On the similarities and differences of non-traumatic sound exposure during the critical period and in adulthood

Eggermont, Jos J.

doi:10.3389/fnsys.2013.00012

Cited by 14 publications

(6 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The notion of auditory sensitive periods in neuronal plasticity (review in Kral, 2013 ) has been established for deaf, cochlear-implanted animals (Kral et al, 2001 , 2002 , 2013 ) and cochlear-implanted children (Ponton and Eggermont, 2001 ; Sharma et al, 2002 , 2005 ), as well as for hearing animals (Zhang et al, 2002 ; Nakahara et al, 2004 ; de Villers-Sidani et al, 2008 ). However, sensitive periods are not observed in all plastic reorganizations in the brain (Noreña et al, 2006 ; Eggermont, 2013 ; Pienkowski et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Unilateral hearing during development: hemispheric specificity in plastic reorganizations

Kral¹,

Heid²,

Hubka³

et al. 2013

Front. Syst. Neurosci.

View full text Add to dashboard Cite

The present study investigates the hemispheric contributions of neuronal reorganization following early single-sided hearing (unilateral deafness). The experiments were performed on ten cats from our colony of deaf white cats. Two were identified in early hearing screening as unilaterally congenitally deaf. The remaining eight were bilaterally congenitally deaf, unilaterally implanted at different ages with a cochlear implant. Implanted animals were chronically stimulated using a single-channel portable signal processor for two to five months. Microelectrode recordings were performed at the primary auditory cortex under stimulation at the hearing and deaf ear with bilateral cochlear implants. Local field potentials (LFPs) were compared at the cortex ipsilateral and contralateral to the hearing ear. The focus of the study was on the morphology and the onset latency of the LFPs. With respect to morphology of LFPs, pronounced hemisphere-specific effects were observed. Morphology of amplitude-normalized LFPs for stimulation of the deaf and the hearing ear was similar for responses recorded at the same hemisphere. However, when comparisons were performed between the hemispheres, the morphology was more dissimilar even though the same ear was stimulated. This demonstrates hemispheric specificity of some cortical adaptations irrespective of the ear stimulated. The results suggest a specific adaptation process at the hemisphere ipsilateral to the hearing ear, involving specific (down-regulated inhibitory) mechanisms not found in the contralateral hemisphere. Finally, onset latencies revealed that the sensitive period for the cortex ipsilateral to the hearing ear is shorter than that for the contralateral cortex. Unilateral hearing experience leads to a functionally-asymmetric brain with different neuronal reorganizations and different sensitive periods involved.

show abstract

Section: Discussionmentioning

confidence: 99%

Unilateral hearing during development: hemispheric specificity in plastic reorganizations

Kral¹,

Heid²,

Hubka³

et al. 2013

Front. Syst. Neurosci.

View full text Add to dashboard Cite

show abstract

“…For example, in the auditory system a CP exists for rapid and permanent alterations of cortical sensory representations in response to sound (Eggermont, 2013, Kral, 2013), with implications that inform cochlear implantation (Kral and Sharma, 2012). Furthermore, in primary somatosensory and auditory cortices critical periods are thought to be regulated via balances in excitatory/inhibitory network activity (Froemke and Jones, 2011, Xiong et al, 2011, Zhang et al, 2011), a suggestion that has been made for the modulation of the CP in V1 as well (Hensch and Fagiolini, 2005, Chen and Nedivi, 2013).…”

Section: Deprivation-induced Plasticity In Visual Cortex: Differencesmentioning

confidence: 99%

Adult cortical plasticity following injury: Recapitulation of critical period mechanisms?

Nahmani

Turrigiano

2014

Neuroscience

View full text Add to dashboard Cite

A primary goal of research on developmental critical periods is the recapitulation of a juvenile-like state of malleability in the adult brain that might enable recovery from injury. These ambitions are often framed in terms of the simple reinstatement of enhanced plasticity in the growth-restricted milieu of an injured adult brain. Here, we provide an analysis of the similarities and differences between deprivation-induced and injury-induced cortical plasticity, to provide for a nuanced comparison of these remarkably similar processes. As a first step, we review the factors that drive ocular dominance plasticity in the primary visual cortex of the uninjured brain during the critical period (CP) and in adults, to highlight processes that might confer adaptive advantage. In addition, we directly compare deprivation-induced cortical plasticity during the CP and plasticity following acute injury or ischemia in mature brain. We find that these two processes display a biphasic response profile following deprivation or injury: an initial decrease in GABAergic inhibition and synapse loss transitions into a period of neurite expansion and synaptic gain. This biphasic response profile emphasizes the transition from a period of cortical healing to one of reconnection and recovery of function. Yet while injury-induced plasticity in adult shares several salient characteristics with deprivation-induced plasticity during the CP, the degree to which the adult injured brain is able to functionally rewire, and the time required to do so, present major limitations for recovery. Attempts to recapitulate a measure of CP plasticity in an adult injury context will need to carefully dissect the circuit alterations and plasticity mechanisms involved while measuring functional behavioral output to assess their ultimate success.

show abstract

“…We confirmed CP plasticity with a second passive exposure to pure tones that led to the expansion of the corresponding frequency region in the primary auditory cortex (A1). The perceptual consequences of this map expansion are incompletely understood and differ based on the mode of induction, with primarily sound-driven—as opposed to neuromodulatory-driven—expansions impairing discrimination for the exposure frequency (Han et al, 2007; Eggermont, 2013; Froemke et al, 2013). Based on the common phenotype of map expansion in both sound-exposed animals and animals with tinnitus, we wondered if the sound exposure used in our previous study could have imparted our rats with tinnitus or another auditory disorder.…”

Section: Introductionmentioning

confidence: 99%

Evidence of Hyperacusis in Adult Rats Following Non-traumatic Sound Exposure

Thomas

Guercio

Drudik

et al. 2019

Front. Syst. Neurosci.

View full text Add to dashboard Cite

Manipulations that enhance neuroplasticity may inadvertently create opportunities for maladaptation. We have previously used passive exposures to non-traumatic white noise to open windows of plasticity in the adult rat auditory cortex and induce frequency-specific functional reorganizations of the tonotopic map. However, similar reorganizations in the central auditory pathway are thought to contribute to the generation of hearing disorders such as tinnitus and hyperacusis. Here, we investigate whether noise-induced reorganizations are accompanied by electrophysiological or behavioral evidence of tinnitus or hyperacusis in adult Long-Evans rats. We used a 2-week passive exposure to moderate-intensity (70 dB SPL) broadband white noise to reopen a critical period for spectral tuning such that a second 1-week exposure to 7 kHz tone pips produced an expansion of the 7 kHz frequency region in the primary auditory cortex (A1). We demonstrate for the first time that this expansion also takes place in the ventral auditory field (VAF). Sound exposure also led to spontaneous and sound-evoked hyperactivity in the anterior auditory field (AAF). Rats were assessed for behavioral evidence of tinnitus or hyperacusis using gap and tone prepulse inhibition of the acoustic startle response. We found that sound exposure did not affect gap-prepulse inhibition. However, sound exposure led to an improvement in prepulse inhibition when the prepulse was a 7 kHz tone, showing that exposed rats had enhanced sensorimotor gating for the exposure frequency. Together, our electrophysiological and behavioral results provide evidence of hyperacusis but not tinnitus in sound-exposed animals. Our findings demonstrate that periods of prolonged noise exposure may open windows of plasticity that can also be understood as windows of vulnerability, potentially increasing the likelihood for maladaptive plasticity to take place.

show abstract

On the similarities and differences of non-traumatic sound exposure during the critical period and in adulthood

Cited by 14 publications

References 39 publications

Unilateral hearing during development: hemispheric specificity in plastic reorganizations

Unilateral hearing during development: hemispheric specificity in plastic reorganizations

Adult cortical plasticity following injury: Recapitulation of critical period mechanisms?

Evidence of Hyperacusis in Adult Rats Following Non-traumatic Sound Exposure

Contact Info

Product

Resources

About