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Feedback inhibition derived from the posterior parietal cortex regulates the neural properties of the mouse visual cortex
Author(s) -
Hishida Ryuichi,
Horie Masao,
Tsukano Hiroaki,
Tohmi Manavu,
Yoshitake Kohei,
Meguro Reiko,
Takebayashi Hirohide,
Yanagawa Yuchio,
Shibuki Katsuei
Publication year - 2019
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.14424
Subject(s) - neuroscience , visual cortex , sensory system , posterior parietal cortex , excitatory postsynaptic potential , cortex (anatomy) , psychology , calcium imaging , surround suppression , disconnection , inhibitory postsynaptic potential , visual perception , chemistry , perception , calcium , organic chemistry , political science , law
Feedback regulation from the higher association areas is thought to control the primary sensory cortex, contribute to the cortical processing of sensory information, and work for higher cognitive functions such as multimodal integration and attentional control. However, little is known about the underlying neural mechanisms. Here, we show that the posterior parietal cortex ( PPC ) persistently inhibits the activity of the primary visual cortex (V1) in mice. Activation of the PPC causes the suppression of visual responses in V1 and induces the short‐term depression, which is specific to visual stimuli. In contrast, pharmacological inactivation of the PPC or disconnection of cortical pathways from the PPC to V1 results in an effect of transient enhancement of visual responses in V1. Two‐photon calcium imaging demonstrated that the cortical disconnection caused V1 excitatory neurons an enhancement of visual responses and a reduction of orientation selectivity index ( OSI ). These results show that the PPC regulates the response properties of V1 excitatory neurons. Our findings reveal one of the functions of the PPC , which may contribute to higher brain functions in mice.