Author
Listed:
- Kasumi Inokuchi
(School of Medical Science, University of Fukui
Graduate School of Science, The University of Tokyo)
- Fumiaki Imamura
(Pennsylvania State University College of Medicine)
- Haruki Takeuchi
(School of Medical Science, University of Fukui)
- Ryang Kim
(Graduate School of Medicine, The University of Tokyo)
- Hiroyuki Okuno
(Graduate School of Medicine, The University of Tokyo)
- Hirofumi Nishizumi
(School of Medical Science, University of Fukui
Graduate School of Science, The University of Tokyo)
- Haruhiko Bito
(Graduate School of Medicine, The University of Tokyo)
- Takefumi Kikusui
(School of Veterinary Medicine, Azabu University)
- Hitoshi Sakano
(School of Medical Science, University of Fukui)
Abstract
Odour information induces various innate responses that are critical to the survival of the individual and for the species. An axon guidance molecule, Neuropilin 2 (Nrp2), is known to mediate targeting of olfactory sensory neurons (primary neurons), to the posteroventral main olfactory bulb (PV MOB) in mice. Here we report that Nrp2-positive (Nrp2+) mitral cells (MCs, second-order neurons) play crucial roles in transmitting attractive social signals from the PV MOB to the anterior part of medial amygdala (MeA). Semaphorin 3F, a repulsive ligand to Nrp2, regulates both migration of Nrp2+ MCs to the PV MOB and their axonal projection to the anterior MeA. In the MC-specific Nrp2 knockout mice, circuit formation of Nrp2+ MCs and odour-induced attractive social responses are impaired. In utero, electroporation demonstrates that activation of the Nrp2 gene in MCs is sufficient to instruct their circuit formation from the PV MOB to the anterior MeA.
Suggested Citation
Kasumi Inokuchi & Fumiaki Imamura & Haruki Takeuchi & Ryang Kim & Hiroyuki Okuno & Hirofumi Nishizumi & Haruhiko Bito & Takefumi Kikusui & Hitoshi Sakano, 2017.
"Nrp2 is sufficient to instruct circuit formation of mitral-cells to mediate odour-induced attractive social responses,"
Nature Communications, Nature, vol. 8(1), pages 1-13, December.
Handle:
RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15977
DOI: 10.1038/ncomms15977
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