多巴胺
多巴胺(dopamine,DA)是一種神經調控分子和單胺類神經傳導物質,屬於兒茶酚胺和苯乙胺衍生物,占了腦中兒茶酚胺的80%。人的腦和腎臟能通過除去前體L-多巴的羧基合成多巴胺,植物和大部分動物同樣能合成多巴胺。多巴胺化學名為 2-(3,4-二羥基苯基)乙胺,其英語 dopamine 是 3,4-dihydroxyphenethylamine 的縮略形式。
臨床資料 | |
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其他名稱 |
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生理學資料 | |
來源組織 | 黑質、腹側被蓋區等 |
目標組織 | 全身 |
受體 | D1、D2、D3、D4、D5、TAAR1[3] |
促效劑 | 直接:阿撲嗎啡、溴隱亭 間接:古柯鹼、苯丙胺 |
拮抗劑 | 抗精神病藥、甲氧氯普胺、多潘立酮 |
前驅物 | 苯丙胺酸、酪胺酸、L-多巴 |
生物合成 | 芳香族L-胺基酸脫羧酶 |
藥物代謝 | MAO、COMT[3] |
識別資訊 | |
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CAS號 | 51-61-6 62-31-7(鹽酸鹽) |
PubChem CID | |
IUPHAR/BPS | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
CompTox Dashboard (EPA) | |
ECHA InfoCard | 100.000.101 |
化學資訊 | |
化學式 | C8H11NO2 |
莫耳質量 | 153.18 g·mol−1 |
3D模型(JSmol) | |
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腦內有幾條不同的多巴胺通路,其中一條在犒賞系統中發揮重要作用。大多數犒賞增加多巴胺在腦中的濃度,[4]許多成癮藥物也會增加多巴胺的分泌,或是阻止它的再攝取。[5]其它多巴胺通路則用於運動系統和控制各種激素的分泌。[5]
大眾普遍認為多巴胺是產生愉悅的物質,但目前藥理學研究認為多巴胺其實是記錄誘因顯著性的物質。[6][7][8]換句話說,多巴胺表示對某個結果的欲望或厭惡,然後推動人去使它實現,或是避免它實現。[8][9]
多巴胺在中樞神經系統以外充當局部旁分泌化學信使。在血管中,它抑制正腎上腺素的分泌,並使血管舒張(正常濃度下);在腎臟中,它增加鈉排泄量和尿量;在胰臟中,它減少胰島素生產;在消化系統中,它減少胃腸蠕動和保護腸胃壁;在免疫系統中,它降低淋巴球的活性。除了血管以外,這些多巴胺都是局部合成,局部發揮作用的。[10]
多巴胺系統的功能障礙與多種重要神經系統疾病有關,而其中一些疾病的治療方式是改變多巴胺的作用。引起身體震顫和運動障礙的帕金森氏症是中腦黑質區中,分泌多巴胺的神經元不足所引起,而帕金森氏症最廣泛使用的治療藥物L-多巴是多巴胺的代謝前體,會轉化為多巴胺。有證據表明思覺失調症涉及多巴胺活性改變,因此大多數常用的抗精神病藥物都是多巴胺拮抗劑,具有降低多巴胺活動的效果。[11]最有效的幾種止吐劑同為多巴胺拮抗劑。不寧腿綜合徵與注意力不足過動症(ADHD)都與多巴胺活性降低有關。[12]高劑量多巴胺會使人上癮,但較低劑量的多巴胺可用於治療ADHD。多巴胺本身是靜脈注射的藥物,可以治療嚴重的心臟衰竭或心源性休克,[13]還能治新生嬰兒的低血壓和敗血性休克。[14]
結構
編輯多巴胺分子由胺基經由乙基鏈連接兒茶酚(有兩個羥基側基的苯環)組成。[15]因此,多巴胺是最簡單的兒茶酚胺,而神經傳導物質正腎上腺素和腎上腺素也同樣是兒茶酚胺。[16]多巴胺中含有苯乙胺結構,因此也是苯乙胺衍生物,而許多精神藥物同樣是苯乙胺衍生物。[17]
多巴胺與大多數胺類似,是一種有機鹼,在酸性環境中可被質子化。[18]質子化的多巴胺極易溶於水,比較穩定,但暴露於氧氣或其它氧化劑下時仍會被氧化。[18]在鹼性環境下,多巴胺沒有被質子化,以游離鹼形式存在,較難溶於水,比較活潑。[18]因為質子化的多巴胺更穩定、更易溶於水,所以用作藥物的多巴胺都是它和鹽酸反應產生的鹽酸鹽,[18]其外觀為白色至黃色細粉。[19]
生物化學
編輯合成
編輯只有少部分細胞(主要是神經元和腎上腺髓質的細胞)可以合成多巴胺,[23]合成路徑如下:
- 主要:L-苯丙胺酸 → L-酪胺酸 → L-多巴 → 多巴胺[20][21]
- 次要:L-苯丙胺酸 → L-酪胺酸 → 酪胺 → 多巴胺[20][21][22]
- 次要:L-苯丙胺酸 → 間酪胺酸 → 間酪胺 → 多巴胺[22][24][25]
多巴胺的直接前體L-多巴可以由必需胺基酸苯丙胺酸或是非必需胺基酸酪胺酸合成。[26]幾乎所有蛋白質都含有苯丙胺酸和酪胺酸,因此很容易從食物中得到這些胺基酸。雖然食物中就有多巴胺,但因為多巴胺無法穿過血腦屏障,所以需要攝取它的前體,然後在腦中合成多巴胺。[27]
在氧氣(O2)和四氫生物蝶呤作為輔因子時,L-苯丙胺酸會被苯丙胺酸羥化酶轉化成L-酪胺酸;而之後四氫生物蝶呤、O2、Fe2+作為輔因子,L-酪胺酸被酪胺酸羥化酶轉化成L-多巴。[26]L-多巴在芳香族L-胺基酸脫羧酶作用下,以磷酸吡哆醛為輔因子,轉化為多巴胺。[26]
多巴胺是神經傳導物質正腎上腺素和腎上腺素的前體。[26]多巴胺在O2和抗壞血酸作為輔因子時會被多巴胺β羥化酶轉化成正腎上腺素,而正腎上腺素在S-腺苷甲硫胺酸作為輔因子時會被苯乙醇胺N-甲基轉移酶轉化成腎上腺素。[26]
代謝
編輯多巴胺會依序被單胺氧化酶(MAO)、兒茶酚-O-甲基轉移酶(COMT)、醛去氫酶(ALDH)代謝。[10]雖然多巴胺有多種代謝路徑,但最終產物主要都是沒有生物活性的高香草酸(HVA),會順著血液經腎臟濾出,然後隨尿液排出體外。[10]下圖是多巴胺代謝成HVA的主要路徑:[28]
在思覺失調症的臨床研究中會測量血漿中高香草酸水平來估計腦內多巴胺水平,但這個估計方法難以分辨由正腎上腺素代謝產生的高香草酸。[29][30]
雖然多巴胺通常由氧化還原酶代謝,但它也可以直接和O2反應,生成醌和各種自由基。[31]反應產生的醌和自由基都會使細胞中毒,且有證據顯示這就是巴金森氏症細胞死亡的原因。[32]
功能
編輯突觸傳導
編輯受體 | 基因 | 種類 | 機理 | |
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類D1受體 | D1 | DRD1 | Gs偶聯 | 活化腺苷酸環化酶, 增加細胞內cAMP水平 |
D5 | DRD5 | |||
類D2受體 | D2 | DRD2 | Gi偶聯 | 抑制腺苷酸環化酶, 降低細胞內cAMP水平 |
D3 | DRD3 | |||
D4 | DRD4 | |||
TAAR | TAAR1 | TAAR1 | Gs偶聯 Gq偶聯 |
增加細胞內cAMP和鈣水平 |
多巴胺通過結合併活化細胞表面受體來發揮其作用。[23]多巴胺在人體內會和各種多巴胺受體以及痕量胺相關受體1(hTAAR1)結合。[3][33]哺乳動物有D1至D5這五種多巴胺受體,[23]全是代謝型的G蛋白偶聯受體,通過複雜的第二信使系統發揮作用。[34]這五種多巴胺受體可分為類D1受體和類D2受體。[23]活化類D1受體(D1、D5)會活化或抑制受體所在的神經元,而活化類D2受體(D2、D3、D4)則會抑制受體所在的神經元。[34]在人的神經系統中,多巴胺受體D1最多,多巴胺受體D2次之,剩下的多巴胺受體都很少。[34]
儲存、釋放、再攝取
編輯多巴胺在腦內充當神經傳導物質和神經調節劑,受所有單胺類神經傳導物質共有的機制控制。[23]多巴胺在合成之後,會被溶質載體VMAT2從胞質溶膠運輸到突觸囊泡。[35]多巴胺會儲存在這些突觸囊泡里,直到因胞吐作用或痕量胺相關受體TAAR1的活動而被釋放到突觸間隙。[33]
多巴胺會和突觸中的多巴胺受體結合併活化它們。[23][36]多巴胺受體在被活化後,會產生動作電位,然後多巴胺就會離開多巴胺受體。這些多巴胺會通過多巴胺轉運體或細胞膜單胺類轉運體回到胞質溶膠,[37]之後部分多巴胺會被單胺氧化酶代謝,剩下的則會被VMAT2運輸到突觸囊泡,等待下一次釋放。[35]
中樞神經系統
編輯腦中的多巴胺在管控功能、運動控制、動機、喚醒、增強、犒賞系統、哺乳、性高潮、噁心中起到重要作用。多巴胺細胞群和多巴胺通路一同組成了神經調節的多巴胺系統。人腦中可以產生多巴胺的神經元很少,只有約400,000個,[38]而且它們的細胞體只出現在腦的少數區域中。[39]但是,它們的軸突可以一直延伸到腦的其它區域,而且可以對傳導對象造成強大影響。[39]這些神經元最早在1964年由安妮卡·達爾斯特羅姆和謝爾·富克塞標繪出來,並給予這些區域A開頭的名字。[40]在他們的模型中,A1-A7區包含正腎上腺素,A8-A14區則包含多巴胺。包含多巴胺的區域包括黑質(A8、A9)、腹側被蓋區(A10)、下視丘後葉(A11)、弓狀核(A12)、未定區(A13)、腦室旁核(A14)。[40]
黑質是中腦基底核的一部分。黑質中的多巴胺神經元主要出現在黑質緻密部這部分(A8)和其周圍(A9)。[39]它們會通過黑質紋狀體通路延伸到紋狀體。這條通路在運動控制和學習新的動作技能中非常重要。[41]若失去大部分此區域的多巴胺神經元,將導致帕金森氏症。[42]
腹側被蓋區(VTA)是中腦的另一部分。它的多巴胺神經元大多通過中腦皮層通路延伸到前額葉皮質,另外一小部分則通過中腦邊緣通路延伸到伏隔核,[39][41]這兩條通路主要和犒賞、動機的功能相關。[41]此外,VTA也有一些多巴胺神經元會將軸突延伸到杏仁核、扣帶皮層、海馬迴、嗅球。[39][41]越來越多文獻表明,多巴胺通過影響腦的多個區域,在厭惡學習中發揮著至關重要的作用。[43][44][45]
下視丘後葉的多巴胺神經元會一直延伸到脊髓,但其功能尚未明確。[46]有證據顯示這個部分的問題和不寧腿症候群(因為強烈想要讓腿部移動而難以入睡的症候群)有關。[46]
弓形核和腦室旁核都位於下視丘。它們的多巴胺神經元通過結節漏斗通路延伸到腦垂腺前葉,抑制催乳素的分泌。[47]產生催乳素的乳促細胞在沒有多巴胺的情況下會不斷產生催乳素,而多巴胺則會抑制催乳素的產生。[47]
位於底視丘未定區多巴胺神經元延伸到下視丘許多部分,參與促性腺激素釋放激素的控制。青春期後生殖系統的發育需要促性腺激素釋放激素的參與。[47]
眼睛視網膜中有一些可以產生多巴胺的神經元。[48]它們是無長突細胞,沒有軸突。[48]它們只在白天活躍,會在細胞外液分泌多巴胺。[48]這些多巴胺可以抑制視桿細胞,同時增強視錐細胞的活動,使人在亮光下對顏色更敏感,但在光線昏暗時相反。[48]
基底核
編輯腦內最大、最重要的多巴胺來源是黑質和腹側被蓋區,它們都位於中腦,彼此密切相關且在許多方面功能相似。[39]它們都會向基底核最大的部分——紋狀體[49]分泌多巴胺。[39]
目前了解基底核功能的進展緩慢,[49]最常見的假說認為基底核在行為選擇扮演主要角色。[50]此假說認為當一個人或動物有多種行為可以選擇執行時,基底核的活動就會決定去執行哪種行為。[51]換句話說,基底核是生物的決策系統。[51]
多巴胺會以兩種方式參與行為選擇的過程。首先,它決定了執行行為的閾值。[50]多巴胺活性越高,去做特定行為所需的動力就越低。[50]因此,多巴胺水平高會導致運動和衝動變多,而多巴胺水平低則會導致蟄伏及反應減慢。[50]會導致行動僵硬遲緩的巴金森氏症就是因黑質中多巴胺大量減少而起。[52]相反,古柯鹼和苯丙胺等可以增加多巴胺分泌的藥物會導致多巴胺活動提高,甚至導致精神躁動和刻板症。[53]
此外,多巴胺還有「教學」的作用。[50]在選擇行為後,如果多巴胺活性提升,那麼基底核神經迴路就會改變,使得下次出現類似情況時更容易做出相同的選擇。[50]這是操作性條件反射的例子。[51]
犒賞
編輯犒賞是極具誘惑的刺激,能夠引導出滿足欲望的行為。[54]愉悅、學習(經典條件反射和操作性條件反射)、趨向行為都是犒賞的產物。[54]愉悅是犒賞的產物,因此可通過刺激能不能帶來愉悅,以確定這種刺激是不是犒賞。[54]不過,雖然所有帶來愉悅的刺激都是犒賞,但有些犒賞(如錢財等外在犒賞)不會直接帶來愉悅。[54][55]犒賞的動機或欲望通過它們引起的接近行為反映出來,而內在犒賞的愉悅則是得到犒賞後的結果。[54]誘因理論中區分了內在犒賞的兩個成分,即反映在趨向行為的欲望,以及反映在完成行為的愉悅。[54][6][56]吸毒者的這兩個成分會分離,他們對毒品的欲望越來越強,但感受到的愉悅會因為藥物耐受性而越來越少。[6]
多巴胺是全腦的犒賞信號,腦對犒賞的多巴胺反應就含有顯著性、價值、犒賞本身的資訊。[54]此外,多巴胺還充當「犒賞預測誤差」信號,即犒賞的意外程度。[54]有假說[57]認為當實際犒賞大於預測犒賞,或是得到意外的犒賞時,突觸的多巴胺會短暫上升;當實際犒賞小於預測犒賞時,多巴胺的分泌水平會下降到初始值。[54]
動物大腦的微電極記錄顯示在有犒賞時,VTA和黑質的多巴胺神經元會變得很活躍。[54]它們與犒賞相關的認知至關重要,是犒賞系統的核心結構。[6][58][59]多巴胺在這裡的作用與軸突的延伸方向有關。[6]從VTA延伸到伏隔核的殼的軸突會為各種犒賞設置其誘因顯著性;從VTA延伸到前額葉皮質的軸突根據各種犒賞的誘因顯著性,不斷更新不同目標的價值;從VTA延伸到杏仁核或海馬迴的軸突鞏固與犒賞相關的記憶的鞏固;從VTA延伸到伏隔核的核以及從黑質延伸到紋狀體的軸突則用於學習有助於獲得犒賞的運動。[6][60]
愉悅
編輯雖然多巴胺在引起反映在趨向行為的欲望的方面很重要,但是更深入的研究發現多巴胺不能簡單與反映在完成行為的愉悅畫上等號,[55]因為介導愉悅的快感中心不僅存在於多巴胺系統中(如伏隔核的殼),也存在於多巴胺系統外(如腹側蒼白球和臂旁核)。[55][56][61]通過直接電擊腦的多巴胺通路,許多動物都會感受到愉悅,且願意為了得到愉悅感做事。[62]降低多巴胺水平的抗精神病藥物會造成失樂,即對原本能夠帶來愉悅的活動失去興趣的現象。[63]諸如性交、飲食、玩電子遊戲等帶來愉悅的活動都能增加多巴胺的分泌。[64]所有會上癮的藥物都會直接或間接影響伏隔核的多巴胺神經傳遞,[6][62]導致對這些藥物的欲望增加。[56]冰毒和古柯鹼等興奮劑會增加突觸間隙的多巴胺水平,導致對它們的欲望增加,但感受到的愉悅並沒有顯著改變。[56][62]海洛因和嗎啡等類阿片則不同,除了增加欲望,也會增加感受到的愉悅。[56]
2019年1月的臨床研究評估了多巴胺前體L-多巴,多巴胺拮抗劑維思通,以及安慰劑對音樂上的抖顫誘發的愉悅程度的影響,發現操縱多巴胺的神經傳遞可以調節愉悅的認知。[65][66]該研究證明多巴胺神經傳遞的增加是音樂造成愉悅的必要條件。[65][66]1998年的另一研究則發現玩電子遊戲時,紋狀體會分泌多巴胺,而這些多巴胺與學習、行為增強、整合感覺-動作關係有關。[67]據該研究,玩電子遊戲的潛在問題與人格特徵有關,如低自尊、低自我效能、焦慮、攻擊性,以及有抑鬱症和焦慮症的臨床症狀。[68]
中樞神經系統以外
編輯因為多巴胺無法通過血腦屏障,所以腦外多巴胺的合成和功能基本獨立於腦內多巴胺的合成和功能。[27]血液中含有相當量的多巴胺,但其作用尚未完全清楚。[10]人的血漿中的多巴胺水平與腎上腺素水平相近,但其中超過95%都以硫酸多巴胺的形式存在,是腸繫膜的SULT1A3酶作用於多巴胺產生的。[10]血漿中的多巴胺水平在飯後可達飯前的五十倍以上,因此人體為了消除這些過量的多巴胺,就會把游離的多巴胺轉化成硫酸多巴胺。[10]硫酸多巴胺沒有生物作用,會隨尿液排出體外。[10]
血液中剩下一小部分的游離多巴胺可能是交感神經、消化系統或其它器官合成的。[10]它們可能會和周圍組織的多巴胺受體結合、被代謝掉,或是被多巴胺β羥化酶轉化成正腎上腺素,然後通過腎上腺髓質分泌到循環系統。[10]多巴胺會和位於動脈壁的多巴胺受體結合,充當血管舒張劑。[69]頸動脈體會在低氧條件下分泌多巴胺來活化這些受體,但目前不知道這些多巴胺受體有沒有其它功能。[69]
此外,多巴胺還能通過外分泌或旁分泌影響免疫系統、腎臟、胰臟。[10]
免疫系統
編輯免疫細胞可以製造和分泌多巴胺。[70]多巴胺可以影響脾臟、骨髓、循環系統的免疫細胞,[71]也可以和淋巴球上的受體結合,[70]抑制淋巴球的活性。這個功能的用途不明,可能是神經系統和免疫系統之間相互作用的途徑,也可能與某些自體免疫性疾病相關。[71]
腎臟
編輯腎臟的多巴胺系統位於腎元的細胞,其中含有所有種類的多巴胺受體。[72]腎小管的細胞可以合成多巴胺,之後分泌到腎小管液。多巴胺在此能增加腎的血液供應、提高腎功能,並增加鈉離子的排泄。當腎髒的多巴胺功能缺失時,會導致鈉離子的排泄減少,造成高血壓。有證據表明腎臟多巴胺系統出問題會導致氧化應激、水腫、高血壓等疾病。[73]基因問題或高血壓有可能使腎臟多巴胺系統產生缺陷。[74]
胰臟
編輯多巴胺在胰臟的功能比較複雜。胰臟可分為兩部分,即外分泌腺部分和內分泌腺部分。外分泌腺會合成消化酶和包括多巴胺在內的其它物質,然後分泌到小腸。[75]這些被分泌到小腸的多巴胺功能不是很明確,可能包括保護腸胃壁以及減少胃腸蠕動。[75]
胰臟的內分泌腺部分就是胰島。它會合成胰島素,然後分泌到循環系統。[75]有證據顯示製造胰島素的胰島β細胞有多巴胺受體,它們受到多巴胺作用時降低胰島素的釋放。[75]這些和胰島β細胞受體結合的多巴胺的來源還沒有釐清的很清楚,可能源自交感神經系統,然後順著血流來到胰島,也有可能是其它胰臟細胞合成的。[75]
醫療用途
編輯多巴胺是列於世界衛生組織基本藥物標準清單的藥物[76]。它通過靜脈注射給藥,最常用於治療嚴重低血壓、心跳過緩、心搏停止,如心肌梗塞、心力衰竭所引起的心源性休克,可增加心排血量、提高心率、增強心肌收縮力,對新生兒的治療更為重要[77][14]。由於多巴胺在血漿中的生物半衰期很短(成年人一分鐘、新生嬰兒兩分鐘、早產兒五分鐘),所以注射多巴胺需要滴注[78]。
多巴胺對心血管的影響源自它對α1、β1、β2腎上腺素受體的作用[79][80],可以增加鈉排泄量和尿量[78]。此外,多巴胺效應依劑量而定,低劑量會提高每搏輸出量和心率,進而提高心輸出量和血壓[81]。更高的劑量還能造成血管收縮,進一步提高血壓[81][82]。較舊的文獻稱極低劑量的多巴胺可在沒有副作用的情況下增強腎功能,但最近的研究得出的結論認為這種劑量無效,甚至可能有害[83]。
多巴胺的副作用包括影響腎功能和心律不整[81]。多巴胺的半數致死量為59mg/kg(小鼠,靜脈注射)、95mg/kg(小鼠,腹腔注射)、163mg/kg(大鼠,腹腔注射)、79mg/kg(狗,靜脈注射)[84]。
疾病與藥理學
編輯多巴胺系統和許多疾病有關,包括巴金森氏症、注意力不足多動症、妥瑞症、思覺失調症、雙相情感障礙、成癮。除了多巴胺以外,很多藥物也可以和人體各處的多巴胺系統產生作用,其中一些被用作藥品或毒品。神經化學家已開發了許多試驗藥物,其中一些和多巴胺受體的親和力高,是它們的促效劑或拮抗劑。多巴胺轉運體抑制劑、VMAT抑制劑、酶抑制劑等藥物也都可以影響多巴胺系統。[85]
大腦老化
編輯許多研究發現年齡與大腦紋狀體和紋外皮層[86]多巴胺合成量、多巴胺受體數量的減少有關。[87]多巴胺受體D1、D2、D3的減少已有充分記錄。[88][89][90]多巴胺隨年齡的減少可能與許多和年齡正相關的神經系統疾病有關,如肢體僵硬。[91]
多發性硬化症
編輯有研究報告稱多巴胺失衡導致了多發性硬化症的疲勞症狀。[92]多發性硬化症病人體內的多巴胺抑制了IL-17和IFN-γ的合成。[93]
巴金森氏症
編輯巴金森氏症是一種與年齡相關的疾病,其症狀是身體僵硬、行動遲緩、四肢顫抖,[52]到了晚期還會發展出失智症,最終死亡。[52]這些症狀導因於黑質里分泌多巴胺的細胞死亡。[94]這些細胞很脆弱,腦炎、多次腦震盪、MPTP中毒都可以使它們大量死亡,導致症狀與巴金森氏症相似的帕金森症候群。[95]不過,大部分巴金森氏症案例都是病因不明症,無法得知細胞死亡的原因。[95]
因為L-多巴在人體內會被轉化成多巴胺,[26]所以帕金森症候群最常用L-多巴治療。[27]不直接使用多巴胺是因為它不能通過血腦屏障,但L-多巴可以。[27]它通常會和卡比多巴或苄絲肼等脫羧酶抑制劑合併使用,減少在腦外就被轉化成多巴胺的量,增加進入腦內的L-多巴含量。[27]雖然長期使用L-多巴會導致異動症等副作用,但它仍是長期治療大多數巴金森氏症病例的最佳選擇。[27]
L-多巴無法補回已經死去的多巴胺細胞,但它可以使其它多巴胺細胞分泌更多多巴胺來彌補。[27]不過到了晚期,已經死亡的多巴胺細胞已經多到其它多巴胺細胞都無法彌補足夠的多巴胺。[27]
用於治療巴金森氏症的此方法有時與多巴胺失調症候群的發展有關。[96][97]
藥物成癮
編輯古柯鹼、苯丙胺衍生物(如甲基苯丙胺)、阿得拉爾、哌甲酯以及各種興奮劑都會通過多種機制來增加腦中的多巴胺水平,發揮作用。[98]古柯鹼和哌甲酯都是多巴胺再攝取抑制劑,[99]會非競爭性抑制多巴胺的再攝取,造成突觸間隙的多巴胺水平增加。[100][101]:54–58苯丙胺衍生物同樣可以增加突觸間隙的多巴胺水平,但機理不同。[102][101]:147–150
興奮劑會使人心率、體溫、出汗增加,警覺性、注意力、耐力提高,且犒賞帶來的快樂增加,但大劑量的興奮劑會導致煩躁、焦慮,甚至與現實失去聯繫。[98]興奮劑因會直接活化腦內的犒賞系統而極易成癮,[98]但小劑量興奮劑可以治療注意力不足多動症(ADHD)和發作性嗜睡病。[103][104]
許多成癮藥物會增加與犒賞系統相關的多巴胺活性。[98]尼古丁、古柯鹼、冰毒等興奮劑都會提升多巴胺的水平,而這似乎是導致這些藥物成癮的主要因素。不過對類阿片海洛因來說,犒賞系統中多巴胺水平的提升並非成癮的主要因素。[105]當已經對興奮劑上癮的人試圖戒掉它們時,他們並不會有像戒酒或戒類阿片的身體上的痛苦,而是會強烈渴望它們,產生煩躁、不安及其它由精神依賴引起的症狀。[106]
多巴胺系統在成癮機制中發揮著至關重要的作用。首先,腦內多巴胺受體的基因差別就足以預測一個人以後認為興奮劑有吸引力,還是令人厭惡。[107]此外,在使用興奮劑後,腦內多巴胺水平就會在接下來幾分鐘到幾小時提高。[98]最後,長期大劑量興奮劑會導致多巴胺慢性升高,引發腦一系列嚴重的結構變化,導致成癮。[108]治療這種藥物成癮非常困難,因為就算停止使用它們,精神依賴帶來的渴望也不會停止;就算渴望看上去停止了,在面對與藥物相關的刺激(如朋友、地點、情況)時仍可能重新出現。[106]
思覺失調和抗精神病藥物
編輯1950年代初,精神科醫生發現了一系列被稱作典型抗精神病藥物(又稱主要鎮靜劑)的藥物可以有效減輕思覺失調症患者的思覺失調症狀,第一個被廣泛使用的抗精神病藥物氯丙嗪就讓許多思覺失調症患者出院。[109]1970年代,研究者了解到這些典型抗精神病藥物都是D2受體的拮抗劑。[109][110]此發現導致思覺失調症的多巴胺假說的出現,它認為思覺失調症因多巴胺功能亢進造成。[111]由於冰毒等可以增強多巴胺功能的興奮劑會加劇思覺失調,而且正常人大量使用這些興奮劑也會產生類似的症狀,這個假說得到了更多支持。[111]
然而,之後的研究對經典的多巴胺假說提出了質疑,因為思覺失調症患者腦內的多巴胺活性通常不會有明顯增加。[111]雖然如此,但是許多精神科醫生和神經科學家仍然認為思覺失調症涉及到多巴胺系統的某種異常。[109]隨著時間的推移,多巴胺假說演變,它所假設的各種功能障礙也往往變得越來越微妙、複雜。[109]
精神藥理學家史蒂芬·史達在2018年的一篇綜述中指出在許多思覺失調症病例中,基於多巴胺、血清素、麩胺酸的三個相互關聯的網絡的問題導致了紋狀體中的多巴胺受體D2過度興奮。[112]
注意力不足多動症
編輯多巴胺神經傳遞的改變與注意力不足多動症(ADHD)有關。[113]多巴胺和ADHD的關係涉及到治療ADHD用的藥,因為最有效的ADHD治療藥物哌甲酯和苯丙胺都可以提升腦中多巴胺和正腎上腺素的水平。[114]這些藥物治療ADHD的機理是間接激動前額葉皮質的多巴胺受體和正腎上腺素受體,具體來說分別是多巴胺受體D1和腎上腺素受體α2。[113][115][116]
疼痛
編輯多巴胺會在中樞神經系統處理疼痛時發揮作用。[117]巴金森氏症經常出現的疼痛症狀和多巴胺水平降低有關,而灼口症候群、纖維肌痛、不寧腿症候群等痛苦的疾病也都與多巴胺系統異常有關。[117]
噁心
編輯噁心號嘔吐主要取決於腦幹延腦腦極後區的活動,而這個區域也含有大量多巴胺受體D2。[118]因此,活化多巴胺受體D2的藥物(如巴金森氏症藥物及阿撲嗎啡等多巴胺受體促效劑[119])很可能會導致嘔吐。[118]反過來說,甲氧氯普胺等多巴胺受體D2拮抗劑則可用作止吐劑。[118]
其它生物中的多巴胺
編輯微生物
編輯至今仍沒有古細菌中有多巴胺的報告,不過在某些細菌以及一種叫四膜蟲的原生動物中已檢測到多巴胺存在。[120]細菌和動物合成多巴胺所用的酶同源,因此有說法稱動物的多巴胺合成路徑來自細菌的基因水平轉移,而這有可能是細菌和真核生物共生,產生粒線體的結果。[121]
動物
編輯大部分多細胞生物都把多巴胺當作神經傳導物質。[122]目前只有一份關於海綿中多巴胺的報告,而且沒有說明其功能。[123]不過,其它徑向對稱物種(如水母、水螅、珊瑚等刺絲胞動物)中的神經系統中都有多巴胺的存在。[124]多巴胺作為神經傳導物質的功能可追溯到5億年前的寒武紀。多巴胺在脊椎動物、棘皮動物、節肢動物、軟體動物、某些蠕蟲里都是神經傳導物質。[125][126]
多巴胺會影響所有動物的運動。[122]它會使扁形動物螺旋運動,還能使水蛭用爬行代替游泳。多巴胺可以活化多種脊椎動物行為的轉換和選擇。[122][127]此外,多巴胺也會影響所有動物的犒賞系統。[122]所有脊椎動物以及線蟲動物、扁形動物、軟體動物、黑腹果蠅等無脊椎動物如果在做一個動作後多巴胺水平持續增加,那麼都可以重複那個動作。[122]多巴胺還能調節猴子[128]和黑腹果蠅[129]的短期和長期記憶。
節肢動物中的多巴胺長期以來都被認為是例外,因為它負責的是厭惡而不是犒賞,而犒賞則是章胺調節的。[130]不過,最近的研究發現多巴胺確實在黑腹果蠅的犒賞學習中發揮作用,而章胺的功能也是因為活化了當時未發現的多巴胺神經元。[130]
植物
編輯許多植物都能合成多巴胺。[131]香蕉的多巴胺含量最高,1公斤小果野蕉果肉里含有42毫克的多巴胺,而1公斤紅皮蕉果肉則含有55毫克的多巴胺。鱷梨、馬鈴薯、西蘭花、可可豆、甘藍的多巴胺含量則較少,1公斤含有約1至7毫克的多巴胺。橙、番茄、茄子、菠菜、菜豆、豌豆的多巴胺含量更低,1公斤含有的多巴胺不到1毫克。[131]這些多巴胺都是從酪胺酸開始合成的,合成路徑和動物一樣。[131]它們可被代謝成黑色素和各種生物鹼。[131]植物中多巴胺的功能尚不明確,但有證據表明它們會對細菌感染等應激源做出反應,有時充當生長因子,以及改變糖的代謝路徑。介導這些作用的受體,以及這些受體的活化機制都尚未確定。[131]
不過,因為多巴胺無法穿過血腦屏障,所以從這些植物中攝取的多巴胺都無法被大腦所用。[27]但是,許多植物也含有多巴胺的代謝前體L-多巴。[132]血藤屬植物的L-多巴含量最高,其中的一個種——刺毛黧豆的L-多巴含量更高。[133]蠶豆的L-多巴含量也很高,但豆里的L-多巴含量要比植物的其它部分少。[134]臘腸樹屬和羊蹄甲屬的種子也含有相當量的L-多巴。[132]
一種叫Ulvaria obscura的綠藻的多巴胺含量極高,預估占了的淨重的4.4%。有證據表明這些多巴胺是它們抵禦被蝸牛和等足目吃的手段。[135]
黑色素的前體
編輯黑色素是存在於許多生物中的一系列深色物質。[136]它們的化學性質與多巴胺相似,且多巴胺經酪胺酸酶氧化後就會產生多巴胺黑色素。[136]多巴胺黑色素不導致皮膚變黑,[136]但有證據表明黑質的黑色源自多巴胺黑色素。[137]除了人以外,其它生物中也含有多巴胺黑色素。植物中的多巴胺很可能是多巴胺黑色素的前體。[138]蝴蝶翅膀上複雜的圖案,以及幼蟲身上的黑白條紋也都因多巴胺黑色素所致。[139]
歷史與發展
編輯多巴胺最早於1910年由喬治·巴格和詹姆斯·尤恩在英國倫敦惠康實驗室合成,[140]之後於1957年由凱瑟琳·蒙塔古首次在人腦中鑑定出來。因為它是L-多巴合成出來的單胺,所以被命名為多巴胺。1958年,阿爾維德·卡爾森和尼爾斯-奧克·希拉普在瑞典國家心臟研究所化學藥理學實驗室中最先發現多巴胺作為神經傳導物質的功能。[141]卡爾森發現多巴胺不僅是正腎上腺素和腎上腺素的前體,自身也是一種神經傳導物質,因此被授予2000年諾貝爾生理學或醫學獎。[142]
聚多巴胺
編輯於2007年對無孔貽貝生物粘合劑的研究促使了聚多巴胺的發現。大多數材料如果放入弱鹼性多巴胺溶液里,就會被一層多巴胺聚合而成的聚多巴胺覆蓋。[143][144]聚多巴胺因多巴胺的氧化產生,[145]通常由多巴胺鹽酸鹽在作為鹼的三羥甲基胺基甲烷水溶液里聚合而成,結構不明。[144]聚多巴胺的性質使它有多種潛在應用,例如防止遇光損壞、輸送藥物的膠囊材料,甚至可作為生物傳感器的基質。[145]
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Listening to pleasurable music is often accompanied by measurable bodily reactions such as goose bumps or shivers down the spine, commonly called "chills" or "frissons." ... Overall, our results straightforwardly revealed that pharmacological interventions bidirectionally modulated the reward responses elicited by music. In particular, we found that risperidone impaired participants' ability to experience musical pleasure, whereas levodopa enhanced it. ... Here, in contrast, studying responses to abstract rewards in human subjects, we show that manipulation of dopaminergic transmission affects both the pleasure (i.e., amount of time reporting chills and emotional arousal measured by EDA) and the motivational components of musical reward (money willing to spend). These findings suggest that dopaminergic signaling is a sine qua non condition not only for motivational responses, as has been shown with primary and secondary rewards, but also for hedonic reactions to music. This result supports recent findings showing that dopamine also mediates the perceived pleasantness attained by other types of abstract rewards (37) and challenges previous findings in animal models on primary rewards, such as food (42, 43).
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In a pharmacological study published in PNAS, Ferreri et al. (1) present evidence that enhancing or inhibiting dopamine signaling using levodopa or risperidone modulates the pleasure experienced while listening to music. ... In a final salvo to establish not only the correlational but also the causal implication of dopamine in musical pleasure, the authors have turned to directly manipulating dopaminergic signaling in the striatum, first by applying excitatory and inhibitory transcranial magnetic stimulation over their participants' left dorsolateral prefrontal cortex, a region known to modulate striatal function (5), and finally, in the current study, by administrating pharmaceutical agents able to alter dopamine synaptic availability (1), both of which influenced perceived pleasure, physiological measures of arousal, and the monetary value assigned to music in the predicted direction. ... While the question of the musical expression of emotion has a long history of investigation, including in PNAS (6), and the 1990s psychophysiological strand of research had already established that musical pleasure could activate the autonomic nervous system (7), the authors' demonstration of the implication of the reward system in musical emotions was taken as inaugural proof that these were veridical emotions whose study has full legitimacy to inform the neurobiology of our everyday cognitive, social, and affective functions (8). Incidentally, this line of work, culminating in the article by Ferreri et al. (1), has plausibly done more to attract research funding for the field of music sciences than any other in this community.
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外部連結
編輯- U.S. National Library of Medicine: Drug Information Portal - Dopamine (頁面存檔備份,存於網際網路檔案館)
- Dopamine: analyte monograph - The Association for Clinical Biochemistry and Laboratory Medicine
- Biochemistry of Parkinson's Disease (頁面存檔備份,存於網際網路檔案館)(英文)