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 　Bromoxyuridine (BrdU) の取り込み実験から、MPOAの主な[[ニューロン]]はラットでは胎生14-18日に第三脳室壁から発生する (Orikasa et al., 2010)。３[[脳胞]]のうち[[前脳]] (forebrain)の尾側端に由来するので、発生学的には[[終脳]] (telencephalon)に属するが、機能的観点から、[[間脳]] (diencephalon)の最吻側部である視床下部と一体とされることがある (Le Gros Clark & Meyer, 1950)。かつては[[脳原基]]の部域化に関わる多くの[[転写因子]]やシグナル分子に[[視床下部]]と共通するものがあり、たとえばDlx5、 Pax6、Nkx2.1aの発現パターンから終脳と間脳の分節境界域 prosomeric boundaryを決定することはできないと論じられた(Puelles and Rubenstein, 2003)。一方、下郡らは異なった発生段階のマウス胎仔のMPOAと視床下部のマイクロアレイ解析からマウス胎児の終脳ではFoxg1が、間脳吻側端にはGdf10が発現し境界が存在することを示した(Blackshaw et al., 2010)。MPOAは終脳のFoxg1陽性細胞に由来し、間脳由来の視床下部とは起源が異なる。また、視床下部のランドマーク遺伝子であるソニックヘッジホッグ (Shh)のノックアウトマウスでは視床下部吻側部が欠損するが、MPOAは形成される。<BR>
-　第三脳室壁から発生するニューロンに加え、[[wikipedia:ja:齧歯類|齧歯類]]では[[性腺刺激ホルモン放出ホルモン]]（gonadotropin releasing hormone, GnRH）産生ニューロンが嗅上皮の原基である内側嗅板medial olfactory placodeに発生し視索前野に移動し定着する(Schwanzel-Fukuda & Pfaff, 1989)。Xp22.3上の[[KAL-1]]遺伝子の異常により生じるヒトのKallmann症候群は[[無嗅覚症]]を伴う伴性低ゴナドトロピン性[[性腺機能不全]]で、GnRHニューロンは前頭の篩骨を透過できずこの移動が起こらない。ただし、正常なrhesusやヒトのではGnRHニューロンはさらに尾側に移動を続け、視床下部内側底部から隆起漏斗部に定着する。この移動・定着の障害が視床下部性性腺機能低下症の一つであるKallman症候の病因である(Schwanzel-Fukuda et al., 1989) [[内側視索前野|下記病態参照]]。<BR>
+　第三脳室壁から発生するニューロンに加え、[[wikipedia:ja:齧歯類|齧歯類]]では[[性腺刺激ホルモン放出ホルモン]]（gonadotropin releasing hormone, GnRH）産生ニューロンが嗅上皮の原基である内側嗅板medial olfactory placodeに発生し視索前野に移動し定着する(Schwanzel-Fukuda & Pfaff, 1989)。Xp22.3上の[[KAL-1]]遺伝子の異常により生じるヒトのKallmann症候群は[[無嗅覚症]]を伴う伴性低ゴナドトロピン性[[性腺機能不全]]で、GnRHニューロンは前頭の篩骨を透過できずこの移動が起こらない。ただし、正常なrhesusやヒトのではGnRHニューロンはさらに尾側に移動を続け、視床下部内側底部から隆起漏斗部に定着する。この移動・定着の障害が視床下部性性腺機能低下症の一つであるKallman症候の病因である(Schwanzel-Fukuda et al., 1989) (下記病態参照)。<BR>
 <BR>== 構造 ==<BR>
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