모노아민 신경전달물질

Monoamine neurotransmitter
도파민
노르에피네프린
세로토닌

모노아민 신경전달물질은 2개의 탄소 사슬(예: -CH-CH-22)에 의해 방향족 고리에 연결된 하나의 아미노기를 포함하는 신경전달물질과 신경조절제이다.예를 들어 도파민, 노르에피네프린, 세로토닌 등이 있다.

모든 모노아민은 방향족 아미노산 탈카르복실화효소 작용에 의해 페닐알라닌, 티로신, 트립토판 등의 방향족 아미노산으로부터 유도된다.그것들은 아민기를 잘라내는 모노아민 산화효소라고 알려진 효소에 의해 체내에서 비활성화된다.

모노아민 신경전달물질을 사용하는 뉴런의 네트워크인 모노아민 시스템은 감정, 각성, 특정 유형의 기억과 같은 과정의 조절에 관여한다.또한 모노아민 신경전달물질은 뉴런 무결성을 유지하고 뉴런에 영양적 [1]지원을 제공하는 화학물질인 성상세포에 의한 신경트로핀-3의 분비 및 생성에 중요한 역할을 하는 것으로 밝혀졌다.

모노아민 신경전달물질의 효과를 증가시키거나 감소시키기 위해 사용되는 약물은 우울증, 불안, 정신분열증, 파킨슨병을 [2]포함한 정신 및 신경학적 장애를 가진 환자들을 치료하는데 사용된다.

예

인간[3][4][5] 뇌의 카테콜아민 및 미량 아민 생합성 경로
The image above contains clickable links
페네틸아민 미량아민 및 카테콜아민은 L-페닐알라닌 유도체이다.
이 섹션의 일부는 트레이스 아민에서 제외됩니다.(이력 편집)
고전 모노아민
트레이스 아민

모노아민을 세포 안이나 밖으로 운반하는 모노아민 트랜스포터라고 불리는 특정 운반체 단백질이 존재한다.외세포막의 도파민 트랜스포터(DAT), 세로토닌 트랜스포터(SERT), 노르에피네프린 트랜스포터(NET), 세포내 [citation needed]소포막의 소포 모노아민 트랜스포터(VMAT1, VMAT2)이다.

시냅스 균열에 방출된 후 시냅스 전 말단에 재흡입함으로써 모노아민 신경전달물질 작용을 종료한다.거기서, 그것들은 시냅스 소포로 재포장되거나 항우울제의 [citation needed]일종인 모노아민 산화효소 억제제의 표적인 효소 모노아민 산화효소(MAO)에 의해 분해될 수 있다.

진화

여러 모노아민 수용체가 서로 어떻게 관련되어 있는지를 나타내는 계통수.

모노아민 신경전달물질 시스템은 거의 모든 척추동물에서 발생하며, 이러한 시스템의 진화 가능성은 척추동물의 다른 [12][13]환경에 대한 적응성을 촉진하는 역할을 했다.

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레퍼런스

  1. ^ Mele, Tina; Čarman-Kržan, Marija; Jurič, Damijana Mojca (2010). "Regulatory role of monoamine neurotransmitters in astrocytic NT-3 synthesis". International Journal of Developmental Neuroscience. 28 (1): 13–9. doi:10.1016/j.ijdevneu.2009.10.003. PMID 19854260. S2CID 25734591.
  2. ^ Kurian, Manju A; Gissen, Paul; Smith, Martin; Heales, Simon JR; Clayton, Peter T (2011). "The monoamine neurotransmitter disorders: An expanding range of neurological syndromes". The Lancet Neurology. 10 (8): 721–33. doi:10.1016/S1474-4422(11)70141-7. PMID 21777827. S2CID 32271477.
  3. ^ Broadley KJ (March 2010). "The vascular effects of trace amines and amphetamines". Pharmacology & Therapeutics. 125 (3): 363–375. doi:10.1016/j.pharmthera.2009.11.005. PMID 19948186.
  4. ^ Lindemann L, Hoener MC (May 2005). "A renaissance in trace amines inspired by a novel GPCR family". Trends in Pharmacological Sciences. 26 (5): 274–281. doi:10.1016/j.tips.2005.03.007. PMID 15860375.
  5. ^ Wang X, Li J, Dong G, Yue J (February 2014). "The endogenous substrates of brain CYP2D". European Journal of Pharmacology. 724: 211–218. doi:10.1016/j.ejphar.2013.12.025. PMID 24374199.
  6. ^ Romero-Calderón R, Uhlenbrock G, Borycz J, Simon AF, Grygoruk A, Yee SK, Shyer A, Ackerson LC, Maidment NT, Meinertzhagen IA, Hovemann BT, Krantz DE (November 2008). "A glial variant of the vesicular monoamine transporter is required to store histamine in the Drosophila visual system". PLOS Genet. 4 (11): e1000245. doi:10.1371/journal.pgen.1000245. PMC 2570955. PMID 18989452. Unlike other monoamine neurotransmitters, the mechanism by which the brain's histamine content is regulated remains unclear. In mammals, vesicular monoamine transporters (VMATs) are expressed exclusively in neurons and mediate the storage of histamine and other monoamines.
  7. ^ a b c d e f g Broadley KJ (March 2010). "The vascular effects of trace amines and amphetamines". Pharmacol. Ther. 125 (3): 363–375. doi:10.1016/j.pharmthera.2009.11.005. PMID 19948186. Trace amines are metabolized in the mammalian body via monoamine oxidase (MAO; EC 1.4.3.4) (Berry, 2004) (Fig. 2) ... It deaminates primary and secondary amines that are free in the neuronal cytoplasm but not those bound in storage vesicles of the sympathetic neurone ... Similarly, β-PEA would not be deaminated in the gut as it is a selective substrate for MAO-B which is not found in the gut ...
    Brain levels of endogenous trace amines are several hundred-fold below those for the classical neurotransmitters noradrenaline, dopamine and serotonin but their rates of synthesis are equivalent to those of noradrenaline and dopamine and they have a very rapid turnover rate (Berry, 2004). Endogenous extracellular tissue levels of trace amines measured in the brain are in the low nanomolar range. These low concentrations arise because of their very short half-life ...
  8. ^ a b Miller GM (January 2011). "The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity". J. Neurochem. 116 (2): 164–176. doi:10.1111/j.1471-4159.2010.07109.x. PMC 3005101. PMID 21073468.
  9. ^ a b c d e f g h i j k Khan MZ, Nawaz W (October 2016). "The emerging roles of human trace amines and human trace amine-associated receptors (hTAARs) in central nervous system". Biomed. Pharmacother. 83: 439–449. doi:10.1016/j.biopha.2016.07.002. PMID 27424325.
  10. ^ a b c d e Lindemann L, Hoener MC (May 2005). "A renaissance in trace amines inspired by a novel GPCR family". Trends Pharmacol. Sci. 26 (5): 274–281. doi:10.1016/j.tips.2005.03.007. PMID 15860375. In addition to the main metabolic pathway, TAs can also be converted by nonspecific N-methyltransferase (NMT) [22] and phenylethanolamine N-methyltransferase (PNMT) [23] to the corresponding secondary amines (e.g. synephrine [14], N-methylphenylethylamine and N-methyltyramine [15]), which display similar activities on TAAR1 (TA1) as their primary amine precursors...Both dopamine and 3-methoxytyramine, which do not undergo further N-methylation, are partial agonists of TAAR1 (TA1). ...
    The dysregulation of TA levels has been linked to several diseases, which highlights the corresponding members of the TAAR family as potential targets for drug development. In this article, we focus on the relevance of TAs and their receptors to nervous system-related disorders, namely schizophrenia and depression; however, TAs have also been linked to other diseases such as migraine, attention deficit hyperactivity disorder, substance abuse and eating disorders [7,8,36]. Clinical studies report increased β-PEA plasma levels in patients suffering from acute schizophrenia [37] and elevated urinary excretion of β-PEA in paranoid schizophrenics [38], which supports a role of TAs in schizophrenia. As a result of these studies, β-PEA has been referred to as the body's 'endogenous amphetamine' [39]
  11. ^ Wainscott DB, Little SP, Yin T, Tu Y, Rocco VP, He JX, Nelson DL (January 2007). "Pharmacologic characterization of the cloned human trace amine-associated receptor1 (TAAR1) and evidence for species differences with the rat TAAR1". The Journal of Pharmacology and Experimental Therapeutics. 320 (1): 475–85. doi:10.1124/jpet.106.112532. PMID 17038507. S2CID 10829497.
  12. ^ Callier S, Snapyan M, Le Crom S, Prou D, Vincent JD, Vernier P (2003). "Evolution and cell biology of dopamine receptors in vertebrates". Biology of the Cell. 95 (7): 489–502. doi:10.1016/s0248-4900(03)00089-3. PMID 14597267. S2CID 18277786. This "evolvability" of dopamine systems has been instrumental to adapt the vertebrate species to nearly all the possible environments.
  13. ^ Vincent JD, Cardinaud B, Vernier P (1998). "[Evolution of monoamine receptors and the origin of motivational and emotional systems in vertebrates]". Bulletin de l'Académie Nationale de Médecine (in French). 182 (7): 1505–14, discussion 1515–6. PMID 9916344. These data suggest that a D1/beta receptor gene duplication was required to elaborate novel catecholamine psychomotor adaptive responses and that a noradrenergic system specifically emerged at the origin of vertebrate evolution.

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