Abstract
Harmful environmental sounds are a prevailing source of chronic hearing impairments, including noise induced hearing loss, hyperacusis, or tinnitus. How these symptoms are related to pathophysiological damage to the sensory receptor epithelia and its effects along the auditory pathway, have been documented in numerous studies. An open question concerns the temporal evolution of maladaptive changes after damage and their manifestation in the balance of thalamocortical and corticocortical input to the auditory cortex (ACx). To address these issues, we investigated the loci of plastic reorganizations across the tonotopic axis of the auditory cortex of male Mongolian gerbils (Meriones unguiculatus) acutely after a sound trauma and after several weeks. We used a residual current-source density analysis to dissociate adaptations of intracolumnar input and horizontally relayed corticocortical input to synaptic populations across cortical layers in ACx. A pure tone-based sound trauma caused acute changes of subcortical inputs and corticocortical inputs at all tonotopic regions, particularly showing a broad reduction of tone-evoked inputs at tonotopic regions around the trauma frequency. At other cortical sites, the overall columnar activity acutely decreased, while relative contributions of lateral corticocortical inputs increased. After 4–6 weeks, cortical activity in response to the altered sensory inputs showed a general increase of local thalamocortical input reaching levels higher than before the trauma. Hence, our results suggest a detailed mechanism for overcompensation of altered frequency input in the auditory cortex that relies on a changing balance of thalamocortical and intracortical input and along the frequency gradient of the cortical tonotopic map.
Highlights
Exposure to harmful environmental sound is a common cause for hearing impairments, including the development of noise-induced hearing loss (NIHL) (Eggermont, 2017a,b)
Whereas peripheral damage initially leads to reduced activity within the damaged region of the cochlea, increased activity has been described for several nuclei along the auditory pathway from the dorsal cochlear nucleus on (Kaltenbach et al, 1998, 2004; Kaltenbach and Afman, 2000; Brozoski et al, 2002; Zacharek et al, 2002; Sun et al, 2009; Holt et al, 2010; Wu et al, 2016) and was interpreted as a potential physiological correlate of tinnitus (e.g., Noreña and Eggermont, 2003; Engineer et al, 2011; Ahlf et al, 2012; Tziridis et al, 2015)
In this report we have described acute and long-term effects of noise trauma on functional neuronal circuitry in auditory cortex (ACx) with particular emphasis on the relative contributions of thalamocortically and intracortically relayed input to a tonotopic site
Summary
Exposure to harmful environmental sound is a common cause for hearing impairments, including the development of noise-induced hearing loss (NIHL) (Eggermont, 2017a,b). Recent studies in rats have demonstrated that while partial hearing loss affects even neighboring audiovisual cortical areas, the loss-induced central gain enhancement was more locally confined to auditory areas (Schormans et al, 2017, 2019) While these data principally demonstrate broad involvement of many nuclei along the auditory pathway as well as corticofugal projections in reflecting and compensating damage of the auditory periphery, relatively little is known about the convergent contribution of thalamocortical and intracortical inputs to these effects. A better understanding of the circuit mechanisms underlying this dynamic temporal process may provide new implications to ameliorate the effects of noiseinduced hearing loss or its common perceptual symptom of chronic tinnitus
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