Thalamocortical Projectional Divergence Leads to Complexity in Functional Organizations in Mouse Auditory Cortex
Shinpei Ohga, Hiroaki TsukanoiD, Masao Horie, Hiroki TerashimaiD, Nana Nishio, Yamato Kubota, Kuniyuki TakahashiiD, Ryuichi HishidaiD, Hirohide TakebayashiiD, Katsuei ShibukiiD
Abstract
Frequency-related topological projections from the ventral division of the medial geniculate body (MGv) relay the tonotopic organization found in primary auditory cortex (A1). However, relaying circuits of the functional organization to higher-order, secondary auditory field (A2) have not been identified so far. Here, using tracing, we found that A2 receives dense topological projections from MGv in mice, and that tonotopy was established in A2 even when primary fields including A1 were removed. These indicate that thalamic inputs to A2 are sufficient for generating its tonotopy. Moreover, neuronal responses in the thalamocortical recipient layer of A2 showed wider bandwidth and greater heterogeneity of the best frequency distribution than those of A1, which was attributed to larger divergence of thalamocortical projections from MGv to A2 than those from MGv to A1. The current study identifies that the functional organization in the auditory cortex can be determined by the structure of thalamocortical input.\n\nSignificant StatementAlthough peripheral input patterns to the primary auditory cortex (A1) of the brain are well understood, how tonal information is relayed to higher-order regions such as the secondary auditory field (A2) remains unclear. This work revealed a new source of auditory information to A2; the tonal map in mouse A2 is primarily produced by orderly projections from the primary auditory thalamus. We also found that the complex behaviour and organization of neurons in A2 is generated by divergent projections from the primary thalamus that converge on neurons in A2. Our findings indicate that thalamocortical projections constitute a major factor that determines the regional properties and functional organization of mouse A2.
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