脊髄内ニューロンのサブ集団による機械的のゲート制御

Steeve Bourane¹, Bo Duan², Stephanie C Koch¹

¹Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.

Science (New York, N.Y.)

|October 31, 2015

まとめ

神経ペプチドY::Cre (NPY::Cre) を発現する脊髄阻害性ニューロンは,ゲートによる機械的を誘発する. これらのニューロンを静止すると慢性的なが起こり機械的なの伝達経路が明らかになります

科学分野:

神経科学
脊髄研究
かゆみ生物学

背景:

軽い接触によって引き起こされる機械的は,通常,機械受容体によって抑制されます.
この抑制は,アロクネシスのような慢性的な状態で失われます.
ゲーティングメカニズムを理解することは慢性的なを治療するのに不可欠です

研究の目的:

脊髄の経路を特定する
神経ペプチドY::Cre (NPY::Cre) が内ニューロンを発現するメカニカルなの伝達における役割を調査する.
慢性的なメカニカルイチに関わる特定の経路を解明する.

主な方法:

ネズミの背中のNPY::Cre-derivedニューロンの選択的消去と静止.
メカニカルなの反応の評価
化学物質に対する敏感性や痛みの評価
ヒスタミン独立性およびガストリン放出ペプチド受容体独立性経路の調査

主要な成果:

NPYの選択的消去または静止: クレニューロンが誘発した機械的.
化学薬品に対する過敏症や痛みに対する過敏症は観察されなかった.
誘発された慢性的なはヒスタミンに依存していない.
ガストリン放出ペプチド受容体発現ニューロンとは独立して発現した.

結論:

脊髄NPY:Cre内ニューロンは,機械的なを遮断する専用の抑制経路を形成する.
この経路の機能の喪失は慢性的なメカニカルなを引き起こします
この経路は化学的なや痛みの感覚に関係する経路とは異なります

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