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

Autor: Pernia M; Instituto de Neurociencias of Castilla y León-INCyL, Universidad de Salamanca, Salamanca, Spain., Díaz I; Instituto de Neurociencias of Castilla y León-INCyL, Universidad de Salamanca, Salamanca, Spain., Colmenárez-Raga AC; Instituto de Neurociencias of Castilla y León-INCyL, Universidad de Salamanca, Salamanca, Spain., Rivadulla C; Centro de Investigaciones Científicas Avanzadas (CICA), Facultad de Ciencias de la Salud, Universidad de A Coruña and Instituto de Investigaciones Biomédicas de A Coruña (INIBIC), A Coruña, Spain., Cudeiro J; Centro de Investigaciones Científicas Avanzadas (CICA), Facultad de Ciencias de la Salud, Universidad de A Coruña and Instituto de Investigaciones Biomédicas de A Coruña (INIBIC), A Coruña, Spain., Plaza I; Instituto de Neurociencias of Castilla y León-INCyL, Universidad de Salamanca, Salamanca, Spain., Merchán MA; Instituto de Neurociencias of Castilla y León-INCyL, Universidad de Salamanca, Salamanca, Spain. merchan@usal.es.
Jazyk: angličtina
Zdroj: Brain structure & function [Brain Struct Funct] 2020 Jan; Vol. 225 (1), pp. 129-148. Date of Electronic Publication: 2019 Nov 28.
DOI: 10.1007/s00429-019-01991-w
Abstrakt: Visual cortex (VC) over-activation analysed by evoked responses has been demonstrated in congenital deafness and after long-term acquired hearing loss in humans. However, permanent hearing deprivation has not yet been explored in animal models. Thus, the present study aimed to examine functional and molecular changes underlying the visual and auditory cross-modal reaction. For such purpose, we analysed cortical visual evoked potentials (VEPs) and the gene expression (RT-qPCR) of a set of markers for neuronal activation (c-Fos) and activity-dependent homeostatic compensation (Arc/Arg3.1). To determine the state of excitation and inhibition, we performed RT-qPCR and quantitative immunocytochemistry for excitatory (receptor subunits GluA2/3) and inhibitory (GABAA-α1, GABAB-R2, GAD65/67 and parvalbumin-PV) markers. VC over-activation was demonstrated by a significant increase in VEPs wave N1 and by up-regulation of the activity-dependent early genes c-Fos and Arc/Arg3.1 (thus confirming, by RT-qPCR, our previously published immunocytochemical results). GluA2 gene and protein expression were significantly increased in the auditory cortex (AC), particularly in layers 2/3 pyramidal neurons, but inhibitory markers (GAD65/67 and PV-GABA interneurons) were also significantly upregulated in the AC, indicating a concurrent increase in inhibition. Therefore, after permanent hearing loss in the rat, the VC is not only over-activated but also potentially balanced by homeostatic regulation, while excitatory and inhibitory markers remain imbalanced in the AC, most likely resulting from changes in horizontal intermodal regulation.
Databáze: MEDLINE