Dopamine
(Synonyms: 2-(3,4-二羟基苯基)乙胺,ASL279 free base) 目录号 : GC62940
An endogenous catecholamine
Cas No.:51-61-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Dopamine is an endogenous catecholamine neurotransmitter synthesized from the amino acid L-tyrosine that acts as an agonist at dopamine receptors (D1-5).1 Dopamine is mainly synthesized in the substantia nigra and ventral tegmental area and is a precursor in norepinephrine and epinephrine biosynthesis. Dopamine-containing neurons in the brain are involved in reward-motivated behavior, motor control, and hormone release. Dopamine is also synthesized in the adrenal glands where it exerts peripheral paracrine functions including control of vasodilation, sodium excretion, insulin production, gastrointestinal motility, and the activity of lymphocytes.2,3 Loss or damage of dopaminergic neurons in the substantia nigra is associated with Parkinson’s disease.4
多巴胺是一种内源性儿茶酚胺神经递质，由氨基酸L-酪氨酸合成，在多巴胺受体（D1-5）上作为激动剂发挥作用。1 多巴胺主要在黑质和腹侧被盖区合成，同时是去甲肾上腺素和肾上腺素合成的前体。大脑中含有多巴胺神经元，它们参与奖赏行为、运动控制和激素释放。多巴胺也在肾上腺中合成，发挥周围副交感作用，包括控制血管扩张、钠排泄、胰岛素分泌、胃肠运动和淋巴细胞活性等。2,3 黑质多巴胺能神经元的丧失或损伤与帕金森病有关。4
1.Missale, C., Nash, S.R., Robinson, S.W., et al.Dopamine receptors: From structure to functionPhysiol. Rev.78(1)190-225(1998) 2.Hayaishi, O.Molecular genetic studies on sleep-wake regulation, with special emphases on the prostaglandin D2 systemJ. Appl. Physiol.92(2)863-868(2015) 3.Garza, J.H.H., and Carr, D.J.J.Neuroendocrine peptide receptors on cells of the immune systemChem. Immunol.69132-154(1997) 4.Angeles, D.C., Ho, P., Dymock, B.W., et al.Antioxidants inhibit neuronal toxicity in Parkinson's disease-linked LRRK2Ann. Clin. Transl. Neurol.3(4)288-294(2016)
| Cas No. | 51-61-6 | SDF | |
| 别名 | 2-(3,4-二羟基苯基)乙胺,ASL279 free base | ||
| 分子式 | C8H11NO2 | 分子量 | 153.18 |
| 溶解度 | 储存条件 | Store at RT,protect from light, stored under nitrogen | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 6.5283 mL | 32.6413 mL | 65.2827 mL |
| 5 mM | 1.3057 mL | 6.5283 mL | 13.0565 mL |
| 10 mM | 0.6528 mL | 3.2641 mL | 6.5283 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
What does Dopamine mean?
Nat Neurosci 2018 Jun;21(6):787-793.PMID:29760524DOI:10.1038/s41593-018-0152-y.
Dopamine is a critical modulator of both learning and motivation. This presents a problem: how can target cells know whether increased Dopamine is a signal to learn or to move? It is often presumed that motivation involves slow ('tonic') Dopamine changes, while fast ('phasic') Dopamine fluctuations convey reward prediction errors for learning. Yet recent studies have shown that Dopamine conveys motivational value and promotes movement even on subsecond timescales. Here I describe an alternative account of how Dopamine regulates ongoing behavior. Dopamine release related to motivation is rapidly and locally sculpted by receptors on Dopamine terminals, independently from Dopamine cell firing. Target neurons abruptly switch between learning and performance modes, with striatal cholinergic interneurons providing one candidate switch mechanism. The behavioral impact of Dopamine varies by subregion, but in each case Dopamine provides a dynamic estimate of whether it is worth expending a limited internal resource, such as energy, attention, or time.
Dopamine, Updated: Reward Prediction Error and Beyond
Curr Opin Neurobiol 2021 Apr;67:123-130.PMID:33197709DOI:10.1016/j.conb.2020.10.012.
Dopamine neurons have been intensely studied for their roles in reinforcement learning. A dominant theory of how these neurons contribute to learning is through the encoding of a reward prediction error (RPE) signal. Recent advances in Dopamine research have added nuance to RPE theory by incorporating the ideas of sensory prediction error, distributional encoding, and belief states. Further nuance is likely to be added shortly by convergent lines of research on Dopamine neuron diversity. Finally, a major challenge is to reconcile RPE theory with other current theories of Dopamine function to account for Dopamine's role in movement, motivation, and goal-directed planning.
Multiple Dopamine functions at different time courses
Annu Rev Neurosci 2007;30:259-88.PMID:17600522DOI:10.1146/annurev.neuro.28.061604.135722.
Many lesion studies report an amazing variety of deficits in behavioral functions that cannot possibly be encoded in great detail by the relatively small number of midbrain Dopamine neurons. Although hoping to unravel a single Dopamine function underlying these phenomena, electrophysiological and neurochemical studies still give a confusing, mutually exclusive, and partly contradictory account of Dopamine's role in behavior. However, the speed of observed phasic Dopamine changes varies several thousand fold, which offers a means to differentiate the behavioral relationships according to their time courses. Thus Dopamine is involved in mediating the reactivity of the organism to the environment at different time scales, from fast impulse responses related to reward via slower changes with uncertainty, punishment, and possibly movement to the tonic enabling of postsynaptic motor, cognitive, and motivational systems deficient in Parkinson's disease.
Dopamine in schizophrenia: a review and reconceptualization
Am J Psychiatry 1991 Nov;148(11):1474-86.PMID:1681750DOI:10.1176/ajp.148.11.1474.
Objective: The initial hypothesis that schizophrenia is a manifestation of hyperdopaminergia has recently been faulted. However, several new findings suggest that abnormal, although not necessarily excessive, Dopamine activity is an important factor in schizophrenia. The authors discuss these findings and their implications. Method: All published studies regarding Dopamine and schizophrenia and all studies on the role of Dopamine in cognition were reviewed. Attention has focused on post-mortem studies, positron emission tomography, neuroleptic drug actions, plasma levels of the Dopamine metabolite homovanillic acid (HVA), and cerebral blood flow. Results: Evidence, particularly from intracellular recording studies in animals and plasma HVA measurements, suggests that neuroleptics act by reducing Dopamine activity in mesolimbic Dopamine neurons. Post-mortem studies have shown high Dopamine and HVA concentrations in various subcortical brain regions and greater than normal Dopamine receptor densities in the brains of schizophrenic patients. On the other hand, the negative/deficit symptom complex of schizophrenia may be associated with low Dopamine activity in the prefrontal cortex. Recent animal and human studies suggest that prefrontal Dopamine neurons inhibit subcortical Dopamine activity. The authors hypothesize that schizophrenia is characterized by abnormally low prefrontal Dopamine activity (causing deficit symptoms) leading to excessive Dopamine activity in mesolimbic Dopamine neurons (causing positive symptoms). Conclusions: The possible co-occurrence of high and low Dopamine activity in schizophrenia has implications for the conceptualization of Dopamine's role in schizophrenia. It would explain the concurrent presence of negative and positive symptoms. This hypothesis is testable and has important implications for treatment of schizophrenia and schizophrenia spectrum disorders.
Imaging Dopamine's role in drug abuse and addiction
Neuropharmacology 2009;56 Suppl 1(Suppl 1):3-8.PMID:18617195DOI:10.1016/j.neuropharm.2008.05.022.
Dopamine is involved in drug reinforcement but its role in addiction is less clear. Here we describe PET imaging studies that investigate Dopamine's involvement in drug abuse in the human brain. In humans the reinforcing effects of drugs are associated with large and fast increases in extracellular Dopamine, which mimic those induced by physiological Dopamine cell firing but are more intense and protracted. Since Dopamine cells fire in response to salient stimuli, supraphysiological activation by drugs is experienced as highly salient (driving attention, arousal, conditioned learning and motivation) and with repeated drug use may raise the thresholds required for Dopamine cell activation and signaling. Indeed, imaging studies show that drug abusers have marked decreases in Dopamine D2 receptors and in Dopamine release. This decrease in Dopamine function is associated with reduced regional activity in orbitofrontal cortex (involved in salience attribution; its disruption results in compulsive behaviors), cingulate gyrus (involved in inhibitory control; its disruption results in impulsivity) and dorsolateral prefrontal cortex (involved in executive function; its disruption results in impaired regulation of intentional actions). In parallel, conditioning triggered by drugs leads to enhanced Dopamine signaling when exposed to conditioned cues, which then drives the motivation to procure the drug in part by activation of prefrontal and striatal regions. These findings implicate deficits in Dopamine activity-inked with prefrontal and striatal deregulation-in the loss of control and compulsive drug intake that results when the addicted person takes the drugs or is exposed to conditioned cues. The decreased Dopamine function in addicted individuals also reduces their sensitivity to natural reinforcers. Therapeutic interventions aimed at restoring brain dopaminergic tone and activity of cortical projection regions could improve prefrontal function, enhance inhibitory control and interfere with impulsivity and compulsive drug administration while helping to motivate the addicted person to engage in non-drug related behaviors.