WordNet

the innermost light-sensitive membrane covering the back wall of the eyeball; it is continuous with the optic nerve
in or relating to the retina of the eye; "retinal cells"

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/04/19 00:01:08」(JST)

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「Retina」はこの項目へ転送されています。アップルの高精細ディスプレイについては「レティナディスプレイ」をご覧ください。

レチナIIa

レチナ（Retina ）は1934年からドイツコダックが製造販売したカメラである。レチナとはドイツ語で網膜の意。

1 概要
2 レチナ式巻き上げレバー
3 カウンターセット
4 126フィルム使用カメラ
5 135フィルム使用カメラ
- 5.1 レチナIシリーズ
- 5.2 レチナIIシリーズ
- 5.3 レチナIIIシリーズ
- 5.4 レチナオートマティックシリーズ
- 5.5 レチナレフレックスシリーズ
- 5.6 デッケルマウント交換レンズ
6 注釈
7 出典
8 参考文献

概要

市場における24×36mm（ライカ）判カメラは1925年にエルンスト・ライツ社から発売されたライカが先鞭を切って成功し、大手光学メーカーのツアイス・イコンが1932年にコンタックスを発売して対抗していたが、いずれも非常に高価格な製品であった。

ドイツコダックの前身・ナーゲルの創設者でもある技術者アウグスト・ナーゲルは、このように高級機に独占されていたライカ版カメラを大衆のものにしようと考えており、1934年^{[注釈 1]}に最初のレチナを発売、同時に親会社のコダックはこれに適合するパトローネ装填済みで扱いやすい135フィルムを発売した^[1]。

レチナは、カール・ツァイス製テッサー、シュナイダー・クロイツナッハ製クセナーなど一流レンズを装着、シャッターもデッケル製コンパーを採用するなど良質なパーツを採用した^[2]製品であったが、その良好な性能に比して廉価^[3]でかつ小型軽量であったことから、市場において歓迎される大ヒット製品となった。

その価格は1934年の発売直後ドイツ本国で75マルクであった。同時代の上級35mmフィルムカメラは、1935年のライカIIIa（エルマー50mmF3.5付き）が307マルク、1938年のコンタックスII型（テッサー50mmF3.5付き）が360マルクであった^[4]。また日本では1935年時点で定価195円^[3]であった。1937年時点でも日本でのレチナは定価195円-240円であったが、ライカはレンズのグレードにより580円から950円、コンタックスはその上をゆく970円-1,600円という超高額品で共に「家が建つほど高い」と言われていた。レチナがいかにバリュー・フォー・マネーな製品であったかを物語る逸話である。

このデザインコンセプトにバルダやウェルタなど多数のメーカーが追随したこともあって、元々映画用だった35mmフィルムの規格を、静止写真用として本格的に大衆に定着させる端緒となった^[4]。

頭に#のついた3桁の数字はレチナ愛好者の間でシュトゥットガルトタイプナンバーと言われているもので、ドイツコダック社内での形式番号である^[1]。

レチナ式巻き上げレバー

ボディー上蓋にレバーを置きフィルムを巻き上げる方式はモータードライブを内蔵しないカメラで現代でも一般的であるが、この方式は1951年にレチナIa/レチナIIaで初めて採用され、エルンスト・ライツ（現ライカ）のライカM3発売までは「レチナ式」と呼ばれていた^[5]。

レチナでレバー式巻上げであっても底部レバーの製品もある。

カウンターセット

機種によっては、逆算式フィルムカウンターが1になるとそれ以上巻き上げできなくなり、「故障した」と考えるユーザーが多い。扇状カウンター窓の中心にあるボタンを押し、背面の扁平な丸いボタンを「→」に沿って右にスライドさせるとカウンターが動いて巻上げできるようになる^[6]。

126フィルム使用カメラ

28×28mm判の一眼レフカメラ。

インスタマチックレフレックス（1968年発売） - デッケルマウントによるレンズ交換が可能。

135フィルム使用カメラ

24×36mm（ライカ）判のコンパクトカメラ。ファインダーのみのレチナIシリーズ、距離計を装備したレチナIIシリーズ、露出計と距離計を装備したレチナIIIシリーズに大きく区分することができる。

レチナIシリーズ

距離計はない。

レチナ - 巻き上げ、巻き戻しともノブ。シャッターレリーズはレンズシャッターのレリーズレバーを直接操作する方法の他、レンズシャッターのレリーズ穴に取り付ける極短いレリーズによる方法もある。この極短いレリーズはスナップに便利で「スケッチ・レリーズ」との名称で販売されていた^[3]。
- #117（1934年7月発売^[1]） - 最初の製品で、「オリジナルレチナ」とも呼ばれる^[1]。巻き上げノブとファインダーの間に巻き止め解除用ノブがあるのが特徴で、撮影後このノブを1/4回転させることで巻き止め機構が解除される^[1]。巻き戻し切り替えレバーは扁平で、巻き上げノブの上にある^[7]。フィルムカウンターがファインダーと巻き戻しノブとの間にある。メーカー資料によればシャッターは最高速1/300秒のコンパー、レンズはシュナイダー・クロイツナッハ製クセナー50mmF3.5のみとされているが、実際には最高速1/500秒のコンパーラピッド、コダック製アナスチグマートエクター50mmF3.5が装着された個体も存在する^[7]。仕上げは黒塗り、ニッケルメッキのみ^[7]。
- #118（1935年7月発売^[7]） - フィルム巻き止めが軍艦部背面のレバーに変更された^[7]。シャッターは最高速1/300秒のコンパーまたは最高速1/500秒のコンパーラピッド^[7]。仕上げは黒塗り、ニッケルメッキのみ^[7]。
- #119（1936年4月発売^[7]） - 巻き上げノブとファインダーの間の軍艦部が高くなり、フィルムカウンターがそちらに移動し、巻き戻しノブとファインダーの間の軍艦部は低く平坦になった^[7]。巻き上げノブ、巻き戻しノブが小径かつ背高になって扱いやすくなった^[7]。レンズがクセナー50mmF3.5またはコダック製エクター50mmF3.5^[7]。仕上げは黒塗り、ニッケルメッキのみ^[7]。
- #126（1936年3月発売^[7]） - アクセサリーシューが装着された^[7]。アクセサリーシューを持たない個体も存在するが、取り付け位置にネジ頭が2本あることで識別できる^[7]。外観に初めてクローム仕上げが採用されたが、黒塗りの個体も存在する^[7]。レンズはクセナー50mmF3.5またはエクター50mmF3.5に加え、カール・ツァイス製テッサー50mmF3.5、アルコー50mmF3.5、ローデンシュトック製イザール50mmF3.5、アンジェニュー製のアンジェニュー50mmF3.5が供給された^[7]。シャッターはコンパーラピッド^[7]。

レチナI - ボディーシャッターとなった^[7]。
- #141（1937年10月発売^[7]） - メーカー資料によればレンズはシュナイダー・クロイツナッハ製クセナー50mmF3.5またはエクター50mmF3.5とされているが、テッサー50mmF3.5が装着された個体も存在する^[7]。シャッターはコンパーまたはコンパーラピッド^[7]。仕上げはクロームメッキのみ^[7]。
- #143（1938年1月発売^[7]） - #141の黒塗り仕上げ版^[7]。クセナー50mmF3.5、コンパーの組み合わせのみでアクセサリーシューなし^[7]。
- #148（1939年3月発売^[7]） - 二重露出防止装置が装備され、それに伴い巻き止め解除レバーがなくなった^[7]。巻き上げノブとファインダーの間の軍艦部が約2mm高くなり、巻き上げノブが#126と同じ厚さに薄くされている^[7]。レンズはクセナー50mmF3.5またはエクター50mmF3.5、シャッターはコンパーまたはコンパーラピッド^[8]。
- #149（1939年3月発売^[8]） - #148とほぼ同様で、ボディー周縁のアルミニウム磨き出し部分が黒色塗装されている^[8]。レンズはクセナー50mmF3.5、シャッターはコンパーのみ^[8]。
- #010（1946年5月発売^[8]） - 第二次世界大戦後#148を再生産したもの^[8]。レンズはクセナー50mmF3.5、エクター50mmF3.5、イザール50mmF3.5など極めて多種雑多で、正確なところが分かっていない^[8]。部品は戦前に生産されたストックを使ったり、資源がない中で新造したりしており低品質の個体も散見される^[8]。
- #013（1949年4月発売^[8]） - 軍艦部がボディー上部全面に設置されファインダーがその中に内蔵された^[8]。イメージを一新する変更で、本当の意味での戦後型と言える^[8]。レンズはクセナー50mmF3.5または50mmF2.8^[8]。
- #013/1（1950年発売） - シンクロ接点を持つコンパーラピッドを装備した。

レチナIa - いわゆる「レチナ式」の、上蓋にあるレバーによりフィルムを巻き上げるようになった。フィルム巻上げでシャッターのセットもされる^[8]。
- #015（1951年1月発売） - レチナI型シリーズでは初めてネックストラップ金具がついた。レンズはシュナイダー・クロイツナッハ製クセナー50mmF2.8、クセナー50mmF3.5、エクター50mmF3.5、ローデンシュトック製ヘリゴン50mmF3.5、シャッターは当初X接点つきコンパーラピッド、7月からMX接点を持つシンクロコンパーを装備した^[8]。

レチナIb - 蛇腹は隠され、近代的な丸みを帯びたボディーデザインとなった^[8]。底蓋にあるレバーによりフィルムを巻き上げる^[8]。ファインダーは少し大型化した^[8]。
- #018（1954年発売^[9]） - レンズはシュナイダー・クロイツナッハ製クセナー50mmF2.8のみ。
- #019^{[注釈 2]}（1957年発売^[8]） - セレン光電池式露出計を装備した。

レチナIB（1958年発売^[6]） - #019にブライトフレームファインダーを組み込んだもの。レンズはシュナイダー・クロイツナッハ製クセナー50mmF2.8のみ。

レチナIIシリーズ

連動距離計が組み込まれている。

レチナII

レチナII/レチナIIa
- #122（1936年10月発売） - 巻き上げは90度折れ曲がった特殊な形のレバー式で、1ストロークでは1コマ巻き上がらず小刻み巻き上げが必要である。レンズはシュナイダー・クロイツナッハ製クセナー50mmF2.8、クセノン50mmF2、エクター50mmF3.5。シャッタ−はコンパーラピッドだが二重露出防止装置が装備されたためT露出はできない。試作的な要素が強いのか製造台数は極めて少なくレチナコレクターにとって最も入手に苦労するタイプ。名称は「レチナII」。
- #142（1937年発売） - 巻き上げが通常のノブ巻き上げとなった。レンズはメーカー資料ではシュナイダー・クロイツナッハ製クセナー50mmF2.8、クセノン50mmF2、エクター50mmF3.5だが、実際にはクセノン50mmF2.5、エクター47mmF2もあるようだという。
- #150（1939年5月発売） - 連動距離計がファインダーと一体となって名称が「レチナIIa」となった。
- #011（1946年4月発売） - #150とほとんど同機構だが軍艦部がワンピース構造となり、ボディーレリーズの傍らにケーブルレリーズ用の穴が設置され、ネックストラップ金具が廃止されるなど細かい違いがある。また名称が「レチナII」に戻された。戦後すぐの混乱期で使用レンズは雑多を極め、クセノン50mmF2、ヘリゴン50mmF2はコートなしとありが存在し、エクター47mmF2も存在する。
- #014（1949年6月発売） - レンズが大幅に整理され、クセノン50mmF2、ヘリゴン50mmF2のみとなった。シャッターはX接点付きコンパーラピッド。
- #016（1951年1月発売） - フィルムがいわゆる「レチナ式」レバー巻き上げとなった。ネックストラップ金具がついた。名称が「レチナIIa」になった。レンズは前期型クセノン50mmF2のみ、7月以降生産された後期型はヘリゴン50mmF2つきが追加された。シャッターは前期型X接点付きコンパーラピッド、後期型MX接点付きシンクロコンパー。

レチナIIc

レチナIIc（1954年発売^[9]） - 蛇腹は隠され、近代的な丸みを帯びたボディーデザインとなった。底蓋にあるレバーによりフィルムを巻き上げる。前玉交換によるレンズ交換が可能だが同一メーカーの交換レンズを用意する必要がある^[9]。レンズは4群6枚レチナクセノンC50mmF2.8またはヘリゴンC50mmF2.8。#020。
レチナIIC（1958年発売^[6]） - ファインダーがブライトフレーム式になり窓が大型化したため「大窓」と俗称される。レンズはシュナイダー・クロイツナッハ製クセノン50mmF2またはローデンシュトック製ヘリゴン50mmF2固定。前玉交換により35mmF5.6、80mmF4としても使用可能だが交換レンズに距離計は連動せず、読み替える必要があり実用性は低い。#029。
レチナIIS（1959年発売） - デッケルマウントによるレンズ交換が可能。折りたたみ機構は持たない。#024。
レチナIIF（1964年発売） - #047。

レチナIIIc

レチナIIIシリーズ

ファインダーに内蔵された連動距離計に加え、セレン光電池式露出計を装備している。当初より近代的な丸みを帯びたボディーデザインである。底蓋にあるレバーによりフィルムを巻き上げる。レンズはシュナイダー・クロイツナッハ製4群6枚クセノン50mmF2のほかローデンシュトック製ヘリゴン50mmF2がある^[9]。

レチナIIIc - レンズ交換が可能だがファインダーに枠はなく外付けファインダーを使用する^[9]。
- #021（1954年発売^[9]） - セレン光電池はスリットのある扉がついた2レンジ式。
- #021/1（1957年発売） - セレン光電池が高感度・広帯域化され1レンジとなった。
レチナIIIC - ファインダーがブライトフレーム式になり窓が大型化したため「大窓」と俗称される^[6]。交換レンズ用の枠も入り、パララックスは自動補正される^[6]。前玉交換により35mmF5.6、80mmF4としても使用可能だが交換レンズに距離計は連動せず、読み替える必要があり実用性は低い。セレン光電池は当初より#021/1に採用された高感度型1レンジ。
- #028（1958年発売^[6]）
- #028/N（1977年限定生産） - ドイツコダック50周年記念で125台が再生産され関係者に贈呈された。シリアルナンバーが99で始まる6桁で、背面貼革にエンボスされる。稀少品のため偽物が多い。
レチナIIIS（1958年発売） - デッケルマウントによるレンズ交換が可能。折りたたみ機構は持たない。ファインダーはレンズ装着に連動してフレームを切り替えられるブライトフレーム式で露出計はシャッタースピード、絞り値、フィルム感度に連動する。#027。

レチナオートマティックI

レチナオートマティックシリーズ

シャッター優先AEを搭載している。ファインダー枠はブライトフレームでパララックスはマークによる補正。

レチナオートマティックI（Retina Automatic I 、1960年発売） - 距離計は内蔵しない。マニュアル露出は不可能。#038。
レチナオートマティックII（Retina Automatic II 、1960年発売） - 距離計は内蔵しない。マニュアル露出も可能。#032。
レチナオートマティックIII（Retina Automatic III 、1961年発売） - 連動距離計内蔵。マニュアル露出も可能。#039。

レチナレフレックスIII

レチナレフレックスシリーズ

24×36mm（ライカ）判の一眼レフカメラ。ツァイス・イコンのコンタフレックスと競合するため少し安価に販売されていたという^[10]が故障が多いという世評もあった^[11]。いずれもフィルム巻き上げまでミラーは上がりっ放しとなる^[12]。

レチナレフレックス（Retina Reflex 、1957年発売） - レンズはレチナクセノンC50mmF2またはレチナヘリゴンC50mmF2。レチナIIc/レチナIIC/レチナIIIc/レチナIIICと交換レンズの互換性があり、前玉交換式でレチナクセノンC50mmF2はレチナカルタークセノンC35mmF4、レチナクセノンC35mmF5.6、ロンガークセノンC80mmF4としても使用可能、同様にレチナヘリゴンC50mmF2はレチナヘリゴンC35mmF4、レチナヘリゴンC5mmF5.6、ヘリゴンC80mmF4としても使用可能^[12]、#025。
レチナレフレックスS（Retina Reflex S 、1959年発売） - デッケルマウントによるレンズ交換が可能になった。露出計がシャッタースピードと連動するようになった。#034^[12]。
レチナレフレックスIII（Retina Reflex III 、1960年発売） - 露出計合致がファインダー内で可能になった。レリーズボタンがボディー前面に移され、特徴的な形状になっている。デッケルマウントによるレンズ交換が可能。#041。
レチナレフレックスIV（Retina Reflex IV 、1964年発売） - ペンタプリズムに小窓がついてファインダーでシャッタースピードが確認できるようになった。スプリットイメージが45度の角度になり縦横両方の線でピント合わせができるようになった。巻き戻しがクランク式になった。デッケルマウントによるレンズ交換が可能^[13]。#051。

デッケルマウント交換レンズ

レチナインスタマチックレフレックス、レチナIIS、レチナIIIS、レチナレフレックスS、レチナレフレックスIII、レチナレフレックスIVに使用できる。ただし後期のレンズは一眼レフカメラでの最短撮影距離短縮を優先しレチナIIIS用の距離計連動カムを内蔵していない。

以下はシュナイダー・クロイツナッハ製。

レチナクルタゴン（Retina-Cultagon ）28mmF4^[12] - レチナIIISに使用する際はファインダー枠が出ないため外付けファインダーを使用することになる。
レチナクルタゴン（Retina-Cultagon ）35mmF2.8^[12]
レチナクセナー（Retina-Xenar ）45mmF2.8^[13] - レチナIIISに使用する際はファインダー枠が出ないため外付けファインダーを使用することになる。ピント合わせは前玉回転式。
レチナクセノン（Retina-Xenon ）50mmF1.9^[12]
レチナクセナー（Retina-Xenar ）50mmF2.8^[12]
レチナテレアートン（Retina-Tele-Arton ）85mmF4^[12]
レチナテレアートン（Retina-Tele-Arton ）90mmF4
レチナテレクセナー（Retina-Tele-Xenar ）135mmF4^[12]
レチナテレクセナー（Retina-Tele-Xenar ）200mmF4.8^[12] - レチナIIS/レチナIIISに装着してもピント精度が不足のため使用不能。

以下はローデンシュトック製。

レチナユリゴン（Retina-Eurygon ）28mmF4^[12] - レチナIIISに使用する際はファインダー枠が出ないため外付けファインダーを使用することになる。
レチナユリゴン（Retina-Eurygon ）30mmF2.8
レチナユリゴン（Retina-Eurygon ）35mmF2.8^[12]
レチナユリゴン（Retina-Eurygon ）35mmF4
レチナヘリゴン（Retina-Heligon ）50mmF1.9^[12]
レチナイザレックス（Retina-Ysarex ）50mmF2.8^[12]
レチナロテラー（Retina-Rotelar ）85mmF4^[12]
レチナロテラー（Retina-Rotelar ）135mmF4^[12]

注釈

^ この箇所には12月とあるが同一記事の中に#117が1934年7月からとあり矛盾する。
^ 文献では型番がレチナIBとなっているが、大窓を大文字にする慣例から外れているため、レチナIbのマイナーチェンジとして扱った。『別冊ステレオサウンドヴィンテージカメラセレクション』p.77もIbがIBになったのは1958年にIIIcがIIICに、IIcがIICに切り替わったのと同時としている。

出典

^ ^a ^b ^c ^d ^e 『クラシックカメラ専科No.4、名機の系譜』p.24。
^ 『ツァイス・イコン物語』p.82。
^ ^a ^b ^c 『クラシックカメラ専科No.2、名機105の使い方』p.34。
^ ^a ^b 『ツァイス・イコン物語』p.83。
^ 『クラシックカメラ専科No.19、ライカブック'92』p.101。
^ ^a ^b ^c ^d ^e ^f 『別冊ステレオサウンドヴィンテージカメラセレクション』p.77。
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y ^z ^aa ^ab ^ac 『クラシックカメラ専科No.4、名機の系譜』p.25。
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r 『クラシックカメラ専科No.4、名機の系譜』p.26。
^ ^a ^b ^c ^d ^e ^f 『別冊ステレオサウンドヴィンテージカメラセレクション』p.76。
^ 『ドイツカメラのスタイリング』p.132。
^ 『ドイツカメラのスタイリング』p.131。
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p 『クラシックカメラ専科No.9、35mm一眼レフカメラ』p.64。
^ ^a ^b 『クラシックカメラ専科No.9、35mm一眼レフカメラ』p.65。

参考文献

『クラシックカメラ専科No.2、名機105の使い方』朝日ソノラマ
『クラシックカメラ専科No.4、名機の系譜』朝日ソノラマ
『クラシックカメラ専科No.9、35mm一眼レフカメラ』朝日ソノラマ
『クラシックカメラ専科No.19、ライカブック'92』朝日ソノラマ
佐貫亦男『ドイツカメラのスタイリング』グリーンアロー出版社 ISBN4-7663-3189-3
竹田正一郎『ツァイス・イコン物語』光人社ISBN978-4-7698-1455-9
『別冊ステレオサウンドヴィンテージカメラセレクション』ステレオサウンド ISBN4-88073-035-1

wiki en

[Wiki en表示]

The vertebrate retina (/ˈrɛtɪnə/ RET-i-nə, pl. retinae, /ˈrɛtiniː/; from Latin rēte, meaning "net") is a light-sensitive layer of tissue, lining the inner surface of the eye. The optics of the eye create an image of the visual world on the retina (through the cornea and lens), which serves much the same function as the film in a camera. Light striking the retina initiates a cascade of chemical and electrical events that ultimately trigger nerve impulses. These are sent to various visual centres of the brain through the fibres of the optic nerve.

In vertebrate embryonic development, the retina and the optic nerve originate as outgrowths of the developing brain, so the retina is considered part of the central nervous system (CNS) and is actually brain tissue.^[1]^[2] It is the only part of the CNS that can be visualized non-invasively.

The retina is a layered structure with several layers of neurons interconnected by synapses. The only neurons that are directly sensitive to light are the photoreceptor cells. These are mainly of two types: the rods and cones. Rods function mainly in dim light and provide black-and-white vision, while cones support daytime vision and the perception of colour. A third, much rarer type of photoreceptor, the intrinsically photosensitive ganglion cell, is important for reflexive responses to bright daylight.

Neural signals from the rods and cones undergo processing by other neurons of the retina. The output takes the form of action potentials in retinal ganglion cells whose axons form the optic nerve. Several important features of visual perception can be traced to the retinal encoding and processing of light.

1 Structure
- 1.1 Development
- 1.2 Blood supply
2 Function
- 2.1 Spatial encoding
3 Clinical significance
- 3.1 Diagnosis and treatment
- 3.2 Retinal gene therapy
4 Society and culture
- 4.1 Retinal scan
5 History
6 In other animals
- 6.1 Vertebrate and cephalopod retina differences
7 Additional Images
8 See also
9 References
10 Further reading
11 External links

Structure

Section of retina

The vertebrate retina has ten distinct layers.^[3] From closest to farthest from the vitreous body - that is, from closest to the front exterior of the head towards the interior and back of the head:

Inner limiting membrane – basement membrane elaborated by Müller cells
Nerve fibre layer – axons of the ganglion cell nuclei (note that a thin layer of Müller cell footplates exists between this layer and the inner limiting membrane)
Ganglion cell layer – contains nuclei of ganglion cells, the axons of which become the optic nerve fibres for messages and some displaced amacrine cells^[1]
Inner plexiform layer – contains the synapse between the bipolar cell axons and the dendrites of the ganglion and amacrine cells.^[1]
Inner nuclear layer – contains the nuclei and surrounding cell bodies (perikarya) of the amacrine cells, bipolar cells and horizontal cells.^[1]
Outer plexiform layer – projections of rods and cones ending in the rod spherule and cone pedicle, respectively. These make synapses with dendrites of bipolar cells.^[1] In the macular region, this is known as the Fiber layer of Henle.
Outer nuclear layer – cell bodies of rods and cones
External limiting membrane – layer that separates the inner segment portions of the photoreceptors from their cell nucleus
Photoreceptor layer – rods/cones
Retinal pigment epithelium - single layer of cuboidal cells (with extrusions not shown in diagram). This is closest to the choroid.

These can be simplified into 4 main processing stages: photoreception, transmission to bipolar cells, transmission to ganglion cells which also contain photoreceptors, the photosensitive ganglion cells, and transmission along the optic nerve. At each synaptic stage there are also laterally connecting horizontal and amacrine cells.

The optic nerve is a central tract of many axons of ganglion cells connecting primarily to the lateral geniculate body, a visual relay station in the diencephalon (the rear of the forebrain). It also projects to the superior colliculus, the suprachiasmatic nucleus, and the nucleus of the optic tract. It passes through the other layers creating the optic disc in primates.^[4]

Additional structures, not directly associated with vision, are found as outgrowths of the retina in some vertebrate groups. In birds, the pecten is a vascular structure of complex shape that projects from the retina into the vitreous humour; it supplies oxygen and nutrients to the eye, and may also aid in vision. Reptiles have a similar, but much simpler, structure.^[5]

In adult humans, the entire retina is approximately 72% of a sphere about 22 mm in diameter. The entire retina contains about 7 million cones and 75 to 150 million rods. The optic disc, a part of the retina sometimes called "the blind spot" because it lacks photoreceptors, is located at the optic papilla, a nasal zone where the optic-nerve fibres leave the eye. It appears as an oval white area of 3mm². Temporal (in the direction of the temples) to this disc is the macula. At its centre is the fovea, a pit that is responsible for our sharp central vision but is actually less sensitive to light because of its lack of rods. Human and non-human primates possess one fovea as opposed to certain bird species such as hawks who actually are bifoviate and dogs and cats who possess no fovea but a central band known as the visual streak. Around the fovea extends the central retina for about 6 mm and then the peripheral retina. The edge of the retina is defined by the ora serrata. The length from one ora to the other (or macula), the most sensitive area along the horizontal meridian is about 32 mm.

Rods, cones and nerve layers in the retina. The front (anterior) of the eye is on the left. Light (from the left) passes through several transparent nerve layers to reach the rods and cones (far right). A chemical change in the rods and cones send a signal back to the nerves. The signal goes first to the bipolar and horizontal cells (yellow layer), then to the amacrine cells and ganglion cells (purple layer), then to the optic nerve fibres. The signals are processed in these layers. First, the signals start as raw outputs of points in the rod and cone cells. Then the nerve layers identify simple shapes, such as bright points surrounded by dark points, edges, and movement. (Based on a drawing by Ramón y Cajal, 1911.)

In section the retina is no more than 0.5 mm thick. It has three layers of nerve cells and two of synapses, including the unique ribbon synapse. The optic nerve carries the ganglion cell axons to the brain and the blood vessels that open into the retina. The ganglion cells lie innermost in the retina while the photoreceptive cells lie outermost. Because of this counter-intuitive arrangement, light must first pass through and around the ganglion cells and through the thickness of the retina, (including its capillary vessels, not shown) before reaching the rods and cones. However it does not pass through the epithelium or the choroid (both of which are opaque).

The white blood cells in the capillaries in front of the photoreceptors can be perceived as tiny bright moving dots when looking into blue light. This is known as the blue field entoptic phenomenon (or Scheerer's phenomenon).

Between the ganglion cell layer and the rods and cones there are two layers of neuropils where synaptic contacts are made. The neuropil layers are the outer plexiform layer and the inner plexiform layer. In the outer the rods and cones connect to the vertically running bipolar cells, and the horizontally oriented horizontal cells connect to ganglion cells.

Distribution of rods and cones along a line passing through the fovea and the blind spot of a human eye^[6]

Illustration of the distribution of cone cells in the fovea of an individual with normal color vision (left), and a color blind (protanopic) retina. Note that the center of the fovea holds very few blue-sensitive cones.

The central retina is cone-dominated and the peripheral retina is rod-dominated. In total there are about seven million cones and a hundred million rods. At the centre of the macula is the foveal pit where the cones are smallest and in a hexagonal mosaic, the most efficient and highest density. Below the pit the other retina layers are displaced, before building up along the foveal slope until the rim of the fovea or parafovea which is the thickest portion of the retina. The macula has a yellow pigmentation from screening pigments and is known as the macula lutea. The area directly surrounding the fovea has the highest density of rods converging on single bipolars. Since the cones have a much lesser power of merging signals, the fovea allows for the sharpest vision the eye can attain.^[1]

Though the rod and cones are a mosaic of sorts, transmission from receptors to bipolars to ganglion cells is not direct. Since there are about 150 million receptors and only 1 million optic nerve fibres, there must be convergence and thus mixing of signals. Moreover, the horizontal action of the horizontal and amacrine cells can allow one area of the retina to control another (e.g. one stimulus inhibiting another). This inhibition is key to the sum of messages sent to the higher regions of the brain. In some lower vertebrates (e.g. the pigeon), there is a "centrifugal" control of messages - that is, one layer can control another, or higher regions of the brain can drive the retinal nerve cells, but in primates this does not occur.^[1]

Development

Retinal development begins with the establishment of the eye fields mediated by Shh and Six3 with subsequent development of the optic vesicles via Pax6 and Lhx2.^[7] The role of Pax6 in eye development was elegantly demonstrated by Walter Gehring and colleagues, who showed that ectopic expression of Pax6 can lead to eye formation on Drosophila antennae, wings, and legs.^[8] The optic vesicle gives rise to three structures: the neural retina, the retinal pigmented epithelium, and the optic stalk. The neural retina contains the retinal progenitor cells (RPCs) that give rise to the seven cell types of the retina. Differentiation begins with the retinal ganglion cells and concludes with production of the Muller glia. Although each cell type differentiates from the RPCs in a sequential order, there is considerable overlap in the timing of when individual cell types differentiate.^[7] The cues that determine a RPC daughter cell fate are coded by multiple transcription factor families including the bHLH and homeodomain factors.^[9]

In addition to guiding cell fate determination, cues exist in the retina to determine the Dorsal/Ventral and Nasal/Temporal axes. The D-V axis is established by a ventral to dorsal gradient of Vax2, whereas the N-T axis is coordinated by expression of the forkhead transcription factors FOXD1 and FOXG1. Additional gradients are formed within the retina that aid in proper targeting of RGC axons that function to establish the retinotopic map.^[7]

Blood supply

The blood vessels in a normal human retina. Veins are darker and slightly wider than corresponding arteries. The optic disc is at left, and the macula lutea is near the centre.

There are two circulations, both supplied by the ophthalmic artery. The uveal circulation consists of arteries entering the globe outside the optic nerve, these supply the uvea and outer and middle layers of the retina. The retinal circulation, on the other hand, supplies the inner layer of the retina and passes with the optic nerve as a branch of the ophthalmic artery called the central artery of the retina.^[1] The central arteriole and venula bifurcate several times and arteriolar and venular branches run mostly in parallel with some crossovers.

The vascular topographical geometry in the retina is known to conform to structural principles that are related to certain physical properties.^[10] The unique structure of the blood vessels in the retina has been used for biometric identification. Changes in the retinal microcirculation are seen with aging,^[11] exposure to air pollution^[12] and may indicate cardiovascular diseases such as hypertension and atherosclerosis.^[13]^[14]^[15] The identification of vascular bifurcations is one of the basic steps in this analysis.^[16] Results of such analyses of the retinal microcirculation can be evaluated against the ground truth data of vascular bifurcations of retinal fundus images that are obtained from the DRIVE data set.

Determining the equivalent width of arterioles and venules near the optic disc is also a widely used technique to identify cardiovascular risks.^[17]

Bird retina is devoid of blood vessels, perhaps to give un-obliterated light for forming image, thus giving better resolution. It is, therefore, a considered view that bird retina depends for nutrition and oxygen supply on a specialized organ, called pecten or pecten oculi, located on blind spot or optic disk. This organ is extremely rich in blood vessels and is thought to supply nutrition and oxygen to bird retina by diffusion through vitreous body. Pecten is highly-rich in alkaline phosphatase activity and polarized cells in its bridge portion - both befitting its secretory role.^[18] Pecten cells are packed with dark melanin granules, which have been theorized to keep this organ warm with absorption of stray light falling on the pecten. This is considered to enhance metabolic rate of pecten, thereby exporting more nutritive molecules to meet stringent energy requirements of retina during long periods of exposure to light.^[19]

Function

An image is produced by the patterned excitation of the cones and rods in the retina. The excitation is processed by the neuronal system and various parts of the brain working in parallel to form a representation of the external environment in the brain.

The cones respond to bright light and mediate high-resolution colour vision during daylight illumination (also called photopic vision). The rods are saturated at daylight levels and don't contribute to pattern vision. However, rods do respond to dim light and mediate lower-resolution, monochromatic vision under very low levels of illumination (called scotopic vision). The illumination in most office settings falls between these two levels and is called mesopic vision. At these light levels, both the rods and cones are actively contributing pattern information to that exiting the eye. What contribution the rod information makes to pattern vision under these circumstances is unclear.

The response of cones to various wavelengths of light is called their spectral sensitivity. In normal human vision, the spectral sensitivity of a cone falls into one of three subgroups. These are often called blue, green, and red cones but more accurately are short, medium, and long wavelength sensitive cone subgroups. It is a lack of one or more of the cone subtypes that causes individuals to have deficiencies in colour vision or various kinds of colour blindness. These individuals are not blind to objects of a particular colour but experience the inability to distinguish between two groups of colours that can be distinguished by people with normal vision. Humans have three different types of cones (trichromatic vision) while most other mammals lack cones with red sensitive pigment and therefore have poorer (dichromatic) colour vision. However, some animals have four spectral subgroups, e.g. the trout adds an ultraviolet subgroup to short, medium and long subgroups that are similar to humans. Some fish are sensitive to the polarization of light as well.

When light falls on a receptor it sends a proportional response synaptically to bipolar cells which in turn signal the retinal ganglion cells. The receptors are also 'cross-linked' by horizontal cells and amacrine cells, which modify the synaptic signal before the ganglion cells. Rod and cone signals are intermixed and combine, although rods are mostly active in very poorly lit conditions and saturate in broad daylight, while cones function in brighter lighting because they are not sensitive enough to work at very low light levels.

Despite the fact that all are nerve cells, only the retinal ganglion cells and few amacrine cells create action potentials. In the photoreceptors, exposure to light hyperpolarizes the membrane in a series of graded shifts. The outer cell segment contains a photopigment. Inside the cell the normal levels of cyclic guanosine monophosphate (cGMP) keep the Na+ channel open and thus in the resting state the cell is depolarised. The photon causes the retinal bound to the receptor protein to isomerise to trans-retinal. This causes receptor to activate multiple G-proteins. This in turn causes the Ga-subunit of the protein to activate a phosphodiesterase (PDE6), which degrades cGMP, resulting in the closing of Na+ cyclic nucleotide-gated ion channels (CNGs). Thus the cell is hyperpolarised. The amount of neurotransmitter released is reduced in bright light and increases as light levels fall. The actual photopigment is bleached away in bright light and only replaced as a chemical process, so in a transition from bright light to darkness the eye can take up to thirty minutes to reach full sensitivity (see Adaptation (eye)).

In the retinal ganglion cells there are two types of response, depending on the receptive field of the cell. The receptive fields of retinal ganglion cells comprise a central approximately circular area, where light has one effect on the firing of the cell, and an annular surround, where light has the opposite effect on the firing of the cell. In ON cells, an increment in light intensity in the centre of the receptive field causes the firing rate to increase. In OFF cells, it makes it decrease. In a linear model, this response profile is well described by a Difference of Gaussians and is the basis for edge detection algorithms. Beyond this simple difference ganglion cells are also differentiated by chromatic sensitivity and the type of spatial summation. Cells showing linear spatial summation are termed X cells (also called parvocellular, P, or midget ganglion cells), and those showing non-linear summation are Y cells (also called magnocellular, M, or parasol retinal ganglion cells), although the correspondence between X and Y cells (in the cat retina) and P and M cells (in the primate retina) is not as simple as it once seemed.

In the transfer of visual signals to the brain, the visual pathway, the retina is vertically divided in two, a temporal (nearer to the temple) half and a nasal (nearer to the nose) half. The axons from the nasal half cross the brain at the optic chiasma to join with axons from the temporal half of the other eye before passing into the lateral geniculate body.

Although there are more than 130 million retinal receptors, there are only approximately 1.2 million fibres (axons) in the optic nerve; a large amount of pre-processing is performed within the retina. The fovea produces the most accurate information. Despite occupying about 0.01% of the visual field (less than 2° of visual angle), about 10% of axons in the optic nerve are devoted to the fovea. The resolution limit of the fovea has been determined at around 10,000 points.^{[clarification needed]} See visual acuity. The information capacity is estimated at 500,000 bits per second (for more information on bits, see information theory) without colour or around 600,000 bits per second including colour.^{[citation needed]}

Spatial encoding

On-centres and off-centres of the retina

The retina does not simply send a picture to the brain. The retina spatially encodes (compresses) the image to fit the limited capacity of the optic nerve. Compression is necessary because there are 100 times more photoreceptor cells than ganglion cells as mentioned above. The retina does so by "decorrelating" the incoming images in a manner to be described below. These operations are carried out by the centre surround structures as implemented by the bipolar and ganglion cells.

There are two types of centre surround structures in the retina—on-centres and off-centres. On-centres have a positively weighted centre and a negatively weighted surround. Off-centres are just the opposite. Positive weighting is more commonly known as excitatory and negative weighting is more commonly known as inhibitory.

These centre surround structures are not physical in the sense that one cannot see them by staining samples of tissue and examining the retina's anatomy. The centre surround structures are logical (i.e., mathematically abstract) in the sense that they depend on the connection strengths between ganglion and bipolar cells. It is believed that the connection strengths between cells is caused by the number and types of ion channels embedded in the synapses between the ganglion and bipolar cells. See Receptive field for figures and more information on centre surround structures.

The centre surround structures are mathematically equivalent to the edge detection algorithms used by computer programmers to extract or enhance the edges in a digital photograph. Thus the retina performs operations on the image to enhance the edges of objects within its visual field. For example, in a picture of a dog, a cat and a car, it is the edges of these objects that contain the most information. In order for higher functions in the brain (or in a computer for that matter) to extract and classify objects such as a dog and a cat, the retina is the first step to separating out the various objects within the scene.

As an example, the following matrix is at the heart of the computer algorithm that implements edge detection. This matrix is the computer equivalent to the centre surround structure. In this example, each box (element) within this matrix would be connected to one photoreceptor. The photoreceptor in the centre is the current receptor being processed. The centre photoreceptor is multiplied by the +1 weight factor. The surrounding photoreceptors are the "nearest neighbors" to the centre and are multiplied by the -1/8 value. The sum of all nine of these elements is finally calculated. This summation is repeated for every photoreceptor in the image by shifting left to the end of a row and then down to the next line.

-1/8	-1/8	-1/8
-1/8	+1	-1/8
-1/8	-1/8	-1/8

The total sum of this matrix is zero if all the inputs from the nine photoreceptors are the same value. The zero result indicates the image was uniform (non-changing) within this small patch. Negative or positive sums mean something was varying (changing) within this small patch of nine photoreceptors.

The above matrix is only an approximation to what really happens inside the retina. The differences are:

The above example is called "balanced". The term balanced means that the sum of the negative weights is equal to the sum of the positive weights so that they cancel out perfectly. Retinal ganglion cells are almost never perfectly balanced.
The table is square while the centre surround structures in the retina are circular.
Neurons operate on spike trains traveling down nerve cell axons. Computers operate on a single Floating point number that is essentially constant from each input pixel. (The computer pixel is basically the equivalent of a biological photoreceptor.)
The retina performs all these calculations in parallel while the computer operates on each pixel one at a time. There are no repeated summations and shifting as there would be in a computer.
Finally, the horizontal and amacrine cells play a significant role in this process but that is not represented here.

Here is an example of an input image and how edge detection would modify it.

Once the image is spatially encoded by the centre surround structures, the signal is sent out the optical nerve (via the axons of the ganglion cells) through the optic chiasm to the LGN (lateral geniculate nucleus). The exact function of the LGN is unknown at this time. The output of the LGN is then sent to the back of the brain. Specifically the output of the LGN "radiates" out to the V1 Primary visual cortex.

Simplified Signal Flow: Photoreceptors → Bipolar → Ganglion → Chiasm → LGN → V1 cortex

Clinical significance

There are many inherited and acquired diseases or disorders that may affect the retina. Some of them include:

Retinitis pigmentosa is a group of genetic diseases that affect the retina and causes the loss of night vision and peripheral vision.
Macular degeneration describes a group of diseases characterized by loss of central vision because of death or impairment of the cells in the macula.
Cone-rod dystrophy (CORD) describes a number of diseases where vision loss is caused by deterioration of the cones and/or rods in the retina.
In retinal separation, the retina detaches from the back of the eyeball. Ignipuncture is an outdated treatment method. The term retinal detachment is used to describe a separation of the neurosensory retina from the retinal pigment epithelium.^[20] There are several modern treatment methods for fixing a retinal detachment: pneumatic retinopexy, scleral buckle, cryotherapy, laser photocoagulation and pars plana vitrectomy.
Both hypertension and diabetes mellitus can cause damage to the tiny blood vessels that supply the retina, leading to hypertensive retinopathy and diabetic retinopathy.
Retinoblastoma is a cancer of the retina.
Retinal diseases in dogs include retinal dysplasia, progressive retinal atrophy, and sudden acquired retinal degeneration.
Lipemia retinalis is a white appearance of the retina, and can occur by lipid deposition in lipoprotein lipase deficiency.

Diagnosis and treatment

A number of different instruments are available for the diagnosis of diseases and disorders affecting the retina. Ophthalmoscopy and fundus photography are used to examine the retina. Recently, adaptive optics has been used to image individual rods and cones in the living human retina and a company based in Scotland have engineered technology that allows physicians to observe the complete retina without any discomfort to patients.^[21]

The electroretinogram is used to measure non-invasively the retina's electrical activity, which is affected by certain diseases. A relatively new technology, now becoming widely available, is optical coherence tomography (OCT). This non-invasive technique allows one to obtain a 3D volumetric or high resolution cross-sectional tomogram of the retinal fine structure with histologic-quality.

OCT scan of a retina at 800nm with an axial resolution of 3µm

Treatment depends upon the nature of the disease or disorder. Transplantation of retinas has been attempted, but without much success. At MIT, The University of Southern California, RWTH Aachen University, and the University of New South Wales, an "artificial retina" is under development: an implant which will bypass the photoreceptors of the retina and stimulate the attached nerve cells directly, with signals from a digital camera.

Retinal gene therapy

Gene therapy holds promise as a potential avenue to cure a wide range of retinal diseases. This involves using a non-infectious virus to shuttle a gene into a part of the retina. Recombinant adeno-associated virus (rAAV) vectors possess a number of features that render them ideally suited for retinal gene therapy, including a lack of pathogenicity, minimal immunogenicity, and the ability to transduce postmitotic cells in a stable and efficient manner.^[22] rAAV vectors are increasingly utilized for their ability to mediate efficient transduction of retinal pigment epithelium (RPE), photoreceptor cells and retinal ganglion cells. Each cell type can be specifically targeted by choosing the appropriate combination of AAV serotype, promoter, and intraocular injection site.

Several clinical trials have already reported positive results using rAAV to treat Leber's Congenital Amaurosis, showing that the therapy was both safe and effective.^[23]^[24] There were no serious adverse events, and patients in all three studies showed improvement in their visual function as measured by a number of methods. The methods used varied among the three trials, but included both functional methods such as visual acuity^[24]^[25]^[26] and functional mobility^[25]^[26]^[27] as well as objective measures that are less susceptible to bias, such as the pupil's ability to respond to light^[23]^[28] and improvements on functional MRI.^[29] Improvements were sustained over the long-term, with patients continuing to do well after more than 1.5 years.^[23]^[24]

The unique architecture of the retina and its relatively immune-privileged environment help this process.^[30] Tight junctions that form the blood retinal barrier separate the subretinal space from the blood supply, thus protecting it from microbes and most immune-mediated damage, and enhancing its potential to respond to vector-mediated therapies. The highly compartmentalized anatomy of the eye facilitates accurate delivery of therapeutic vector suspensions to specific tissues under direct visualization using microsurgical techniques.^[31] In the sheltered environment of the retina, AAV vectors are able to maintain high levels of transgene expression in the retinal pigmented epithelium (RPE), photoreceptors, or ganglion cells for long periods of time after a single treatment. In addition, the eye and the visual system can be routinely and easily monitored for visual function and retinal structural changes after injections with noninvasive advanced technology, such as visual acuities, contrast sensitivity, fundus auto-fluorescence (FAF), dark-adapted visual thresholds, vascular diameters, pupillometry, electroretinography (ERG), multifocal ERG and optical coherence tomography (OCT).^[32]

This strategy is effective against a number of retinal diseases that have been studied, including neovascular diseases that are features of age-related macular degeneration, diabetic retinopathy and retinopathy of prematurity. Since the regulation of vascularization in the mature retina involves a balance between endogenous positive growth factors, such as vascular endothelial growth factor (VEGF) and inhibitors of angiogenesis, such as pigment epithelium-derived factor (PEDF), rAAV-mediated expression of PEDF, angiostatin, and the soluble VEGF receptor sFlt-1, which are all antiangiogenic proteins, have been shown to reduce aberrant vessel formation in animal models.^[33] Since specific gene therapies cannot readily be used to treat a significant fraction of patients with retinal dystrophy, there is a major interest in developing a more generally applicable survival factor therapy. Neurotrophic factors have the ability to modulate neuronal growth during development to maintain existing cells and to allow recovery of injured neuronal populations in the eye. AAV encoding neurotrophic factors such as fibroblast growth factor (FGF) family members and GDNF either protected photoreceptors from apoptosis or slowed down cell death.^[34]

Society and culture

Retinal scan

A retinal scan may be used as a method of biometric identification.

History

George Wald, Haldan Keffer Hartline and Ragnar Granit won the 1967 Nobel Prize in Physiology or Medicine for their scientific research on the retina.^[35]

A recent University of Pennsylvania study calculated the approximate bandwidth of human retinas is 8.75 megabits per second, whereas guinea pig retinas transfer at 875 kilobits.^[36]

MacLaren & Pearson and colleagues at University College London and Moorfields Eye Hospital in London showed in 2006 that photoreceptor cells could be transplanted successfully in the mouse retina if donor cells were at a critical developmental stage.^[37] Recently Ader and colleagues in Dublin showed using the electron microscope that transplanted photoreceptors formed synaptic connections.^[38]

In 2012 Sebastian Seung and his lab at MIT have launched EyeWire, an online Citizen science game where players trace neurons in the retina.^[39] The goals of the EyeWire project are to identify specific cell types within the known broad classes of retinal cells, and to map the connections between neurons in the retina, which will help to determine how vision works.^[40]^[41]

In other animals

Vertebrate and cephalopod retina differences

The vertebrate retina is inverted in the sense that the light sensing cells sit at the back side of the retina, so that light has to pass through layers of neurons and capillaries before it reaches the rods and cones. By contrast, the cephalopod retina has the photoreceptors at the front side of the retina, with processing neurons and capillaries behind them. Because of this, cephalopods do not have a blind spot.

The cephalopod retina does not originate as an outgrowth of the brain, as the vertebrate one does. It is arguable that this difference shows that vertebrate and cephalopod eyes are not homologous but have evolved separately.

The difference between vertebrate and cephalopod retinas presents an interesting puzzle of evolutionary path which is not yet fully settled. From an evolutionary perspective, a convoluted structure such as the inverted retina can generally come about as a consequence of two alternative processes; (a) an advantageous "good" compromise between competing functional limitations, or (b) as a historical maladaptive relic of the convoluted path of organ evolution and transformation. Vision is an important adaptation in higher vertebrates. Therefore, if the retina is indeed "wired wrongly" or "badly designed" (from an optical engineering point of view) then it is sensible to look for it to possibly have some very significant physiological advantage. One such suggestion is based on the argument that the mammalian photoreceptor amplification process requires vast quantities of metabolic energy, and consequently, it requires massive and homogeneous supply of blood. Indeed, a unique network of blood vessels is well adapted to provide the photoreceptor layer with copious quantities of blood. This shows that the inverted retina is an adaptation to deliver abundant quantities of oxygen to the retina commensurate with its high energy demands and provide it with good maintenance by the retinal pigment epithelial (RPE) cells against photo-oxidative damage,^[42] which, while at first glance should be worsened by the oxygen-rich blood in the choroid, is nonetheless eliminated by the process of opsin disc recycling the RPE enables.^[43] This latter effect allows the photoreceptor cells to have a long (i.e. decades) useful life. The combination of this process and the chemical resetting^[44] of retinal after the phototransduction cascade may be the real reason that the vertebrate retina requires the "vast quantities of metabolic energy" referred to above.

The cephalopods have a non-inverted retina which is comparable in resolving power to the eyes of many vertebrates. Squid eyes do not have an analog of the vertebrate RPE. Although their photoreceptors contain a protein, retinochrome, that recycles retinal and replicates one of the functions of the vertebrate RPE, one could argue that the photoreceptor as a whole is not maintained as well overall in cephalopods as in vertebrates.^[45] A third possibility, of having easily replaced stalk-eyes (some lobsters) or retinae (some spiders, such as Deinopis^[46]) is rare.

Additional Images

The structures of the eye labeled
Another view of the eye and the structures of the eye labeled
Illustration of image as 'seen' by the retina independent of optic nerve and striate cortex processing.

References

^ ^a ^b ^c ^d ^e ^f ^g ^h "Sensory Reception: Human Vision: Structure and function of the Human Eye" vol. 27, Encyclopaedia Britannica, 1987
^ http://www.uphs.upenn.edu/news/News_Releases/jul06/retinput.htm
^ The Retinal Tunic. Virginia-Maryland Regional College of Veterinary Medicine
^ Shepherd, Gordon (2004). The Synaptic Organization of the Brain. New York, NY: Oxford University Press. pp. 217–225. ISBN 978-0-19-515956-1.
^ Romer, Alfred Sherwood; Parsons, Thomas S. (1977). The Vertebrate Body. Philadelphia, PA: Holt-Saunders International. p. 465. ISBN 0-03-910284-X.
^ Foundations of Vision, Brian A. Wandell
^ ^a ^b ^c Heavner, W; Pevny, L (Dec 1, 2012). "Eye development and retinogenesis.". Cold Spring Harbor perspectives in biology 4 (12). doi:10.1101/cshperspect.a008391. PMID 23071378.
^ Halder, G; Callaerts, P; Gehring, WJ (Mar 24, 1995). "Induction of ectopic eyes by targeted expression of the eyeless gene in Drosophila.". Science 267 (5205): 1788–92. doi:10.1126/science.7892602. PMID 7892602.
^ Hatakeyama, J; Kageyama, R (Feb 2004). "Retinal cell fate determination and bHLH factors.". Seminars in cell & developmental biology 15 (1): 83–9. doi:10.1016/j.semcdb.2003.09.005. PMID 15036211.
^ Sherman, T: On connecting large vessels to small - the meaning of murray law. Journal of General Physiology vol. 78, pp. 431–453, 1981
^ Adar SD, Klein R, Klein BE, Szpiro AA, Cotch MF, Wong TY et al. (2010). "Air Pollution and the microvasculature: a crosssectional assessment of in vivo retinal images in the population based multiethnic study of atherosclerosis (MESA)". PLoS Med 7: e1000372. doi:10.1371/journal.pmed.1000372.
^ Louwies, T; Int Panis, L; Kicinski, M; De Boever, P; Nawrot, Tim S (2013). "Retinal Microvascular Responses to Short-Term Changes in Particulate Air Pollution in Healthy Adults Journal = Environmental Health Perspectives". doi:10.1289/ehp.1205721.
^ Tso, M., Jampol, L.: Path-physiology of hypertensive retinopathy. Ophthalmology vol. 89, 1982
^ Chapman N., Dell'omo G., Sartini M., Witt N., Hughes A., Thom S., Pedrinelli R. (2002). "Peripheral vascular disease is associated with abnormal arteriolar diameter relationships at bifurcations in the human retina". Clinical Science 103.
^ Patton, N., Aslam, T., MacGillivray, T., Deary, I., Dhillon, B., Eikelboom, R., Yogesan, K., Constable, I. (2006) Retinal image analysis: Concepts, applications and potential. Progress in Retinal and Eye Research vol. 25, pp. 99–127,
^ Azzopardi G., Petkov N. (2011). "Detection of retinal vascular bifurcations by trainable V4-like filters, in Computer Analysis of Images and Patterns (CAIP), Seville". Lecture Notes in Computer Science 6854: 451–459. doi:10.1007/978-3-642-23672-3_55.
^ Wong TY, Knudtson MD, Klein R, Klein BE, Meuer SM, Hubbard LD (2004). "Computer assisted measurement of retinal vessel diameters in the Beaver Dam Eye Study: methodology, correlation between eyes, and effect of refractive errors". Ophthalmology 111: 1183. doi:10.1016/j.ophtha.2003.09.039.
^ Bawa S.R., YashRoy R.C. (1972). "Effect of dark and light adaptation on the retina and pecten of chicken". Experimental Eye Research 13: 92–97. doi:10.1016/0014-4835(72)90129-7.
^ Bawa, S.R.; YashRoy, R.C. (1974). "Structure and function of vulture pecten". Cells Tissues Organs 89: 473–480. doi:10.1159/000144308.
^ Oh, Kean, "Pathogenetic Mechanisms of Retinal Detachment", in Retina, ed. Ryan, S.J., Elsevier Health Sciences, Philadelphia, PA, 2006, p. 2013-2015
^ Seeing into the Future Ingenia, March 2007
^ Dinculescu Astra, Glushakova Lyudmyla, Seok-Hong Min, Hauswirth William W (2005). "Adeno-associated virus-vectored gene therapy for retinal disease". Human Gene Therapy 16 (6): 649–663. doi:10.1089/hum.2005.16.649. PMID 15960597.
^ ^a ^b ^c Cideciyan A. V., Hauswirth W. W., Aleman T. S., Kaushal S., Schwartz S. B., Boye S. L., Windsor E. A. M. et al. (2009). "Human RPE65 gene therapy for Leber congenital amaurosis: persistence of early visual improvements and safety at 1 year". Human gene therapy 20 (9): 999–1004. doi:10.1089/hum.2009.086. PMC 2829287. PMID 19583479.
^ ^a ^b ^c Simonelli F., Maguire A. M., Testa F., Pierce E. A., Mingozzi F., Bennicelli J. L., Rossi S. et al. (2010). "Gene therapy for Leber's congenital amaurosis is safe and effective through 1.5 years after vector administration". Molecular therapy : the journal of the American Society of Gene Therapy 18 (3): 643–650. doi:10.1038/mt.2009.277. PMC 2839440. PMID 19953081.
^ ^a ^b Maguire A. M., Simonelli F., Pierce E. A., Pugh E. N., Mingozzi F., Bennicelli J., Banfi S. et al. (2008). "Safety and efficacy of gene transfer for Leber's congenital amaurosis The". The New England Journal of Medicine 358 (21): 2240–2248. doi:10.1056/NEJMoa0802315. PMC 2829748. PMID 18441370.
^ ^a ^b Maguire A. M., High K. A., Auricchio A., Wright J. F., Pierce E. A., Testa F., Mingozzi F. et al. (2009). "Age-dependent effects of RPE65 gene therapy for Leber's congenital amaurosis: a phase 1 dose-escalation trial". Lancet 374 (9701): 1597–1605. doi:10.1016/S0140-6736(09)61836-5. PMID 19854499.
^ Bainbridge J. W. B., Smith A. J., Barker S. S., Robbie S., Henderson R., Balaggan K., Viswanathan A. et al. (2008). "Effect of gene therapy on visual function in Leber's congenital amaurosis". The New England Journal of Medicine 358 (21): 2231–2239. doi:10.1056/NEJMoa0802268. PMID 18441371.
^ Hauswirth W. W., Aleman T. S., Kaushal S., Cideciyan A. V., Schwartz S. B., Wang L., Conlon T. J. et al. (2008). "Treatment of Leber Congenital Amaurosis Due to RPE65Mutations by Ocular Subretinal Injection of Adeno-Associated Virus Gene Vector: Short-Term Results of a Phase I Trial". Human gene therapy 19 (10): 979–990. doi:10.1089/hum.2008.107. PMC 2940541. PMID 18774912.
^ Ashtari M., Cyckowski L. L., Monroe J. F., Marshall K. A., Chung D. C., Auricchio A., Simonelli F. et al. (2011). "The human visual cortex responds to gene therapy-mediated recovery of retinal function". The Journal of Clinical Investigation 121 (6): 2160–2168. doi:10.1172/JCI57377. PMC 3104779. PMID 21606598.
^ Bennett J (2003). "Immune response following intraocular delivery of recombinant viral vectors". Gene therapy 10 (11): 977–982. doi:10.1038/sj.gt.3302030. PMID 12756418.
^ Curace Enrico M., Auricchio Alberto (2008). "Versatility of AAV vectors for retinal gene transfer". Vision Research 48: 353–359. doi:10.1016/j.visres.2007.07.027.
^ Anneke , Roepmana Ronald, Koenekoopb Robert K., Cremersa Frans P.M. (2008). "Leber congenital amaurosis: Genes, proteins and disease mechanisms". Progress in Retinal and Eye Research 27 (4): 391–419. doi:10.1016/j.preteyeres.2008.05.003. PMID 18632300.
^ Rolling F (2004). "Recombinant AAV-mediated gene transfer to the retina: gene therapy perspectives". Gene Therapy 11: S26–S32. doi:10.1038/sj.gt.3302366. PMID 15454954.
^ Rolling F (2004). "Recombinant AAV-mediated gene transfer to the retina: gene therapy perspectives". Gene Therapy 11: S26–S32. doi:10.1038/sj.gt.3302366. PMID 15454954.
^ The Nobel Prize in Physiology or Medicine 1967
^ Calculating the speed of sight - being-human - 28 July 2006 - New Scientist
^ "Retinal repair by transplantation of photoreceptor precursors". Nature 444 (7116): 203–7. November 2006. doi:10.1038/nature05161. PMID 17093405.
^ Bartsch, U.; Oriyakhel, W.; Kenna, P. F.; Linke, S.; Richard, G.; Petrowitz, B.; Humphries, P.; Farrar, G. J.; Ader, M. (2008). "Retinal cells integrate into the outer nuclear layer and differentiate into mature photoreceptors after subretinal transplantation into adult mice". Experimental Eye Research 86 (4): 691–700. doi:10.1016/j.exer.2008.01.018. PMID 18329018. edit
^ "About << EyeWire". Retrieved March 26, 2012.
^ "Retina << EyeWire". Retrieved March 27, 2012.
^ "EyeWire". Retrieved March 27, 2012.
^ Photobiology of the retina http://www.photobiology.info/Rozanowska.html
^ Diagrammatic representation of disc shedding and phagosome retrieval into the pigment epithelial cell http://webvision.med.utah.edu/imageswv/photphag.jpeg
^ Visual phototransduction
^ Retinochrome http://jgp.rupress.org/content/65/2/235.full.pdf
^ http://www.australianmuseum.net.au/How-spiders-see-the-world

External links

Eye, Brain, and Vision - online book - by David Hubel
Kolb, H., Fernandez, E., & Nelson, R. (2003). Webvision: The neural organization of the vertebrate retina. Salt Lake City, Utah: John Moran Eye Center, University of Utah. Retrieved July 22, 2014.
Demo: Artificial Retina, MIT Technology Review, September 2004. Reports on implant research at Technology Review
Successful photoreceptor transplantation, MIT Technology Review, November 2006. How stem cells might restore sight Technology Review
Australian Vision Prosthesis Group, Graduate School of Biomedical Engineering, University of New South Wales
RetinaCentral, Genetics and Diseases of the Human Retina at University of Würzburg
Retinal layers image. NeuroScience 2nd Ed at United States National Library of Medicine
Jeremy Nathans's seminars: "The Vertebrate Retina: Structure, Function, and Evolution"
Retina - Cell Centered Database
Histology image: 07901loa — Histology Learning System at Boston University
MedlinePlus Encyclopedia 002291

UpToDate Contents

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1. 尋常性ざ瘡の治療 treatment of acne vulgaris
2. 光による老化 photoaging
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5. 急性前骨髄球性白血病の分子生物学 molecular biology of acute promyelocytic leukemia

English Journal

Identification of anti-retinal antibodies in patients with age-related macular degeneration.

Morohoshi K, Ohbayashi M, Patel N, Chong V, Bird AC, Ono SJ.SourceDepartment of Ophthalmology, Tokyo Medical and Dental University, Tokyo, Japan; Department of Ophthalmology, Emory University School of Medicine and Emory Eye Center, Dobbs Ocular Immunology Laboratories, Atlanta, GA, USA; Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children's Hospital, Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Experimental and molecular pathology.Exp Mol Pathol.2012 Oct;93(2):193-9. Epub 2012 Mar 19.
Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in industrial counties. Recent findings indicate that the autoimmunity is involved in the pathogenesis of the disease. However, there is no autoantibody biomarker applied in a clinical setting for diagnosis and pro
PMID 22465421

P53 is required for the developmental restriction in Müller glial proliferation in mouse retina.

Ueki Y, Karl MO, Sudar S, Pollak J, Taylor RJ, Loeffler K, Wilken MS, Reardon S, Reh TA.SourceDepartment of Biological Structure, University of Washington, Seattle, Washington.
Glia.Glia.2012 Oct;60(10):1579-89. doi: 10.1002/glia.22377. Epub 2012 Jul 6.
Müller glia are normally mitotically quiescent cells, but in certain pathological states they can re-enter the mitotic cell cycle. While several cell cycle regulators have been shown to be important in this process, a role for the tumor suppressor, p53, has not been demonstrated. Here, we investiga
PMID 22777914

Japanese Journal

Retinal remodeling

Jones B. W.,Kondo M.,Terasaki H. [他]
Japanese journal of ophthalmology : the official English-language journal of the Japanese Ophthalmological Society 56(4), 289-306, 2012-07
NAID 40019342209

Passive component based multifunctional Jones matrix swept source optical coherence tomography for Doppler and polarization imaging

Lim Yiheng,Hong Young-Joo,Duan Lian,Yamanari Masahiro,Yasuno Yoshiaki,安野嘉晃
Optics letters 37(11), 1958-1960, 2012-06
… The optic nerve head of a retina was measured in vivo. …
NAID 120004368691

Related Pictures

★リンクテーブル★

リンク元	「100Cases 59」「網膜」「retinal」「retinae」
拡張検索	「acute retinal necrosis syndrome」「blood-retinal barrier」

「100Cases 59」

Retina
	Right human eye cross-sectional view, eyes vary significantly among animals.
Details
Artery	central retinal artery
Identifiers
Gray's	p.1014
MeSH	A09.371.729
Dorlands; /Elsevier	Retina
TA	A15.2.04.002
FMA	58301
	Anatomical terminology

　　[★]

☆case59　尿中の血液

52歳　ビジネスマン

顕微鏡的血尿のため泌尿器科医に紹介があった。

主訴：顕微鏡的血尿

現病歴：6ヶ月前、new jofのためのisurance medicalで血尿を指摘された。以来、家庭医に2回血尿指摘された。以前の尿検査は正常だった。一度も顕微鏡は指摘されたことが無く、泌尿器系の症状もなかった。顕微鏡的血尿であることを除けば健康である。視覚、聴覚に問題なし。タバコ1日30本、アルコール35 unit/week(缶ビール(350ml)20本/週)

既往歴：特記無し。

家族歴：特記無し。腎臓病の家族歴無し

・身体所見

　栄養状態良く体調はよい。心拍：72/分、整。血圧：146/102 mmHg。心血管系、呼吸器系、腹部、神経学所見：異常なし。眼底鏡でarteriovenous nippingを認める。

・検査

(血液生化学)

　上昇：尿素、クレアチニン、γ-GTP

(尿検査)

蛋白：＋＋。血尿：＋＋。赤血球：>100 red cells

24時間尿蛋白：1.2g; 正常値 <200mg/24hr

(その他)

ECG：左室拡大。腎超音波検査：大きさは正常

(第一パラグラフ)

　・顕微鏡的血尿の原因は腎臓と尿路系のものがある(ex.前立腺病変、結石)。

　・顕微鏡的血尿　＋　高度のタンパク尿　＋　高血圧　＋　腎障害　＝　慢性糸球体腎炎の病態

　・γ-GTP 高値はアルコールの過剰摂取による肝臓病であることに適合する

　・男性で推奨されるアルコール摂取の上限は、28unit/週 ()

(第二パラグラフ)IgA 腎症

　・IgA 腎症は先進国における一般的な糸球体腎炎。メサンギウム領域におけるIgAの蓄積が特徴的

　・患者はしばしば、上気道感染と同時におこる顕微鏡血尿のエピソードがある

　・IgA 腎症は多くは特発性だけど、ヘノッホ-シェーンライン紫斑病(Henoch-Schonlein purpura)とアルコール性肝硬変(alcoholic cirrhosis)と関連するのが普通である。

　・IgA 腎症の患者の20%は20年の経過で末期腎不全(end-stage renal failure)に陥る。

(第三パラグラフ)基底膜病・アルポート症候群

　・菲薄基底膜病はisolated microscopic hematuria、minimal proteinuria及び正常腎機能(悪化しない)をしめす家族性の疾患である。

　・電顕的にはびまん性の糸球体基底膜の菲薄化が見られる(300-400nm -> 150-225nm)

　・アルポート症候群は進行性糸球体病態であり、聴覚消失と視覚異常と関連している。ふつうX連鎖優性遺伝で、男性がひどく影響を受ける。

(第四パラグラフ)What further incestigations would you organize?

　・腎生検

　・age>50: 尿細胞診、前立腺特異抗原、膀胱鏡　→　除外診断のため(膀胱・前立腺病変)

　・肝超音波検査が必要で、肝生検を考慮するべき。

(第五パラグラフ)What advice would you give this patient

　・指導：禁酒、血圧のコントロール

　・経過観察：透析、腎移植に移行しうるため

　・血清/血漿クレアチニン：これはGFRが50%減らないと上昇しない　→　この症例では軽度のクレアチニンの上昇は腎機能は正常の腎機能の40%であることを示す。

　・治療：免疫抑制薬がIgA 腎症の大部分で透析導入を遅らせるという証拠はない

■KEYPOINT

　・50歳以下の血尿のみを訴える患者はまず腎臓専門医に紹介すべき。

　・50歳以上の血尿のみを訴える患者は、膀胱や前立腺の疾患を除外するためにまず泌尿器科医に紹介すべき

　・血清/血漿クレアチニンのわずかな上昇は腎機能の大きな喪失を示している。

　・大量のアルコール摂取による肝障害は明らかな徴候なく起こるかもしれない。

■もっとも一般的な顕微鏡的血尿をきたす糸球体による原因

IgA 腎症

菲薄基底膜病(thin basement membrane disease)

アルポート症候群(XR)

■高血圧の病理的帰結 HIM.1552

・高血圧が生み出すリスクファクター：粥状硬化症

・高血圧が悪化因子？(predisposing factor)となる疾患：心不全、冠動脈疾患、梗塞、腎臓病、末梢動脈疾患

　心臓：高血圧性心疾患は高血圧に対する機能的・構造的適応　→　左心室肥大、拡張期機能不全(diastolic dysfunction)、うっ血性心不全、血行異常(冠状動脈の粥状硬化・微小血管障害による)、不整脈

　左心室肥大(1遺伝的要因と血行動態要因による)　→　↑リスク：冠動脈心疾患、梗塞、慢性心不全、突然死

　拡張期機能不全：(左心室壁が肥厚して拡張期に十分拡張できないという意味での機能不全(written by s))

　脳：(高血圧は脳梗塞と脳出血のリスクファクター)

　　・認知症(脳梗塞による)

　　・高血圧脳症(autoreguration(50-150mmHg)が傷害され、重度の頭痛、悪心・嘔吐、巣状神経徴候(focal neurologic sign)、精神状態の変調をきたす)

　腎臓：高血圧は腎障害と末期腎臓病のリスクファクター。

　　・腎臓における粥状硬化性の高血圧に関連した血管損傷は、最初に糸球体の前の細動脈に及ぶ。これにより糸球体と糸球体の後の構造に虚血性の変化を起こす。

　　・糸球体の損傷は糸球体の高灌流による糸球体毛細血管の損傷の結果かもしれない。

　　・糸球体の病理は糸球体硬化症を呈し、そして尿細管は虚血により萎縮する。

　末梢動脈：長期にわたって持続する高血圧により、下肢の動脈を狭窄させる　→　跛行

　網膜：交差現象(http://www.1stretinalscreen.com/ra_DR_NonDR.asp )

AV nipping is indicative of hypertension and describes the changes which occur at arteriovenous crossings in the retina where an artery crosses a vein. In patients with hypertension and associated arteriolosclerosis (narrowing of the artery) the artery applies increased pressure on the vein at the point where it passes over the top of the vein.

■顕微鏡的血尿

　血尿のうち、肉眼的には血尿ではないが、尿沈渣で400倍毎視野1個以上の赤血球を認める場合をいう。しかしそれでは再現性に乏しいので、一般的には5個以上の赤血球を認める場合を顕微鏡的血尿といい病的意義をもつ。

■glossary

modest adj. 謙虚な。慎み深い、控えめな、遠慮がちの。(主に女性が)しとやかにした、ひどく上品な。質素な、地味な。適度の、穏当な。大きくない、ささやかな。

「網膜」

　　[★]

英: retina
関: 眼、眼球

図：SP.275,

組織学

10層よりなる (SP.275)

構造	層		細胞体
脈絡膜
網膜
1	色素上皮層		色素上皮細胞	pigment epithelium cell
2	杆体錐体層	rod and cone layer
3	外境界膜
4	外顆粒層	outer nuclear layer	視細胞	photoreceptor
5	外網状層	outer plexiform layer
6	内顆粒層	inner nuclear layer	双極細胞	bipolar cell
			水平細胞	horizontal cell
			アマクリン細胞	amacrine cell
7	内網状層	inner plexiform layer
8	神経節細胞層	ganglion cell layer	神経節細胞	ganglion cell
9	神経線維層	optic nerve fiber layer
10	内境界膜

視細胞層(外顆粒層)には以下の細胞が存在

杆状体細胞　明暗　ロドプシン　　 rhodopsin　＝　オプシン(opsin)　　　　　＋　レチナール(retinal)
錐状体細胞　色覚　ヨードプシン　 iodopsin　＝　フォトプシン(photopsin)　＋　レチナール(retinal)

感覚網膜(神経上皮)　＋　網膜色素上皮　の２つの上皮からなる。

臨床関連

黄斑変性症
網脈絡膜変性疾患

網膜色素変性症

「retinal」

　　[★]

網膜の、(βカロチン誘導体の視物質アルデヒド帯)レチナール

関: 11-cis-retinal、retina、retinae、retinaldehyde, retinol

「retinae」

　　[★]

網膜

関: retina、retinal

「acute retinal necrosis syndrome」

　　[★]

(網膜剥離や視力低下を伴う網膜炎)急性網膜壊死症候群

関: acute retinal necrosis

「blood-retinal barrier」

　　[★]

血液網膜関門、血液網膜柵

[1] この箇所には12月とあるが同一記事の中に#117が1934年7月からとあり矛盾する。

[11] 文献では型番がレチナIBとなっているが、大窓を大文字にする慣例から外れているため、レチナIbのマイナーチェンジとして扱った。『別冊ステレオサウンドヴィンテージカメラセレクション』p.77もIbがIBになったのは1958年にIIIcがIIICに、IIcがIICに切り替わったのと同時としている。

[clacamesenka4-24-2] 『クラシックカメラ専科No.4、名機の系譜』p.24。

[3] 『ツァイス・イコン物語』p.82。

[clacamesenka2-34-4] 『クラシックカメラ専科No.2、名機105の使い方』p.34。

[zeissikonstory83-5] 『ツァイス・イコン物語』p.83。

[6] 『クラシックカメラ専科No.19、ライカブック'92』p.101。

[stereosoundvintagecamera-77-7] ^ ^a ^b ^c ^d ^e ^f 『別冊ステレオサウンドヴィンテージカメラセレクション』p.77。

[clacamesenka4-25-8] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y ^z ^aa ^ab ^ac 『クラシックカメラ専科No.4、名機の系譜』p.25。

[clacamesenka4-26-9] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r 『クラシックカメラ専科No.4、名機の系譜』p.26。

[stereosoundvintagecamera-76-10] ^ ^a ^b ^c ^d ^e ^f 『別冊ステレオサウンドヴィンテージカメラセレクション』p.76。

[12] 『ドイツカメラのスタイリング』p.132。

[13] 『ドイツカメラのスタイリング』p.131。

[clacamesenka9-64-14] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p 『クラシックカメラ専科No.9、35mm一眼レフカメラ』p.64。

[clacamesenka9-65-15] 『クラシックカメラ専科No.9、35mm一眼レフカメラ』p.65。

[eb-1] ^ ^a ^b ^c ^d ^e ^f ^g ^h "Sensory Reception: Human Vision: Structure and function of the Human Eye" vol. 27, Encyclopaedia Britannica, 1987

[2] ttp://www.uphs.upenn.edu/news/News_Releases/jul06/retinput.htm

[3] The Retinal Tunic. Virginia-Maryland Regional College of Veterinary Medicine

[4] Shepherd, Gordon (2004). The Synaptic Organization of the Brain. New York, NY: Oxford University Press. pp. 217–225. ISBN 978-0-19-515956-1.

[VB-5] Romer, Alfred Sherwood; Parsons, Thomas S. (1977). The Vertebrate Body. Philadelphia, PA: Holt-Saunders International. p. 465. ISBN 0-03-910284-X.

[6] Foundations of Vision, Brian A. Wandell

[Heavner-7] Heavner, W; Pevny, L (Dec 1, 2012). "Eye development and retinogenesis.". Cold Spring Harbor perspectives in biology 4 (12). doi:10.1101/cshperspect.a008391. PMID 23071378.

[8] Halder, G; Callaerts, P; Gehring, WJ (Mar 24, 1995). "Induction of ectopic eyes by targeted expression of the eyeless gene in Drosophila.". Science 267 (5205): 1788–92. doi:10.1126/science.7892602. PMID 7892602.

[9] Hatakeyama, J; Kageyama, R (Feb 2004). "Retinal cell fate determination and bHLH factors.". Seminars in cell & developmental biology 15 (1): 83–9. doi:10.1016/j.semcdb.2003.09.005. PMID 15036211.

[Sherman81-10] Sherman, T: On connecting large vessels to small - the meaning of murray law. Journal of General Physiology vol. 78, pp. 431–453, 1981

[11] Adar SD, Klein R, Klein BE, Szpiro AA, Cotch MF, Wong TY et al. (2010). "Air Pollution and the microvasculature: a crosssectional assessment of in vivo retinal images in the population based multiethnic study of atherosclerosis (MESA)". PLoS Med 7: e1000372. doi:10.1371/journal.pmed.1000372.

[Louwies-12] Louwies, T; Int Panis, L; Kicinski, M; De Boever, P; Nawrot, Tim S (2013). "Retinal Microvascular Responses to Short-Term Changes in Particulate Air Pollution in Healthy Adults Journal = Environmental Health Perspectives". doi:10.1289/ehp.1205721.

[Tso82-13] Tso, M., Jampol, L.: Path-physiology of hypertensive retinopathy. Ophthalmology vol. 89, 1982

[Chapman02-14] Chapman N., Dell'omo G., Sartini M., Witt N., Hughes A., Thom S., Pedrinelli R. (2002). "Peripheral vascular disease is associated with abnormal arteriolar diameter relationships at bifurcations in the human retina". Clinical Science 103.

[Patton06-15] Patton, N., Aslam, T., MacGillivray, T., Deary, I., Dhillon, B., Eikelboom, R., Yogesan, K., Constable, I. (2006) Retinal image analysis: Concepts, applications and potential. Progress in Retinal and Eye Research vol. 25, pp. 99–127,

[Azzopardi2011-16] Azzopardi G., Petkov N. (2011). "Detection of retinal vascular bifurcations by trainable V4-like filters, in Computer Analysis of Images and Patterns (CAIP), Seville". Lecture Notes in Computer Science 6854: 451–459. doi:10.1007/978-3-642-23672-3_55.

[17] Wong TY, Knudtson MD, Klein R, Klein BE, Meuer SM, Hubbard LD (2004). "Computer assisted measurement of retinal vessel diameters in the Beaver Dam Eye Study: methodology, correlation between eyes, and effect of refractive errors". Ophthalmology 111: 1183. doi:10.1016/j.ophtha.2003.09.039.

[18] Bawa S.R., YashRoy R.C. (1972). "Effect of dark and light adaptation on the retina and pecten of chicken". Experimental Eye Research 13: 92–97. doi:10.1016/0014-4835(72)90129-7.

[19] Bawa, S.R.; YashRoy, R.C. (1974). "Structure and function of vulture pecten". Cells Tissues Organs 89: 473–480. doi:10.1159/000144308.

[20] Oh, Kean, "Pathogenetic Mechanisms of Retinal Detachment", in Retina, ed. Ryan, S.J., Elsevier Health Sciences, Philadelphia, PA, 2006, p. 2013-2015

[21] Seeing into the Future Ingenia, March 2007

[22] Dinculescu Astra, Glushakova Lyudmyla, Seok-Hong Min, Hauswirth William W (2005). "Adeno-associated virus-vectored gene therapy for retinal disease". Human Gene Therapy 16 (6): 649–663. doi:10.1089/hum.2005.16.649. PMID 15960597.

[Cideciyan_2009-23] Cideciyan A. V., Hauswirth W. W., Aleman T. S., Kaushal S., Schwartz S. B., Boye S. L., Windsor E. A. M. et al. (2009). "Human RPE65 gene therapy for Leber congenital amaurosis: persistence of early visual improvements and safety at 1 year". Human gene therapy 20 (9): 999–1004. doi:10.1089/hum.2009.086. PMC 2829287. PMID 19583479.

[Simonelli_2010-24] Simonelli F., Maguire A. M., Testa F., Pierce E. A., Mingozzi F., Bennicelli J. L., Rossi S. et al. (2010). "Gene therapy for Leber's congenital amaurosis is safe and effective through 1.5 years after vector administration". Molecular therapy : the journal of the American Society of Gene Therapy 18 (3): 643–650. doi:10.1038/mt.2009.277. PMC 2839440. PMID 19953081.

[Maguire_2008-25] Maguire A. M., Simonelli F., Pierce E. A., Pugh E. N., Mingozzi F., Bennicelli J., Banfi S. et al. (2008). "Safety and efficacy of gene transfer for Leber's congenital amaurosis The". The New England Journal of Medicine 358 (21): 2240–2248. doi:10.1056/NEJMoa0802315. PMC 2829748. PMID 18441370.

[Maguire_2009-26] Maguire A. M., High K. A., Auricchio A., Wright J. F., Pierce E. A., Testa F., Mingozzi F. et al. (2009). "Age-dependent effects of RPE65 gene therapy for Leber's congenital amaurosis: a phase 1 dose-escalation trial". Lancet 374 (9701): 1597–1605. doi:10.1016/S0140-6736(09)61836-5. PMID 19854499.

[Bainbridge_2008-27] Bainbridge J. W. B., Smith A. J., Barker S. S., Robbie S., Henderson R., Balaggan K., Viswanathan A. et al. (2008). "Effect of gene therapy on visual function in Leber's congenital amaurosis". The New England Journal of Medicine 358 (21): 2231–2239. doi:10.1056/NEJMoa0802268. PMID 18441371.

[Hauswirth_2008-28] Hauswirth W. W., Aleman T. S., Kaushal S., Cideciyan A. V., Schwartz S. B., Wang L., Conlon T. J. et al. (2008). "Treatment of Leber Congenital Amaurosis Due to RPE65Mutations by Ocular Subretinal Injection of Adeno-Associated Virus Gene Vector: Short-Term Results of a Phase I Trial". Human gene therapy 19 (10): 979–990. doi:10.1089/hum.2008.107. PMC 2940541. PMID 18774912.

[Ashtari_2011-29] Ashtari M., Cyckowski L. L., Monroe J. F., Marshall K. A., Chung D. C., Auricchio A., Simonelli F. et al. (2011). "The human visual cortex responds to gene therapy-mediated recovery of retinal function". The Journal of Clinical Investigation 121 (6): 2160–2168. doi:10.1172/JCI57377. PMC 3104779. PMID 21606598.

[30] Bennett J (2003). "Immune response following intraocular delivery of recombinant viral vectors". Gene therapy 10 (11): 977–982. doi:10.1038/sj.gt.3302030. PMID 12756418.

[31] Curace Enrico M., Auricchio Alberto (2008). "Versatility of AAV vectors for retinal gene transfer". Vision Research 48: 353–359. doi:10.1016/j.visres.2007.07.027.

[32] Anneke , Roepmana Ronald, Koenekoopb Robert K., Cremersa Frans P.M. (2008). "Leber congenital amaurosis: Genes, proteins and disease mechanisms". Progress in Retinal and Eye Research 27 (4): 391–419. doi:10.1016/j.preteyeres.2008.05.003. PMID 18632300.

[Rolling2004-33] Rolling F (2004). "Recombinant AAV-mediated gene transfer to the retina: gene therapy perspectives". Gene Therapy 11: S26–S32. doi:10.1038/sj.gt.3302366. PMID 15454954.

[ReferenceA-34] Rolling F (2004). "Recombinant AAV-mediated gene transfer to the retina: gene therapy perspectives". Gene Therapy 11: S26–S32. doi:10.1038/sj.gt.3302366. PMID 15454954.

[35] The Nobel Prize in Physiology or Medicine 1967

[36] Calculating the speed of sight - being-human - 28 July 2006 - New Scientist

[37] "Retinal repair by transplantation of photoreceptor precursors". Nature 444 (7116): 203–7. November 2006. doi:10.1038/nature05161. PMID 17093405.

[38] Bartsch, U.; Oriyakhel, W.; Kenna, P. F.; Linke, S.; Richard, G.; Petrowitz, B.; Humphries, P.; Farrar, G. J.; Ader, M. (2008). "Retinal cells integrate into the outer nuclear layer and differentiate into mature photoreceptors after subretinal transplantation into adult mice". Experimental Eye Research 86 (4): 691–700. doi:10.1016/j.exer.2008.01.018. PMID 18329018. edit

[39] "About << EyeWire". Retrieved March 26, 2012.

[40] "Retina << EyeWire". Retrieved March 27, 2012.

[41] "EyeWire". Retrieved March 27, 2012.

[42] Photobiology of the retina http://www.photobiology.info/Rozanowska.html

[43] Diagrammatic representation of disc shedding and phagosome retrieval into the pigment epithelial cell http://webvision.med.utah.edu/imageswv/photphag.jpeg

[44] Visual phototransduction

[45] Retinochrome http://jgp.rupress.org/content/65/2/235.full.pdf

[46] ttp://www.australianmuseum.net.au/How-spiders-see-the-world

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retina