Reduction of corpus callosum activity during whisking leads to interhemispheric decorrelation

Yael Oran, Yonatan Katz, Michael Sokoletsky, Katayun Cohen-Kashi Malina, Ilan Lampl*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Interhemispheric correlation between homotopic areas is a major hallmark of cortical physiology and is believed to emerge through the corpus callosum. However, how interhemispheric correlations and corpus callosum activity are affected by behavioral states remains unknown. We performed laminar extracellular and intracellular recordings simultaneously from both barrel cortices in awake mice. We find robust interhemispheric correlations of both spiking and synaptic activities that are reduced during whisking compared to quiet wakefulness. Accordingly, optogenetic inactivation of one hemisphere reveals that interhemispheric coupling occurs only during quiet wakefulness, and chemogenetic inactivation of callosal terminals reduces interhemispheric correlation especially during quiet wakefulness. Moreover, in contrast to the generally elevated firing rate observed during whisking epochs, we find a marked decrease in the activity of imaged callosal fibers. Our results indicate that the reduction in interhemispheric coupling and correlations during active behavior reflects the specific reduction in the activity of callosal neurons.
Interhemispheric correlations are mediated by the corpus callosum, an extensive fiber bundle connecting the cortical hemispheres. The authors show that interhemispheric correlations between the somatosensory cortices of awake mice are reduced during whisking as a result of lower callosal activity.
Original languageEnglish
Article number4095
Number of pages19
JournalNature Communications
Volume12
Issue number1
DOIs
Publication statusPublished - 1 Dec 2021

Funding

I.L. is the incumbent of the Norman and Helen Asher Professorial Chair at the Weizmann Institute of Science. Y.K. is incumbent of the Marianne Manoville Beck Research Fellow Chair in Brain Research. We thank A. Parabucki and for making the schematic illustrations and both her and A. Marmelshtein for constructive comments on an earlier version of this manuscript. This research was supported by DFG (SFB 1089), EraNet (DeCipher Neuron 01EW1606), Human Frontier Science Program Grant, Israel Science Foundation (ISF 1539/ 17), BSF grant 2019251, Minerva, and the Marianne Manoville Beck Laboratory for Research in Neurobiology in Honor of her Parents Elisabeth and Miksa Manoville, all awarded to I.L.

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