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

Abstract

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.

Cross-modal reaction of auditory and visual cortices after long-term bilateral hearing deprivation in the rat

“…c-Fos is a marker of neuronal activity which is rapidly induced after neuronal depolarisation (Greenberg et al 1986;Morgan and Curran 1988;Bartel et al 1989;Joo et al 2016). Accordingly, increased VC activation is confirmed by the overexpression of the activity-dependent early gene c-Fos (present results) and by significant increases in immunoreactive neurons in the VC (Pernia et al 2017). Furthermore, a link between Arc/Arg3.1 expression and neuronal electrical activity has been demonstrated by the increase in Arc/Arg3.1 gene expression after high-frequency stimulation of the hippocampus (Lyford et al 1995;Steward et al 1998Steward et al , 2015.…”

“…In deaf mice, a potential increase in VC activation has been demonstrated by c-Fos overexpression (Teichert and Bolz 2017). In addition, after bilateral long-term deafness, c-Fos and Arc/Arg3.1 expression is significantly increased in immunoreactive neurons in the VC (Pernia et al, 2017). Thus, these data indicate that hearing deprivation induces long-term bimodal adaptive reorganisation of cortical neuronal networks and altered functional interactions between the VC and AC.…”

“…Surgery and hearing loss validation in this animal model of long-term hearing deprivation have been extensively detailed in a previous paper published by our laboratory (Pernia et al 2017). Deep anaesthesia was induced by intramuscular injections of ketamine chlorhydrate (30 mg/kg BW; Imalgene 1000, Rhone Méreuse, Lyon, France) and 5 mg/ kg xylazine chlorhydrate (5 mg/kg BW; Rompun, Bayer, Leverkusen, Germany).…”

Expression and Localization of Kv1.1 and Kv3.1b Potassium Channels in the Cochlear Nucleus and Inferior Colliculus after Long-Term Auditory Deafferentation

“…Bilateral cochlear lesions were performed as previously described [16]. Animals were anesthetized using a mixture of ketamine chlorohydrate (30 mg/kg Imalgene 1000, Rhone Méreuse, Lyon, France) and xylazine chlorohydrate (5 mg/kg, Rompun, Bayer, Leverkusen, Germany) and placed on a warm pad.…”

“…Activity deprivation triggers complex post-lesion adaptive mechanisms at different central levels up to the auditory cortex. Several deafness-related plasticity mechanisms are known, including central connectivity rearrangements and adaptations of inhibitory and excitatory synaptic input in response to loss of primary excitatory drive [15][16][17][18]. Plastic adaptations involving regulation of several classes of potassium channels, including Kv1.1 and Kv3.1b, were also reported [1,13,[19][20][21][22][23].…”