Prolonged non-traumatic early auditory deprivation increases hearing thresholds, leads to memory deficits, and reduces doublecortin-positive neurons in mice.

The critical period following hearing onset in rodents and humans is a window of plasticity essential for auditory system development. Additionally, multiple studies have demonstrated that auditory deprivation can lead to cognitive impairments in both animals and humans. Therefore, early acoustic deprivation (EAD) can negatively influence the development and function of hearing and mental processes, potentially affecting the well-being of individuals with early-life deafness. However, there is limited experimental evidence on how EAD impacts auditory processing, memory, and hippocampal function. In this study, we used a simple, non-invasive, and straightforward method of auditory deprivation: a reversible elastomer earplug applied to mice, kept in place for 30 days. This method raised the auditory threshold by 30 dB, and this elevation persisted for five days after the earplugs were removed. The mice showed deficits in Paired Pulse Inhibition (PPI) of the startle reflex and in gap-prepulse inhibition of acoustic startle (GPIAS). They also displayed memory problems, as tested by novel object recognition and placement tasks, without changes in hippocampal long-term potentiation. Moreover, although there were no changes in dendritic spine numbers in hippocampal granule neurons, a significant reduction in hippocampal and doublecortin-positive cells was observed, suggesting a decrease in the population of immature neurons in the dentate gyrus. We conclude that a 30-day EAD affects not only auditory processing but also leads to notable memory deficits with possible implications for developing persistent hearing and learning disorders.