Hemispheric asymmetries in subcortical visual and auditory relay structures in congenital deafness

Neuroplasticity - the capacity of the brain to change as a response to internal and external pressures - has been studied from a number of different perspectives. Perhaps one of the most powerful models is the study of populations that have been congenitally deprived of a sense. It has been shown that the right Auditory Cortex (AC) of congenitally deaf humans is neuroplastically modified in order to represent visual properties of a stimulus. One unresolved question is how this visual information is routed to the AC of congenitally deaf individuals. Here, we performed volumetric analysis of subcortical auditory and visual brains regions - namely the thalamus (along with three thalamic nuclei: the pulvinar, the lateral geniculate nucleus and the medial geniculate nucleus), and the inferior and superior colliculi - in deaf and hearing participants in order to identify which structures may be responsible for relaying visual information toward the altered AC. Because there is a hemispheric asymmetry in the neuroplastic changes observed in the AC of the congenitally deaf, we reasoned that subcortical structures that also showed a similar asymmetry in their total volume could have been enlisted in the effort of relaying visual information to the neuroplastically altered right AC. We show that for deaf, but not for hearing individuals, the right thalamus, right lateral geniculate nucleus and right inferior colliculus are larger than their left counterparts. These results suggest that these subcortical structures may be responsible for rerouting visual information to the AC in congenital deafness.
LA is supported by Fundacao BIAL (http://www.bial.com/en/). AG-A is supported by Fundacao para a Ciencia e a Tecnologia Doctoral Grant number SFRH/BD/80945/2011 and Programa COMPETE. AO is funded by Sao Paulo Research Foundation (FAPESP) grant number 2014/06777-0, by the National Council for Scientific and Technological Development (CNPq) grant number 487188/2013-6 and by MackPesquisa grant number 105/2015. FF is funded by the NSFC of China (30925014; 31230029). DH is supported in part by a Postdoctoral Fellowship funded by the Peking-Tsinghua Center for Life Sciences. BZM and QC were supported by NIH grant R01NS089609 to BZM. YB is funded by NNSF of China (31171073; 31222024). JA is funded by Fundacao para a Ciencia e a Tecnologia projects PTDC/MHC-PCN/6805/2014 and PTDC/MHC-PCN/0522/2014, Programa COMPETE and by Fundacao BIAL 112/12. This research was supported by Fundacao BIAL (http://www.bial.com/en/).
info:eu-repo/semantics/publishedVersion