Rapid modifications in calretinin immunostaining in the deep layers of the superior colliculus after unilateral cochlear ablation

Alvarado, Juan Carlos; Fuentes–Santamaría, Verónica; Henkel, Craig K.

doi:10.1016/j.heares.2008.10.005

Cited by 11 publications

(12 citation statements)

References 60 publications

(89 reference statements)

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“…Thus, our model reproduces an abrupt cessation of peripheral synaptic auditory input, accompanied by progressive structural damage of first order neurons and their central synapses (Butler & Lomber, ; Wang, O'Donohue, & Manis, ). Animal models of deafness induced by cochlear mechanical lesion have been previously used to investigate post‐lesion plasticity in the auditory pathway (Vale & Sanes, ; Illing, Kraus, & Meidinger, ; Rubio, ; Alvarado, Fuentes‐Santamaría, & Henkel, ).…”

Section: Discussionmentioning

confidence: 99%

c‐Fos and Arc/Arg3.1 expression in auditory and visual cortices after hearing loss: Evidence of sensory crossmodal reorganization in adult rats

Pernìa

Estévez

Poveda

et al. 2017

J of Comparative Neurology

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Cross-modal reorganization in the auditory and visual cortices has been reported after hearing and visual deficits mostly during the developmental period, possibly underlying sensory compensation mechanisms. However, there are very few data on the existence or nature and timeline of such reorganization events during sensory deficits in adulthood. In this study, we assessed long-term changes in activity-dependent immediate early genes c-Fos and Arc/Arg3.1 in auditory and neighboring visual cortical areas after bilateral deafness in young adult rats. Specifically, we analyzed qualitatively and quantitatively c-Fos and Arc/Arg3.1 immunoreactivity at 15 and 90 days after cochlea removal. We report extensive, global loss of c-Fos and Arc/Arg3.1 immunoreactive neurons in the auditory cortex 15 days after permanent auditory deprivation in adult rats, which is partly reversed 90 days after deafness. Simultaneously, the number and labeling intensity of c-Fos-and Arc/Arg3.1-immunoreactive neurons progressively increase in neighboring visual cortical areas from 2 weeks after deafness and these changes stabilize three months after inducing the cochlear lesion. These findings support plastic, compensatory, long-term changes in activity in the auditory and visual cortices after auditory deprivation in the adult rats. Further studies may clarify whether those changes result in perceptual potentiation of visual drives on auditory regions of the adult cortex.

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Section: Discussionmentioning

confidence: 99%

c‐Fos and Arc/Arg3.1 expression in auditory and visual cortices after hearing loss: Evidence of sensory crossmodal reorganization in adult rats

Pernìa

Estévez

Poveda

et al. 2017

J of Comparative Neurology

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“…For each section, three microscopic 60× fields (dorsal, middle, and ventral) extending through the rostrocaudal dimension of the nucleus were selected, photographed and analyzed. As described elsewhere (Fuentes-Santamaría et al, 2003 , 2005 , 2007a , b ; Alvarado et al, 2004 , 2009a ), the immunostaining was evaluated by using the public domain image analysis software Scion Image for Windows (version beta 4.0.2; developed by Scion Corp). For suitable comparisons of the staining across samples, a macro was used to process and analyze the captured images (Alvarado et al, 2004 ).…”

Section: Methodsmentioning

confidence: 99%

The Role of Glia in the Peripheral and Central Auditory System Following Noise Overexposure: Contribution of TNF-α and IL-1β to the Pathogenesis of Hearing Loss

et al. 2017

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Repeated noise exposure induces inflammation and cellular adaptations in the peripheral and central auditory system resulting in pathophysiology of hearing loss. In this study, we analyzed the mechanisms by which noise-induced inflammatory-related events in the cochlea activate glial-mediated cellular responses in the cochlear nucleus (CN), the first relay station of the auditory pathway. The auditory function, glial activation, modifications in gene expression and protein levels of inflammatory mediators and ultrastructural changes in glial-neuronal interactions were assessed in rats exposed to broadband noise (0.5–32 kHz, 118 dB SPL) for 4 h/day during 4 consecutive days to induce long-lasting hearing damage. Noise-exposed rats developed a permanent threshold shift which was associated with hair cell loss and reactive glia. Noise-induced microglial activation peaked in the cochlea between 1 and 10D post-lesion; their activation in the CN was more prolonged reaching maximum levels at 30D post-exposure. RT-PCR analyses of inflammatory-related genes expression in the cochlea demonstrated significant increases in the mRNA expression levels of pro- and anti-inflammatory cytokines, inducible nitric oxide synthase, intercellular adhesion molecule and tissue inhibitor of metalloproteinase-1 at 1 and 10D post-exposure. In noise-exposed cochleae, interleukin-1β (IL-1β), and tumor necrosis factor α (TNF-α) were upregulated by reactive microglia, fibrocytes, and neurons at all time points examined. In the CN, however, neurons were the sole source of these cytokines. These observations suggest that noise exposure causes peripheral and central inflammatory reactions in which TNF-α and IL-1β are implicated in regulating the initiation and progression of noise-induced hearing loss.

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“…The immunostaining analysis was performed by using the public domain image analysis software Scion Image for Windows (version beta 4.0.2; developed by Scion Corp), as described elsewhere (Fuentes-Santamaría et al, 2003 , 2005b , 2007a , b ; Alvarado et al, 2004 , 2009a ). Immunostained cochlear and CN sections were examined via brightfield illumination using a Nikon Eclipse 80i photomicroscope (Nikon Instruments Europe B.V.).…”

Section: Methodsmentioning

confidence: 99%

Noise-Induced “Toughening” Effect in Wistar Rats: Enhanced Auditory Brainstem Responses Are Related to Calretinin and Nitric Oxide Synthase Upregulation

et al. 2016

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An appropriate conditioning noise exposure may reduce a subsequent noise-induced threshold shift. Although this “toughening” effect helps to protect the auditory system from a subsequent traumatic noise exposure, the mechanisms that regulate this protective process are not fully understood yet. Accordingly, the goal of the present study was to characterize physiological processes associated with “toughening” and to determine their relationship to metabolic changes in the cochlea and cochlear nucleus (CN). Auditory brainstem responses (ABR) were evaluated in Wistar rats before and after exposures to a sound conditioning protocol consisting of a broad-band white noise of 118 dB SPL for 1 h every 72 h, four times. After the last ABR evaluation, animals were perfused and their cochleae and brains removed and processed for the activity markers calretinin (CR) and neuronal nitric oxide synthase (nNOS). Toughening was demonstrated by a progressively faster recovery of the threshold shift, as well as wave amplitudes and latencies over time. Immunostaining revealed an increase in CR and nNOS levels in the spiral ganglion, spiral ligament, and CN in noise-conditioned rats. Overall, these results suggest that the protective mechanisms of the auditory toughening effect initiate in the cochlea and extend to the central auditory system. Such phenomenon might be in part related to an interplay between CR and nitric oxide signaling pathways, and involve an increased cytosolic calcium buffering capacity induced by the noise conditioning protocol.

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Rapid modifications in calretinin immunostaining in the deep layers of the superior colliculus after unilateral cochlear ablation

Cited by 11 publications

References 60 publications

c‐Fos and Arc/Arg3.1 expression in auditory and visual cortices after hearing loss: Evidence of sensory crossmodal reorganization in adult rats

c‐Fos and Arc/Arg3.1 expression in auditory and visual cortices after hearing loss: Evidence of sensory crossmodal reorganization in adult rats

The Role of Glia in the Peripheral and Central Auditory System Following Noise Overexposure: Contribution of TNF-α and IL-1β to the Pathogenesis of Hearing Loss

Noise-Induced “Toughening” Effect in Wistar Rats: Enhanced Auditory Brainstem Responses Are Related to Calretinin and Nitric Oxide Synthase Upregulation

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