Visual Abstract

Dichromatic vision is common in many mammals. However, color processing in the primary visual cortex (V1) of dichromatic mammals is relatively unknown compared to the trichromatic primates. In this study, we investigated the functional organization of color processing in mouse V1. The mouse retina has a graded expression pattern of two opsins along its dorsoventral axis. However, it is not clear whether and how this expression pattern is reflected in the cortical representation at local (several hundred microns) and areal (V1) level. Using in vivo two-photon calcium (Ca2+) imaging and wide-field Ca2+ imaging, we revealed that V1 neurons responded to S (UV)- and M (green)-opsin isolating stimuli with slightly biased color preference depending on retinotopic position in V1. This was consistent with the distribution of retinal opsins. At the cellular level, preferences for S- and M-opsin isolating stimuli were intermingled in a local region encompassing several hundred microns. These results suggest that functional organizations of color information are locally intermingled, but slightly biased depending on the retinotopic position in mouse V1.

Developing neurons initially form excessive neurites and then remodel them based on molecular cues and neuronal activity. Developing mitral cells in the olfactory bulb initially extend multiple primary dendrites. They then stabilize single primary dendrites while eliminating others. However, the mechanisms underlying selective dendrite remodeling remain elusive. Using CRISPR-Cas9-based knockout screening combined with in utero electroporation, we identify BMPR-2 as a key regulator for selective dendrite stabilization. Bmpr2 knockout and its rescue experiments show that BMPR-2 inhibits LIMK without ligands and thereby permits dendrite destabilization. In contrast, the overexpression of antagonists and agonists indicates that ligand-bound BMPR-2 stabilizes dendrites, most likely by releasing LIMK. Using genetic and FRET imaging experiments, we demonstrate that free LIMK is activated by NMDARs via Rac1, facilitating dendrite stabilization through F-actin formation. Thus, the selective stabilization of primary dendrites is ensured by concomitant inputs of BMP ligands and neuronal activity.

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