Dopamine receptors play vital roles in processes such as the control of learning, motivation, fine motor control and modulation of neuroendocrine signaling (Giralt JA and Greengard P, 2004). Abnormalities in dopamine receptor signaling may lead to neuropsychiatric disorders such as Parkinson's disease and schizophrenia. Dopamine receptors are prominent in the CNS and the neurotransmitter dopamine is the primary endogenous ligand for these receptors. In humans, there are five distinct types of dopamine receptor, D1-D5. They are subdivided into two families; D1-like family (D1 and D5) which couple with the G protein alpha-s and are excitatory and D2-like family (D2,D3 and D4) which couple with the G protein alpha-i and are inhibitory (Kebabian JW and Calne DB, 1979).

The neurotransmitter dopamine has been shown to play an important role in modulating behavioural, morphological and life-history responses to food abundance. However, costs of expressing high dopamine levels remain poorly studied and are essential for understanding the evolution of the dopamine system. Negative maternal effects on offspring size from enhanced maternal dopamine levels have previously been documented in Daphnia. Here, we tested whether this translates into fitness costs in terms of lower starvation resistance in offspring. We exposed Daphnia magna mothers to aqueous dopamine (2.3 mg/L or 0 mg/L for the control) at two food levels (ad libitum versus 30% ad libitum) and recorded a range of maternal life history traits. The longevity of their offspring was then quantified in the absence of food. In both control and dopamine treatments, mothers that experienced restricted food ration had lower somatic growth rates and higher age at maturation. Maternal food restriction also resulted in production of larger offspring that had a superior starvation resistance, compared to ad libitum groups. However, although dopamine exposed mothers produced smaller offspring than controls at restricted food ration, these smaller offspring survived longer under starvation. Hence, maternal dopamine exposure provided an improved offspring starvation resistance.

The data in this data repository was used to generate an article published in Biosensors and Bioelectronics titled "Real-time selective detection of dopamine and serotonin at nanomolar concentration from complex in vitro systems", available through the DOI:10.1016/j.bios.2023.115579

Dopamine is an organic chemical of the catecholamine and phenethylamine families that plays several important roles in the brain and body. It is an amine synthesized by removing a carboxyl group from a molecule of its precursor chemical L-DOPA, which is synthesized in the brain and kidneys. Dopamine is also synthesized in plants and most animals. The dopamine system plays a central role in several significant medical conditions, including Parkinson's disease. Parkinson's disease is an age-related disorder characterized by movement disorders such as stiffness of the body, slowing of movement, and trembling of limbs when they are not in use. The main symptoms are caused by the loss of dopamine-secreting cells in the substantia nigra. These dopamine cells are especially vulnerable to damage, and a variety of insults, including encephalitis (as depicted in the book and movie "Awakenings"), repeated sports-related concussions, and some forms of chemical poisoning such as MPTP, can lead to substantial cell loss, producing a parkinsonian syndrome that is similar in its main features to Parkinson's disease. The most widely used treatment for parkinsonism is administration of L-DOPA, the metabolic precursor for dopamine. L-DOPA is converted to dopamine in the brain and various parts of the body by the enzyme DOPA decarboxylase. L-DOPA is used rather than dopamine itself because, unlike dopamine, it is capable of crossing the blood-brain barrier. Description source: [https://en.wikipedia.org/wiki/Dopamine Wikipedia] Proteins on this pathway have targeted assays available via the [https://assays.cancer.gov/available_assays?wp_id=WP2436 CPTAC Assay Portal]

Dopamine receptors are members of the rhodopsin-like G-protein coupled receptor family and are prominent in the vertebrate central nervous system (CNS). Dysfunction of dopaminergic neurotransmission in the CNS has been implicated in a variety of neuropsychiatric disorders , including social phobia , Tourette's syndrome , Parkinson's disease , schizophrenia , neuroleptic malignant syndrome , attention-deficit hyperactivity disorder (ADHD) and drug and alcohol dependence . As a result, dopamine receptors are common drug targets; antipsychotics are often dopamine receptor antagonists while psychostimulants are typically indirect agonists of dopamine receptors .There are at least five different known subtypes of dopamine receptors designated D1, D2, D3, D4 and D5 . They are distinguished by their G-protein coupling, ligand specificity, anatomical distribution and physiological effects. Dopamine receptors are divided into two further subfamilies. The D1-like family consists of D1 and D5 receptors, which couple to Gs and mediate excitatory neurotransmission. The D2-like family, meanwhile, consists of D2, D3 and D4 receptors, which couple to Gi/Go and mediate inhibitory neurotransmission. Although dopamine receptors are widely distributed in the brain, they are found in different locations that have different receptor type densities, presumably reflecting different functional roles . D1 and D2 receptor subtypes are found at 10-100 times the levels of the D3, D4, D5 subtypes .

This page, "Dopamine", is part of the NIST Chemistry WebBook. This site and its contents are part of the NIST Standard Reference Data Program.

Dopamine, a major neurotransmitter, plays a role in a wide range of brain sensorimotor functions. Parkinson's disease and schizophrenia are two major human neuropsychiatric disorders typically associated with dysfunctional dopamine activity levels, which can be alleviated through the druggability of the dopaminergic systems. Meanwhile, several studies suggest that optimal brain dopamine activity levels are also significantly impacted in other serious neurological conditions, notably stroke, but this has yet to be fully appreciated at both basic and clinical research levels. This is of utmost importance as there is a need for better treatments to improve recovery from stroke. Here, we discuss the state of knowledge regarding the modulation of dopaminergic systems following stroke, and the use of dopamine boosting therapies in animal stroke models to improve stroke recovery. Indeed, studies in animals and humans show stroke leads to changes in dopamine functioning. Moreover, evidence from animal stroke models suggests stimulation of dopamine receptors may be a promising therapeutic approach for enhancing motor recovery from stroke. With respect to the latter, we discuss the evidence for several possible receptor-linked mechanisms by which improved motor recovery may be mediated. One avenue of particular promise is the subtype-selective stimulation of dopamine receptors in conjunction with physical therapy. However, results from clinical trials so far have been more mixed due to a number of potential reasons including, targeting of the wrong patient populations and use of drugs which modulate a wide array of receptors. Notwithstanding these issues, it is hoped that future research endeavors will assist in the development of more refined dopaminergic therapeutic approaches to enhance stroke recovery.

This dataset contains the data presented in the paper Dopamine neurons projecting to medial shell of the nucleus accumbens drive heroin reinforcement. (doi: 10.7554/eLife.39945 )

Dopamine neurotransmitter cycle occurs in dopaminergic neurons. Dopamine is synthesized and loaded into the clathrin sculpted monoamine transport vesicles. The vesicles are docked, primed and fused with the plasmamembrane in the synapse to release dopamine into the synaptic cleft.

This dataset contains the data of 25 healthy young adults who completed a delay discounting task during fMRI scanning and on a separate vist, completed a PET scan with the high-affinity dopamine D2/3 receptor tracer [18F]fallypride. PET data for each participant were acquired in 3 sessions separated with short breaks for participant comfort. Dynamic tomograph images from the 3 sessions provided have been merged and realigned. PET images were reconstructed with decay correction, attenuation correction, scatter correction, and calibration. PET data for each participant are provided in three ways: (1.) raw unprocessed timeseries with timing information, (2.) binding potential (BPND) parametric image calculated using the simplified reference tissue method (SRTM) in the participant's original PET space (smoothed with a 5 mm FWHM Gaussian kernel), and (3.) BPND parametric image calculated using SRTM (from PET space map) transformed to MNI152 2mm standard space using the participant's structural T1. Calculation of BPND using the SRTM was carried out using Pmod software with the putamen as the receptor-rich region and the cerebellum as the reference region.

Dopaminergic neurotransmission has been investigated extensively, yet direct optical probing of dopamine has not been possible in live cells. Here we image intracellular dopamine with sub-micrometer three-dimensional resolution by harnessing its intrinsic mid-ultraviolet (UV) autofluorescence. Two-photon excitation with visible light (540 nm) in conjunction with a non-epifluorescent detection scheme is used to circumvent the UV toxicity and the UV transmission problems. The method is established by imaging dopamine in a dopaminergic cell line and in control cells (glia), and is validated by mass spectrometry. We further show that individual dopamine vesicles/vesicular clusters can be imaged in cultured rat brain slices, thereby providing a direct visualization of the intracellular events preceding dopamine release induced by depolarization or amphetamine exposure. Our technique opens up a previously inaccessible mid-ultraviolet spectral regime (excitation ~270 nm, emission < 320 nm) for label-free imaging of native molecules in live tissue.

Datafile for: "Dopamine and the creative mind: Individual differences in creativity are predicted by interactions between dopamine genes DAT and COMT."

Protein-Protein, Genetic, and Chemical Interactions for Ostadali MR (2004):The Detection of Dopamine Gene Receptors (DRD1-DRD5) Expression on Human Peripheral Blood Lymphocytes by Real Time PCR. curated by BioGRID (https://thebiogrid.org); ABSTRACT: There is interrelationship between the immune and nervous systems that is accomplished by the molecular mediators. Dopamine is one of the most important neurotransmitters. Five different dopamine receptor genes (DRD1, DRD2, DRD3, DRD4, and DRD5) have been recognized and cloned. The expression of the dopamine receptors is well characterized in the brain but little work has been done to examine their expression in other organ tissues. In certain diseases of the immune and nervous systems, alterations in dopamine receptors gene expression in different cells have been reported. This suggests that dopamine and its receptors have important role in pathophysiology of above-mentioned diseases.In the present study, using Real Time Polymerase Chain Reaction (PCR) technique, we investigated dopamine receptors genes expression in PBMC of normal individuals. The PBMC was separated from normal whole blood by Ficoll-hypaque; the total cellular RNA was then extracted and the cDNA was synthesized. This process followed by real time-PCR using primer pairs specific for five dopamine receptors mRNAs and beta-actin as internal control. The results showed the presence of all types of dopamine receptors in lymphocytes of normal individuals. The specificities of the obtained PCR products for the respective dopamine receptors fragments were confirmed by sequenced analysis capillary system. In conclusion, the present study has shown that human lymphocytes express five dopamine receptors DR1-DR5. However, the conclusive evidence on the possible function of these receptors in lymphocytes remains unknown. Because lymphocytes express all of the five neuronal dopamine receptors, it is quite reasonable to consider them as a model of dopaminergic neuron.

Four groups of this dataset were used as negative samples for testing subtype selectivity of our developed multi-label machine learning models.

This MassBank record with Accession MSBNK-Keio_Univ-KO003149 contains the MS2 mass spectrum of Dopamine with the InChIkey VYFYYTLLBUKUHU-UHFFFAOYSA-N.

This MassBank record with Accession MSBNK-Osaka_Univ-OUF00207 contains the MS mass spectrum of Dopamine with the InChIkey VYFYYTLLBUKUHU-UHFFFAOYSA-N.

Nicotine is an alkaloid found in tobacco plants. It is a substance that acts as a stimulant in humans and is one of the main factors responsible for tobacco dependence. When nicotine enters the body, it is distributed quickly through the bloodstream, and it can cross the blood-brain barrier to enter the central nervous system (CNS). It binds to two main types of nicotinic acetylcholine receptors: the ganglion type and the CNS type. In dopaminergic neurons in the CNS, nicotine binds to the CNS-type nicotinic acetylcholine receptors. The main type of CNS receptor is composed of alpha 4 beta 2 (CHRNA4, CHRNB2) subunits. It has been shown that alpha 6, alpha 5, and beta 3 can also be in the receptor complex to modulate binding sensitivity. By binding to the receptor, nicotine causes cell depolarization and release of dopamine from the cell through the SNARE complex. Dopamine then binds to dopamine receptors (DRD2, DRD3, DRD4) on dopaminergic terminals and activates Gi alpha (GNAI1), initiating a feedback loop to inhibit dopamine release. One of the key players mediating dopamine signaling is PPP1R1B (also called DARPP-32, dopamine and cyclic AMP-regulated phospho-protein). PPP1R1B is a bifunctional signal transduction molecule which, by distinct mechanisms, inhibits either a serine/threonine kinase (PPKACA or PKA) or a serine/threonine phosphatase (PPP1CA or protein phosphatase 1). When PPP1R1B is phosphorylated by PPKACA at threonine 34, it is an inhibitor of protein phosphatase 1 (PPP1CA), which inhibits dopamine secretion through the SNARE complex. When PPP1R1B is phosphorylated by CDK5 at threonine 75, it is converted to an inhibitor of PPKACA. Binding of dopamine to D2-like dopamine receptors leads to inhibition of adenylate cyclase (ADCY2) via G-protein GNAI1, and decreases PKA-stimulated phosphorylation of DARPP-32 at Thr34. This, in turn, relieves the inhibition of protein phosphatase 1 (PPP1CA), and inhibits further dopamine release. Sources: [http://www.pharmgkb.org/do/serve?objId=PA162355621&objCls=Pathway PharmGKB:Nicotine in Dopaminergic Neurons], [http://en.wikipedia.org/wiki/Nicotine Wikipedia:Nicotine]

Dopaminergic neurons of the substantia nigra exist in a persistent state of vulnerability resulting from high baseline oxidative stress, high energy demand, and broad unmyelinated axonal arborizations. Impairments in the storage of dopamine compound this stress due to cytosolic reactions that transform the vital neurotransmitter into an endogenous neurotoxicant, and this toxicity is thought to contribute to the dopamine neuron degeneration that occurs Parkinson's disease. We have previously identified synaptic vesicle glycoprotein 2C (SV2C) as a modifier of vesicular dopamine function, demonstrating that genetic ablation of SV2C in mice results in decreased dopamine content and evoked dopamine release in the striatum. Here, we adapted a previously published in vitro assay utilizing false fluorescent neurotransmitter 206 (FFN206) to visualize how SV2C regulates vesicular dopamine dynamics and identified that SV2C promotes the uptake and retention of FFN206 within vesicles. In addition, we present data indicating that SV2C enhances the retention of dopamine in the vesicular compartment with radiolabeled dopamine in vesicles isolated from immortalized cells and from mouse brain. Further, we demonstrate that SV2C enhances the ability of vesicles to store the neurotoxicant 1-methyl-4-phenylpyridinium (MPP+) and that genetic ablation of SV2C results in enhanced 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced vulnerability in mice. Together, these findings establish that SV2C functions to enhance storage of dopamine and toxicants and helps maintain the integrity of dopaminergic neurons.

Protein-Protein, Genetic, and Chemical Interactions for Qin ZH (1994):Dopamine receptor blockade increases dopamine D2 receptor and glutamic acid decarboxylase mRNAs in mouse substantia nigra. curated by BioGRID (https://thebiogrid.org); ABSTRACT: To study the influence of dopaminergic activity on the expression of dopamine D2 receptors and glutamic acid decarboxylase in substantia nigra, mice were treated daily for several days with an irreversibly acting dopamine D1 and dopamine D2 receptor antagonist N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) or with a selective irreversible D2 dopamine receptor antagonist fluphenazine-N-mustard. Mice were killed 24 h after the last injection. Dopamine D1 and dopamine D2 receptors were determined by receptor autoradiography, and dopamine D1 and dopamine D2 receptor mRNA and glutamic acid decarboxylase mRNA were determined by in situ hybridization histochemistry. The results showed that treatment with EEDQ, which blocked 80% to 85% of the dopamine D2 and dopamine D1 receptors in substantia nigra, increased the levels of dopamine D2 receptor mRNA in substantia nigra by about 27%. Treatment with fluphenazine-N-mustard, which blocked about 85% of the dopamine D2 receptors in substantia nigra but had no significant effect on dopamine D1 receptors, increased the levels of dopamine D2 receptor mRNA by about 34%. There were no detectable levels of dopamine D1 receptors, increased the levels of dopamine D2 receptor mRNA by about 34%. There were no detectable levels of dopamine D1 receptor mRNA in substantia nigra either in control animals or in animals treated with the dopamine receptor antagonists. Glutamic acid decarboxylase mRNA was expressed in several regions of the mid-brain but only that expressed in substantia nigra was altered by treatment with dopamine receptor antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)