Biology subjects

Mowery, T. M.

Publications and source records attributed to Mowery, T. M..

4 recordsLinked to original sources

bioRxiv2026

Noise-induced hearing loss delays auditory learning and reduces the influence of acoustic evidence on choice

Noise-induced hearing loss (NIHL) degrades auditory sensitivity, but how it affects the learning of sound-guided decisions remains unclear. We trained adult Mongolian gerbils with normal-hearing (NH) or permanent NIHL, induced by a 2-hour exposure to 120 dB SPL broadband noise, to discriminate 4- versus 12-Hz amplitude-modulated (AM) broadband noise presented in a two-alternative forced-choice task. Stimuli were presented at comparable sensation levels across groups. Relative to NH animals, NIHL animals required approximately 2.5 times more sessions and 2.9 times more trials to reach task acquisition criterion. This learning delay was not explained by reduced task engagement, response latency, or auditory brainstem response threshold shift. Video tracking showed that spatial occupancy refined with training in both groups, whereas trial-by-trial movement path trajectories became less variable in NH animals. Per-session and dynamic trial-by-trial logistic regression models revealed that the influence of the task-relevant acoustic stimulus increased with training in both groups but remained consistently lower in NIHL animals, whereas sound-independent choice tendencies were largely unchanged. Together, these results suggest that NIHL delays auditory learning by reducing the influence of acoustic evidence on choice, indicating that hearing loss can alter how sensory experience is used to acquire new behaviors.

animal behavior and cognition↗

bioRxiv2024

Auditory decision-making deficits after permanent noise-induced hearing loss

Loud noise exposure is one of the leading causes of permanent hearing loss. Individuals with noise-induced hearing loss (NIHL) suffer from speech comprehension deficits and experience impairments to cognitive functions such as attention and decision-making. Here, we tested whether a specific sensory deficit, NIHL, can directly impair auditory cognitive function. Gerbils were trained to perform an auditory decision-making task that involves discriminating between slow and fast presentation rates of amplitude-modulated (AM) noise. Decision-making task performance was assessed across pre-versus post-NIHL sessions within the same gerbils. A single exposure session (2 hours) to loud broadband noise (120 dB SPL) produced permanent NIHL with elevated threshold shifts in auditory brainstem responses (ABRs). Following NIHL, decision-making task performance was tested at sensation levels comparable to those prior to noise exposure in all animals. Our findings demonstrate NIHL diminished perceptual acuity, reduced attentional focus, altered choice bias, and slowed down evidence accumulation speed. Finally, video-tracking analysis of motor behavior during task performance demonstrates that NIHL can impact sensory-guided decision-based motor execution. Together, these results suggest that NIHL impairs the sensory, cognitive, and motor factors that support auditory decision-making.

neuroscience↗

bioRxiv2023

Developmental hearing loss-induced perceptual deficits are rescued by cortical expression of GABAB receptors

Even transient periods of developmental hearing loss during the developmental critical period have been linked to long-lasting deficits in auditory perception, including temporal and spectral processing, which correlate with speech perception and educational attainment. In gerbils, hearing loss-induced perceptual deficits are correlated with a reduction of both ionotropic GABAA and metabotropic GABAB receptor-mediated synaptic inhibition in auditory cortex, but most research on critical period plasticity has focused on GABAA receptors. We developed viral vectors to express both endogenous GABAA or GABAB receptor subunits in auditory cortex and tested their capacity to restore perception of temporal and spectral auditory cues following critical period hearing loss in the Mongolian gerbil. HL significantly impaired perception of both temporal and spectral auditory cues. While both vectors similarly increased IPSCs in auditory cortex, only overexpression of GABAB receptors improved perceptual thresholds after HL to be similar to those of animals without developmental hearing loss. These findings identify the GABAB receptor as an important regulator of sensory perception in cortex and point to potential therapeutic targets for developmental sensory disorders. Significance StatementHearing loss in children can induce deficits in aural communication that persevere even after audibility has returned to normal, suggesting permanent changes to the auditory central nervous system. In fact, a reduction in cortical synaptic inhibition has been implicated in a broad range of developmental disorders, including hearing loss. Here, we tested the hypothesis that developmental hearing loss-induced perceptual impairments in gerbils are caused by a permanent reduction of auditory cortical inhibitory synapse strength. We found that virally-mediated expression of a GABAB receptor subunit in gerbil auditory cortex was able to restore two auditory perceptual skills in juvenile animals reared with hearing loss, suggesting that cortical synaptic inhibition is a plausible therapeutic target for sensory processing disorders.

neuroscience↗

bioRxiv2021

Auditory processing remains sensitive to environmental experience during adolescence

Development is a time of great opportunity. A heightened period of neural plasticity contributes to dramatic improvements in perceptual, motor, and cognitive skills. However, developmental plasticity poses a risk: greater malleability of neural circuits exposes them to environmental factors that may impede behavioral maturation. While these risks are well-established prior to sexual maturity (i.e., critical periods), the degree of neural vulnerability during adolescence remains uncertain. To address this question, we induced a transient period of hearing loss (HL) spanning adolescence in the gerbil, confirmed by assessment of circulating sex hormones, and asked whether behavioral and neural deficits are diminished. Wireless recordings were obtained from auditory cortex neurons during perceptual task performance, and within-session behavioral and neural sensitivity were compared. We found that a transient period of adolescent HL caused a significant perceptual deficit (i.e., amplitude modulation detection thresholds) that could be attributed to degraded auditory cortex processing, as confirmed with both single neuron and population-level analyses. In contrast, perceptual deficits did not occur when HL of the same duration was induced in adulthood. To determine whether degraded auditory cortex encoding was attributable to an intrinsic change, we obtained auditory cortex brain slices from adolescent HL animals, and recorded synaptic and discharge properties from auditory cortex pyramidal neurons. There was a clear and novel phenotype, distinct from critical period HL: excitatory postsynaptic potential amplitudes were elevated in adolescent HL animals, whereas inhibitory postsynaptic potentials were unchanged. This is in contrast to critical period deprivation, where there are large changes to synaptic inhibition. Taken together, these results show that diminished adolescent sensory experience can cause long-lasting behavioral deficits that originate, in part, from a dysfunctional cortical circuit. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=84 SRC="FIGDIR/small/439537v2_ufig1.gif" ALT="Figure 1"> View larger version (18K): org.highwire.dtl.DTLVardef@50b787org.highwire.dtl.DTLVardef@1410662org.highwire.dtl.DTLVardef@a0fa6org.highwire.dtl.DTLVardef@897b1c_HPS_FORMAT_FIGEXP M_FIG Summary of experimental design and main findings. C_FIG

neuroscience↗