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Analyzed sessions data structure for all data collected. Data structures include multidimensional behavioral data extracted from video and external sensors as well as simultaneous photometry recordings from multiple locations in the mouse brain. All datasets are aligned to include the first ~1000 trials of learning for >20 animals. A subset of animals received optogenetic perturbations during learning as described in the paper / methods.
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This page, "Dopamine, N-acetate, PFP", is part of the NIST Chemistry WebBook. This site and its contents are part of the NIST Standard Reference Data Program.
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According to Cognitive Market Research, the global Dopamine market size was USD XX million in 2024. It will expand at a compound annual growth rate (CAGR) of 5.00% from 2024 to 2031.
North America held the major market share for more than 40% of the global revenue with a market size of USD XX million in 2024 and will grow at a compound annual growth rate (CAGR) of 3.2% from 2024 to 2031.
Europe accounted for a market share of over 30% of the global revenue with a market size of USD XX million.
Asia Pacific held a market share of around 23% of the global revenue with a market size of USD XX million in 2024 and will grow at a compound annual growth rate (CAGR) of 7.0% from 2024 to 2031.
Latin America had a market share of more than 5% of the global revenue with a market size of USD XX million in 2024 and will grow at a compound annual growth rate (CAGR) of 4.4% from 2024 to 2031.
Middle East and Africa had a market share of around 2% of the global revenue and was estimated at a market size of USD XX million in 2024 and will grow at a compound annual growth rate (CAGR) of 4.7% from 2024 to 2031.
The depressive disorders category is the fastest growing segment of the Dopamine industry
Market Dynamics of Dopamine Market
Key Drivers for Dopamine Market
Increasing Prevalence of Neurological Disorders to Boost Market Growth
The rising incidence of neurological disorders, such as Parkinson's disease, depression, schizophrenia, and bipolar disorder, is a major driving factor for the dopamine market. Dopamine, a key neurotransmitter involved in mood regulation, movement, and reward processing, plays a critical role in these conditions. For instance, dopamine deficiency is associated with Parkinson's disease, leading to motor symptoms like tremors and rigidity. The demand for treatments targeting dopamine receptors, such as dopamine agonists, is growing rapidly as healthcare systems focus on improving the quality of life for patients suffering from these conditions. Furthermore, with the increasing ageing population globally, the number of individuals at risk of developing dopamine-related disorders is expanding, thus driving demand for dopamine-based therapies. Advancements in understanding dopamine's role in mental health are also prompting the development of new drugs and treatments, further expanding the market.
Growth in the Pharmaceutical and Biotechnology Sectors to Drive Market Growth
The continuous advancements in the pharmaceutical and biotechnology industries are fueling the growth of the dopamine market. Research into dopamine-related therapies has expanded due to breakthroughs in understanding its mechanisms in various neurological and psychiatric disorders. Pharmaceutical companies are focusing on developing dopamine agonists and antagonists that can treat a wide range of conditions, from Parkinson’s disease to mood disorders. Additionally, dopamine is a key target in the development of new treatments for addiction, obesity, and other metabolic conditions. The growing number of biotech startups and multinational corporations investing in dopamine-targeting drugs further strengthens market demand. Increased research funding, collaboration between academic institutions and pharmaceutical companies, and regulatory support for innovative drug development have accelerated market growth.
Restraint Factor for the Dopamine Market
Regulatory and Safety Concerns will Limit Market Growth
The market for dopamine, particularly in pharmaceutical applications, faces significant regulatory hurdles. Dopamine is primarily used in medical treatments for conditions like Parkinson's disease and dopamine deficiency. Due to its critical role in the central nervous system, its use is heavily regulated by government bodies such as the FDA. The approval process for dopamine-based treatments and related drugs is stringent, leading to long development timelines and high costs for manufacturers. Additionally, the safety concerns associated with dopamine treatments, such as the potential for side effects like hypertension, tachycardia, or arrhythmia, can limit the market’s growth. The strict regulations and safety requirements add layers of complexity, which can inhibit innovation and slow market expansion.
Impact of Covid-19 on the Dopamine Market
The COVID-19 pandemic had a notable impact on the dopamine market, particularly in the pharmaceutical sector. D...
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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.
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Background: The dopaminergic system has been associated with the progression of Alzheimer's disease. But previous studies found inconsistent results regarding the relationship between Alzheimer's disease and dopamine when looking at dopamine receptor concentrations.Objective: The aim of this review was to synthesize, using a random-effects model of meta-analysis, the link between the dopaminergic system and Alzheimer's disease.Methods: A detailed analysis protocol was registered at the PROSPERO database prior to data extraction (CRD42018110798). Electronic databases of PubMed, Embase, Web of Science, and Psyc-ARTICLES were searched up to December 2018 for studies that examined dopamine and dopamine receptors in relation to Alzheimer's disease. Standardized mean differences (SMD) were calculated to assess group differences in the levels of dopaminergic neurometabolites.Results: Seventeen studies met the eligibility criteria. Collectively, they included 512 patients and 500 healthy controls. There were significantly lower levels of dopamine in patients with Alzheimer's disease compared with controls (SMD = −1.56, 95% CI: −2.64 to −0.49). In addition, dopamine 1 receptor (SMD = −5.05, 95% CI: −6.14 to −3.97) and dopamine 2 receptor (SMD = −1.13, 95% CI: −1.52 to −0.74) levels were decreased in patients with Alzheimer's disease compared with controls. The results of network meta-analysis indicated that the rank of correlation with Alzheimer's disease from highest to lowest was dopamine (0.74), dopamine 2 receptor (0.49), dopamine 3 receptor (0.46), dopamine 4 receptor (0.33), dopamine 5 receptor (0.31), and dopamine 1 receptor (0.64).Conclusions: Overall, decreased levels of dopaminergic neurotransmitters were linked with the pathophysiology of Alzheimer's disease. Nonetheless, there is a clear need for more prospective studies to validate these hypotheses.
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TwitterBackground Though the dysfunction of central dopaminergic system has been proposed, the etiology or pathogenesis of schizophrenia is still uncertain partly due to limited accessibility to dopamine receptor. The purpose of this study was to define whether or not the easily accessible dopamine receptors of peripheral lymphocytes can be the peripheral markers of schizophrenia. Results 44 drug-medicated schizophrenics for more than 3 years, 28 drug-free schizophrenics for more than 3 months, 15 drug-naïve schizophrenic patients, and 31 healthy persons were enrolled. Sequential reverse transcription and quantitative polymerase chain reaction of the mRNA were used to investigate the expression of D3 and D5 dopamine receptors in peripheral lymphocytes. The gene expression of dopamine receptors was compared in each group. After taking antipsychotics in drug-free and drug-naïve patients, the dopamine receptors of peripheral lymphocytes were sequentially studied 2nd week and 8th week after medication. In drug-free schizophrenics, D3 dopamine receptor mRNA expression of peripheral lymphocytes significantly increased compared to that of controls and drug-medicated schizophrenics, and D5 dopamine receptor mRNA expression increased compared to that of drug-medicated schizophrenics. After taking antipsychotics, mRNA of dopamine receptors peaked at 2nd week, after which it decreases but the level was above baseline one at 8th week. Drug-free and drug-naïve patients were divided into two groups according to dopamine receptor expression before medications, and the group of patients with increased dopamine receptor expression had more severe psychiatric symptoms. Conclusions These results reveal that the molecular biologically-determined dopamine receptors of peripheral lymphocytes are reactive, and that increased expression of dopamine receptor in peripheral lymphocyte has possible clinical significance for subgrouping of schizophrenis.
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TwitterDopaminergic 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, w..., , , # Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity
This dataset contains the raw data corresponding to the manuscript Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity. Inclusive in this dataset is the following: 1) a GraphPad Prism file containing all of the data found in the manuscript with statistical analysis and graphs; 2) individual .csv files containing the data for each graph of data found in the manuscript including a separate .csv for corresponding statistics (files ending in _stats); 3) individual PDFs of graphs generated in GraphPad Prism; and 4) raw image files for microscopy and Western blots. These data demonstrate the principal findings for the manuscript that the protein SV2C: 1) enhances vesicular storage of dopamine and dopamine analogues (e.g., FFN206 and MPP+), and 2) confers neuroprotection against dopaminergic toxicity.
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TwitterSee the file README.docx for description of data files.
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Brain dopamine is critically involved in movement control, and its deficiency is the primary cause of motor symptoms in Parkinson disease. Here we report development of an animal model of acute severe dopamine deficiency by using mice lacking the dopamine transporter. In the absence of transporter-mediated recycling mechanisms, dopamine levels become entirely dependent on de novo synthesis. Acute pharmacological inhibition of dopamine synthesis in these mice induces transient elimination of striatal dopamine accompanied by the development of a striking behavioral phenotype manifested as severe akinesia, rigidity, tremor, and ptosis. This phenotype can be reversed by administration of the dopamine precursor, L-DOPA, or by nonselective dopamine agonists. Surprisingly, several amphetamine derivatives were also effective in reversing these behavioral abnormalities in a dopamine-independent manner. Identification of dopamine transporter- and dopamine-independent locomotor actions of amphetamines suggests a novel paradigm in the search for prospective anti-Parkinsonian drugs.
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TwitterFour groups of this dataset were used as negative samples for testing subtype selectivity of our developed multi-label machine learning models.
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TwitterReward motivation is known to enhance cognitive control. However, detrimental effects have also been observed, which have been attributed to overdosing of already high baseline dopamine levels by further dopamine increases elicited by reward cues. Aarts et al. (2014) indeed demonstrated, in 14 individuals, that reward effects depended on striatal dopamine synthesis capacity, measured with [18F]FMT-PET: promised reward improved Stroop control in low-dopamine individuals, while impairing it in high-dopamine individuals. Here, we aimed to assess this same effect in 44 new participants, who had previously undergone an [18F]DOPA-PET scan to quantify dopamine synthesis capacity. This sample performed the exact same rewarded Stroop paradigm as in the prior study. However, we did not find any correlation between reward effects on cognitive control and striatal dopamine synthesis capacity. Critical differences between the radiotracers [18F]DOPA and [18F]FMT are discussed, as the discrepancy between the current and our previous findings might reflect the use of the potentially less sensitive [18F]DOPA radiotracer in the current study.
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Twitterhttps://doi.org/10.5061/dryad.qnk98sfs5
Title: Relating genetic variations in dopamine brain transmission to task performance with and without rewards
Contact: Diane Damiano, National Institutes of Health, damianod@cc.nih.gov
Date created: 2024/09/17
Licenses or restrictions: none
Methods for data collection: a specialized computer program that provided instruction to participants, administered all items and recorded reaction time, error rate for SRTT and proportion correct and reaction time for WPT.
Description: Excel file includes participant group, age group at enrollment (1 = 6-10, 2 = 11-15, 3 = 16-20, 4 = 21-25), sex, gene group, individual gene variant scores (COMT = catechol-O -...
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Results of regression analysis examining the association between individual differences in cognitive flexibility as measured with the difference between part b and a in the trail making test and individual differences in dopamine D2 receptor availability as measured with PET and the radioligand [18F]fallypride controlling for age in an adult life-span sample of healthy humans. Regression analysis included the continuous cognitive score (trail making test b-a) and age as continuous independent variables with dopamine D2-like binding potential as the dependent variable. Data collected at Vanderbilt University in the Zald lab.
Two studies of healthy, human adults examining associations between adult chronological age, dopamine D2-like receptors measured with [18F]Fallypride in one study and [11C]FLB457 in the other study, and neuropsychological measures of cognition and psychomotor speed. Fallypride data set collected at Vanderbilt University in the Zald Lab. FLB457 data set collected at Yale University in the Samanez-Larkin Lab. Data analyzed at Duke University in the Samanez-Larkin Lab.
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TwitterDopamine in the striatum strongly regulates behavioral output in a heterogenous across the various striatal subregions. Moreover, dopamine dynamics not only displays heterogeneity across brain structures but also within males and females. The purpose of this dataset was to evaluate the dopamine dynamics in male and female mice and rats across five subregions: the dorsolateral caudate, ventromedial caudate, nucleus accumbens core, nucleus accumbens lateral shell, and the nucleus accumbens medial shell. Fast scan cyclic voltammetry (FSCV) was employed to measure dopamine release and uptake following a single pulse electrical stimulation in each of these subregions within a single brain slice. The dopamine dynamics were also observed across a variety of stimulation amplitudes. The goal of this dataset was to produce systematic FSCV measurements of dopamine across the rodent striatum using FSCV which would be available as a resource for further investigation of DA terminal function., Detailed methods can be found in the manuscript., , # Comparison of dopamine release and uptake parameters across sex, species and striatal subregions
https://doi.org/10.5061/dryad.sf7m0cgcn
This data set includes 12 mice (6 male, 6 female) and 12 rats (6 male, 6 female). One rostral (mouse: 1.33-1.09 AP; rat: 2.20-1.60 AP) and one caudal (mouse: 0.97-0.73 AP, rat: 1.20-0.70 AP) brain slice from each animal hemisected so that a total of 4 data points were collected per animal. All slices were run in parallel, and an additional slice was collected from each animal to serve as a control for slice health and electrode stability throughout the recording period. Data identifiers have been designated as follows: Species (Ms= mouse or Rt=rat), Sex (M=male; F=female), animal number, slice identity (r=rostral, c=caudal), slice number. Example: MsM1_r1 would be mouse, male 1, rostral slice 1.Â
The study was designed to maximize the data collected, allowing...
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TwitterTransient increases in dopamine within the striatum can encode reward prediction errors, critical signals for updating predictions of future rewards. However, it is unclear how this mechanism can provide suitable feedback for predictions across a wide range of time horizons: from seconds or less (if singing a song) to potentially hours or more (if hunting for food). Here we report that dopamine transients in distinct striatal subregions convey prediction errors over distinct time scales. Dopamine dynamics systematically accelerated from ventral to dorsal- medial to dorsal-lateral striatum, in the tempo of their spontaneous fluctuations, their temporal integration of prior rewards, and their discounting of future rewards. This spectrum of time scales for evaluative computations can help achieve efficient learning and adaptive motivation for a wide range of behaviors.
, , , # Subregion Specific Dynamics of Striatal Dopamine
The dataset included in this repository follows the standard format used by the Berke lab. It contains the necessary files and data required to replicate the experiments and findings described in the research article. Additionally, we have provided MATLAB code that can be utilized to read and interpret the data, as well as generate figures related to our results.
The dataset consists of three *.zip files. Each zip file contains MATLAB/python scripts and data files required to reproduce the graphs in corresponding figures. Following is the description for each data file.
This text contains data and MATLAB scripts to replicate Fig2. The data is saved in .mat format, which can be loaded in MATLAB as a 1x41 struct. Each struct has recordings from one behavioral session of the bandit task and has these elements:
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TwitterHigh-resolution bright-field microscopy images of coronal brain sections showing dopamine 2 receptor positive neurons across the adult (70 days old) mouse brain. The dataset consists of seven image series covering the rostral part of the brain from Drd2-EGFP mice. For each brain, every fourth section was processed by diaminobenzidine (DAB) immunohistochemistry using a polyclonal anti-GFP (RRID:AB_300798) antibody. The publication related to the dataset furthermore includes stereological counts of positive neurons in the prelimbic, infralimbic and insula cortex, as well as in dorsal and ventral striatum.
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ABSTRACT
Dopamine release defects are an early and consistently-observed pathological feature of Parkinson’s disease, however the underlying drivers of disease have not yet been elucidated. Here we demonstrate dopamine release is reduced in patient-derived dopamine neurons with the SNCA-triplication mutation and find that this is due to impaired synaptic vesicle loading resulting in reduced dopamine content and increased dopamine turnover while dopamine synthesis remains intact. Supplementation with L-DOPA rescues these observed dopamine release defects. We find that impaired dopamine vesicle loading results in decreased synaptic vesicle pool size. In contrast, glutamate release is intact in Parkinson’s patient neurons, revealing specificity in dopaminergic dysfunction. In combination, these data reveal dopamine loading into synaptic vesicles as a critical target in Parkinson’s disease therapies.
This repository contains the following files:
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TwitterLearning causal relationships relies on understanding how often one event precedes another. To gain an understanding of how dopamine neuron activity and neurotransmitter release change when a retrospective relationship is degraded for a specific pair of events, we used outcome-selective Pavlovian contingency degradation in rats. Two cues were paired with distinct food rewards, one of which was also delivered in the absence of either cue. Conditioned responding was attenuated for the cue-reward contingency that was degraded. Dopamine neuron activity in the midbrain and dopamine release in the ventral striatum in response to the cue and subsequent reward were attenuated during degraded versus non-degraded trials, and contingency degradation also abolished the trial-by-trial history dependence of dopamine responses at the time of trial outcome. This profile of changes in cue- and reward-evoked responding is not easily explained by a standard reinforcement learning model. An alternative mod..., , , # Mesostriatal dopamine is sensitive to changes in specific cue-reward contingencies
https://doi.org/10.5061/dryad.q573n5tr1
This dataset includes two types of behavioral data. First, there are conditioned port entry rates from five separate cohorts of rats: those that underwent fiber photometry recordings using GCaMP6f in ventral tegmental area (VTA) dopamine neurons, those that underwent fiber photometry recordings using dLight1.2 in the nucleus accumbens (NAc) core, those that underwent a context manipulation, those that underwent optogenetic inhibition of VTA dopamine neurons, and those that underwent optogenetic inhibition of dopamine release. Second, there are behavioral measures derived from videos: conditioned head velocities and distances between head and mid-tail derived from DeepLabCut, and conditioned rates of rearing and rotating derived from video hand-scoring.
This dataset also includes fiber photometry data taken from rats th...
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TwitterIntroduction: The nematode, Caenorhabditis elegans (C. elegans), is an advantageous model for studying developmental toxicology due to its well defined developmental stages and homology to humans. It has been established that across species, dopaminergic neurons are highly vulnerable to neurotoxicant exposure, resulting in developmental neuronal dysfunction and age-induced degeneration. C. elegans, with genetic perturbations in dopamine system proteins, can provide insight into the mechanisms of dopaminergic neurotoxicants. In this study, we present a comprehensive analysis on the effect of gene mutations in dopamine-related proteins on body size, development, and behavior in C. elegans. Methods: We studied C. elegans that lack the ability to sequester dopamine (OK411) and that overproduce dopamine (UA57) and a novel strain (MBIA) generated by the genetic crossing of OK411 and UA57, which both lack the ability to sequester dopamine into vesicles and, additionally, endogenously overprodu..., , , # Effect of altered production and storage of dopamine on development and behavior in C. elegans
https://doi.org/10.5061/dryad.hhmgqnkpf
This dataset contains the raw data corresponding to the manuscript "Effect of altered production and storage of dopamine on development and behavior in C. elegans." The data presented here was in effort to understand and characterize the role of dopamine neurotransmission in C. elegans development utilizing genetic models. A novel strain was generated that lacks the protein cat-1, which is responsible for vesicular sequestration of dopamine, and over-expresses the gene cat-2, which is responsible for dopamine synthesis. Thus, this novel strain (MBIA) has compounded effects on the amount of cytosolic dopamine. We characterized this strain, the parent strains used to generate MBIA, and wild-type C. elegans to determine what role dopamine synthesis and sequestration has on body size, development through lar...
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TwitterWe trained naive or trained mice to associate odor cues with outcome (water, air puff or no outcome), and recorded dopamine cell body activity in the vetral tegmental area (VTA), dopamine axon activity in the ventral striatum (VS) or dopamine release in VS with optic fiber fluorometry (photometry). In different set of mice, single dopamine neuron activiy was recorded with 2-photon microscope. In some of these mice, we reversed odor-outcome contingency so that an odor that was associated with no outcome or air puff became associated with water reward. Licking pattern was also recorded.
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Analyzed sessions data structure for all data collected. Data structures include multidimensional behavioral data extracted from video and external sensors as well as simultaneous photometry recordings from multiple locations in the mouse brain. All datasets are aligned to include the first ~1000 trials of learning for >20 animals. A subset of animals received optogenetic perturbations during learning as described in the paper / methods.