3 was mostly localized in a type of Gnat3+ and CD45+ immune cells, suggesting changes of immune cell distribution in the gut of stressed mice. Together, our study revealed broad effects of CSDS on the peripheral taste system and the gut, which may contribute to stress-associated changes in eating behavior.