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Raclopride

Raclopride is a radioligand used in positron emission tomography (PET) imaging to study the dopamine D2 receptor in the brain.
It has been widely used in research to investigate the role of dopamine in various neurological and psychiatric disorders, such as Parkinson's disease, schizophrenia, and addiction.
Raclopride provides a quantitative measure of D2 receptor availability, allowing researchers to understand the underlying neurochemical mechanisms involved in these conditions.
The selection of appropriate experimental protocols is crucial for ensuring the reproducibility and accuracy of Raclopride-based studies.
PubCompare.ai's AI-driven platform helps researchers identify the most effective Raclopride protocols from literature, preprints, and patents, optimizing for reproducibility and accuracy.
This unique tool streamlines the research process and enhancse outcomes in Raclopride-related studies.

Most cited protocols related to «Raclopride»

Volumetric PET images were collected for 19 different neurotransmitter receptors and transporters across multiple studies. To protect patient confidentiality, individual participant maps were averaged within studies before being shared. Details of each study, the associated receptor/transporter, tracer, number of healthy participants, age and reference with full methodological details can be found in Table 1. A more extensive table can be found in the supplementary material (Supplementary Table 3), which additionally includes the PET camera, number of males and females, PET modeling method, reference region, scan length, modeling notes and additional references, if applicable. In all cases, only healthy participants were scanned (n = 1,238; 718 males and 520 females). Images were acquired using best practice imaging protocols recommended for each radioligand56 . Altogether, the images are an estimate proportional to receptor densities, and we, therefore, refer to the measured value (that is, binding potential and tracer distribution volume) simply as density. Note that the NMDA receptor tracer ([18F]GE-179) binds to open (that is, active) NMDA receptors86 (link),95 (link). PET images were all registered to the MNI-ICBM 152 non-linear 2009 (version c, asymmetric) template and then parcellated to 100, 200 and 400 regions according to the Schaefer atlas12 (link). Receptors and transporters with more than one mean image of the same tracer (that is, 5-HT1B, D2, mGluR5 and VAChT) were combined using a weighted average after confirming that the images are highly correlated to one another (Supplementary Fig. 13a). Finally, each tracer map corresponding to each receptor/transporter was z-scored across regions and concatenated into a final region by receptor matrix of relative densities.
In some cases, more than one tracer map was available for the same neurotransmitter receptor/transporter. We show the comparisons between tracers in Supplementary Fig. 13b for the following neurotransmitter receptors/transporters: 5-HT1A9 (link),69 (link), 5-HT1B9 (link),69 (link),70 (link), 5-HT2A9 (link),69 (link),96 (link), 5-HTT9 (link),69 (link), CB1 (refs. (89 (link),97 (link))), D2 (refs. (59 (link),60 (link),98 (link),99 (link))), DAT64 (link),100 (link), GABAA8 (link),64 (link), MOR93 (link),101 (link) and NET65 (link),102 (link). Here, we make some specific notes: (1) 5-HTT and GABAA involve comparisons between the same tracers (DASB and flumazenil, respectively), but one map is converted to density using autoradiography data (see ref. 9 (link) and ref. 8 (link)) and the other is not7 ,64 (link),69 (link); (2) raclopride is a popular D2 tracer but has unreliable binding in the cortex and is, therefore, an inappropriate tracer to use for mapping D2 densities in the cortex, but we show its comparison to FLB457 and another D2 tracer, fallypride, for completeness98 (link),99 (link),103 ; and (3) the chosen carfentanil (MOR) map was collated across carfentanil images in the PET Turku Centre database—because our alternative map is a partly overlapping subset of participants, we did not combine the tracers into a single mean map93 (link),101 (link).
Synapse density in the cortex was measured in 76 healthy adults (45 males, 48.9 ± 18.4 years of age) by administering [11C]UCB-J, a PET tracer that binds to the synaptic vesicle glycoprotein 2A (SV2A)104 (link). Data were collected on an HRRT PET camera for 90 minutes after injection. Non-displaceable binding potential (BPND) was modeled using SRTM2, with the centrum semiovale as reference and k fixed to 0.027 (population value). This group-averaged map was first presented in ref. 105 (link).
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Publication 2022
Adult Autoradiography carfentanil Cortex, Cerebral fallypride Females Flumazenil Glycoproteins GRM5 protein, human Healthy Volunteers HTR1B protein, human Males Membrane Transport Proteins Microtubule-Associated Proteins N-Methyl-D-Aspartate Receptors N-Methylaspartate Neurotransmitter Receptor Neurotransmitter Transport Proteins Raclopride SLC6A2 protein, human Synapses Synaptic Vesicles
Following behavioral testing, rats were deeply anesthetized with an overdose of sodium pentobarbital. Rats in which Fos plumes were measured were perfused and brains treated as described previously (Reynolds and Berridge, 2008 (link)). These included rats behaviorally tested in the environmental shift group (n=10; which therefore received a 7th final drug or vehicle microinjection and behavioral test 90 minutes prior to perfusion) and a separate dedicated Fos group (n = 36; which were histologically assessed after just a single drug or vehicle microinjection into locations staggered throughout medial shell, administered under conditions identical to the first day of testing for behavioral rats). The purpose of the dedicated Fos group was to assess maximal local impact radius, and avoid danger of under-estimating plume size due to progressive necrosis/gliosis over a series of microinjections that might shrink a final plume. If shrinkage occurred in the behaviorally tested group, that in turn could give rise to overly precise estimates of localization of function in brain maps. This potential distortion of impact estimates by plume shrinkage was prevented in the dedicated group that received only one microinjection.
All rats used for Fos analysis were anesthetized and transcardially perfused 90 minutes after their final or sole bilateral microinjection of vehicle (n=10), DNQX alone (n=13), DNQX plus SCH23390 (n=6), DNQX plus raclopride (n=10), DNQX plus raclopride and SCH23390 (n=3) or no solution (normal, n=3). Brain slices were processed for Fos-like immunoreactivity using NDS, goat anti-cfos (Santa Cruz Biotechnology, Santa Cruz, CA) and donkey anti-goat Alexa Fluor 488 (Invitrogen, Carlsbad, CA) (Faure et al., 2008 (link); Reynolds and Berridge, 2008 (link)). Sections were mounted, air-dried and coverslipped with ProLong Gold antifade reagent (Invitrogen). Zones where the expression of fluorescent Fos was elevated in neurons surrounding microinjection sites (“Fos plumes”) were assessed via microscope as described previously (Reynolds and Berridge, 2008 (link)).
Other brains were removed and fixed in 10% paraformaldehyde for 1–2 days and in 25% sucrose solution (0.1 M NaPB) for 3 days. For assessment of microinjection site locations in behaviorally tested rats, brains were sliced at 60 microns on a freezing microtome, mounted, air-dried and stained with cresyl violet for verification of microinjection sites. Bilateral microinjection sites for each rats were placed on coronal slices from a rat brain atlas (Paxinos and Watson, 2007 ), which were used to extrapolate the position of each site on one sagittal slice. Mapping in the sagittal view allows for the presentation on the same map of the entire rostrocaudal and dorsoventral extents of NAc medial shell. Functional effects on appetitive and fearful behaviors were mapped using color-coding to express the intensity of changes in motivated behaviors for individual behaviorally-tested rats. Symbols were sized to match the maximal diameter of Fos plumes measured as described below. Sites were classified as rostral shell if their NAc placements were located +1.4 to +2.6 mm ahead of bregma, and as caudal shell if their placements were located +0.4 to +1.4 mm ahead of bregma.
Publication 2011
6,7-dinitroquinoxaline-2,3-dione alexa fluor 488 Brain Brain Mapping cresyl violet Drug Overdose Equus asinus Fear Gliosis Goat Gold Microinjections Microscopy Microtomy Necrosis Neurons paraform Pentobarbital Sodium Perfusion Pharmaceutical Preparations Raclopride Radius Rattus norvegicus SCH 23390 Sucrose
The effect of different compounds in vivo depends on the dose, brain penetration, and target engagement of the compound. Therefore, the best way to compare the effects of compounds is to normalize the concentration of the compounds against the apparent D2 receptor occupancy displacement of specific radiotracers such as 11C-raclopride and 125I-IBZM. Ideally, one would like to quantify the binding of a specific radiotracer before and after neuroleptic treatment to correct for any individual baseline variability of the D2 receptor. Although this is possible with our model, it is usually difficult in the clinical setting; hence, many studies define a binding index (Eq. 1) compared to a normal control population.
where Am and Cerm are the specific radioactive signals in the region of interest, ie, in the striatum and cerebellum, respectively.
We used a radiotracer at a concentration of 1 pM. The Kd of raclopride, IBZM, and FLB457 for the D2 receptor are 1.3 nM, 0.6 nM, and 0.018 nM, respectively.20 (link),21 (link) We defined the apparent D2 receptor occupancy as
where Rdrug and Rcontrol are the receptor tracer occupancies, respectively, in the presence and the absence of the D2 receptor modulator. Because the density of radioactive-sensitive D2 receptor binding sites is about 100-fold lower in the cerebellum than that in the striatum,22 (link) our simulations indicate that applying Eq. 2 results in between 1% and 1.5% error, compared to the correct use of Eq. 1 (data not shown).
Figure 3 shows the effect of different radiotracers on the calculated receptor occupancy for a range of haloperidol doses. The observation that the calculated D2 receptor occupancy level decreases when higher-affinity tracers are used is in line with reported differences between apparent receptor occupancy measured with raclopride and IBZM in the same subjects.23 (link) This can be partially explained by the fact that the greater the affinity a tracer has for a receptor, the more difficult it is for the drug to compete with it and dislodge it.
Publication 2010
3-iodo-2-hydroxy-6-methoxy-N-((1-ethyl-2-pyrrolidinyl)methyl)benzamide A-A-1 antibiotic Antipsychotic Agents Binding Sites Brain Cerebellum Dopamine D2 Receptor Haloperidol Pharmaceutical Preparations Raclopride Radioactivity Striatum, Corpus
A computer-interfaced rotarod accelerating from 4–40 rotations per min over 300 s was used (ENV-575M, Med Associates). Animals were trained with ten trials per day for either 1 d or 8 d (trained every other day). This training protocol was chosen on the basis of studies determining the time course of sensitivity of this task to interference, protein synthesis blockers (data not shown) and dopamine receptor antagonists (Fig. 5d). Each trial ended when the mouse fell off the rotarod or after 300 s had elapsed and there was a resting period of approximately 300 s between trials. Yoked animals were handled and placed in the rotarod in the same manner as the trained animals, but without the rotation of the rod. During the in vivo recordings, the beginning and end of the running period were signaled to the MAP recording system (Plexon) as events. The D1 receptor antagonist SCH-23390 (0.4 mg per kg of body weight, Sigma-Aldrich) and D2 receptor antagonist raclopride (2.0 mg per kg, Sigma-Aldrich) were dissolved in phosphate-buffered saline with 1% DMSO by volume (control injection) and injected intra-peritoneally at 10 ml kg–1 (these doses completely block the effects of 3,4-dihydroxy-l-phenylalanine after dopamine depletion49 (link), indicating complete block of D1 and D2 receptors in vivo).
Publication 2009
A 300 Animals Body Weight Cardiac Arrest Dopamine Dopamine Antagonists Dopamine D1 Receptor Dopamine D2 Receptor Hypersensitivity Levodopa Mice, House Phosphates Protein Biosynthesis Raclopride Saline Solution SCH 23390 Sulfoxide, Dimethyl
Intact brains from ~500 g male Sprague-Dawley rats at age of 5 months and a 5 kg male rhesus monkey at age of 6 years (euthanized due to a pancreatic tumor) were flash frozen in dry ice, precooled in isopentane, and stored at −80°C until used. Coronal sections (20 μm) were cut with a Microm cryotome and mounted on superfrost plus glass slides (Fisher Scientific, Pittsburgh, PA). Sections were incubated with 4 nM of [3H]WC-10 or 10 nM of [3H]raclopride in the same buffer used for binding assays, in the presence or absence of 1 μM cold S(−)-Eticlopride (to define nonspecific binding) for 30 min, and then rinsed five times at 1 min intervals each time with ice-cold buffer. Slides were incubated in the wide open staining jar, and the free radioligand concentration loss was less than 5% after ligands bound to brain sections. Slides were dried and made conductive by coating the free side with a copper foil tape. Slides were then placed in the gas chamber [mixture of argon and triethylamine (Sigma-Aldrich, USA)] of a gaseous detector system, the Beta Imager 2000Z Digital Beta Imaging System (Biospace, France). After the gas was well mixed and a homogenous state was reached, further exposure for 24 h yielded high-quality images. [3H]Microscale (American Radiolabeled Chemicals, St. Louis, MO) was counted at the same time as a reference for total radioactivity quantitative analysis. Quantitative analysis was performed with the program β-Vision Plus (BioSpace, France) for the anatomical ROI.
In comparison with digital Beta Imager, the dried slides with brains sections were also exposed to a 3H-sensitive film (3H-Hyperfilm, Amersham, Buckinghamshire, UK) for 1 or 3 months, and the film was developed with a Kodak X-OMAT 2000A processor.
Publication 2010
Argon Biological Assay Brain Buffers Cold Temperature Copper Dry Ice Electric Conductivity eticlopride Fingers Freezing Homozygote isopentane Ligands Macaca mulatta Males Pancreatic Neoplasm Raclopride Radioactivity Rats, Sprague-Dawley triethylamine Vision

Most recents protocols related to «Raclopride»

Time-activity curves (TACs) for [11C]raclopride in the cerebellum were simulated using a one-tissue compartment model operational equation for the instantaneous tissue concentration, dCrtdt=K1rCptk2rCrt, with uptake rate constant K1r=0.092 mL/min g and clearance rate constant k2r=0.45 min−1 (see ref. 18 (link)), and a plasmatic input function given by either the tri-exponential function Cpt=A1+A2+A3tpeaktift<tpeaki=13Aiexpln(2)Tittpeakifttpeak, with A=A1,A2,A3=288.6, 1.1, 409.7Bq/ml , T=T1,T2,T3=4.28, 735.5, 183.5sec , and tpeak = 110 s (see ref. 30 (link)) for IV-MP, or the probability density function of a standard gamma distribution with time-to-peak, tpeak = 90 min, for oral-MP. Note that oral-MP is rapidly absorbed from the gastrointestinal tract achieving peak blood levels in 60 to 120 min53 (link). TACs for the striatum were simulated using the LSSRM operational equation18 (link), CTt=R1Crt+k20tCruduk2a0tCTuduγ0tCTuh(u)du, with ratio of tracer delivery R1 = 1.154, clearance rate constant k2 = 0.45 min−1, uptake rate constant k2a = 0.065 min−1, and amplitude of ligand displacement γ = 0.003, and h(t) accounts for the dynamics of the dopamine–raclopride competition for D2/3 receptor binding30 (link). All parameters ( A , T , tpeak, K1r , k2r , R1 , k2 , k2a , γ, and λ) were varied 10 and 4% (100*standard deviation/mean) across 1000 simulations, using a normal random generator, to simulate between- and within-subjects physiologic variability, respectively. Two alternative mechanistic models for h(t) were tested: (model 1) the fractional occupancy of DAT by MP (see below); and (model 2) the relative extracellular dopamine increases induced by MP (see below). In addition we tested the popular heuristic model for h(t) which is based on a gamma variate function15 (link), ht=0ift<tDttDtptDθexpθ1ttDtptDifttD with tD = 31 min, tp = 45 min, and θ=1 5 (see ref. 30 (link)), but the results did not explain the dynamic changes in the experimental data. Dynamic standardized uptake value ratios were simulated as SUVrt=CT(t)/Cr(t) , and the dynamic SUVr changes between placebo (PL) and MP conditions were simulated as ΔSUVrt=SUVrPLtSUVrMPt.
The simulations were implemented in the interactive data language (IDL, L3Harris Geospatial, Boulder, CO) and the Livermore solver for ordinary differential equations54 .
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Publication 2023
BLOOD Cerebellum Dopamine Dopamine D2 Receptor Gamma Rays Gastrointestinal Tract Ligands Metabolic Clearance Rate Obstetric Delivery physiology Placebos Plasma Raclopride Striatum, Corpus Tissues
A 3-dimensional ordered-subset expectation-maximization (OSEM) algorithm61 (link) with 3 iterations, 21 subsets, an all-pass filter, 344 × 344 × 127 matrix, and a model of the point spread function of the system was used for PET image reconstruction. The reconstructed PET time series consisted of 48 time windows (30 frames of 1 min, followed by 12 frames of 2.5 min, and 6 frames of 5 min) each with 2.086-mm in-plane resolution and 2.032-mm slice thickness. Attenuation coefficients (μ-maps) estimated from the UTE data using a fully convolutional neural network62 were used to correct for scattering and attenuation of the head, the MRI table, the gantry, and the radiofrequency coil. Standardized uptake values (SUVs) for [11C]raclopride were calculated after normalization for body weight and injected dose and spatially normalized to MNI space using HCP pipelines. Relative SUV time series, SUVr(t), were computed in MNI space by normalizing each SUV volume by its mean SUV in the cerebellum, as defined in individual FreeSurfer segmentations.
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Publication 2023
Biological Models Body Weight Cerebellum Head Microtubule-Associated Proteins Nervousness Raclopride Reading Frames
We tested twenty healthy adults who underwent 90-min long PET scans collected in 3 randomly ordered sessions (placebo, oral-MP, and IV-MP; double-blind) while simultaneously recording their self-reported ‘high’ ratings (0–10) under resting conditions, using oral- and IV-MP as pharmacological challenges. In each session, each of the 20 participants was given an oral pill (60mg-MP or placebo) 30 min before injection of the PET tracer ([11C]raclopride), followed 30 min after the tracer by an IV administration (0.25 mg/kg-MP or placebo). Note that these IV- and oral-MP doses were selected because they led to roughly equivalent levels of DA transporter occupancy6 (link), and their administration times were chosen to ensure that peak concentrations of MP in the striatum had similar timing for oral-MP and IV-MP, relative to imaging initiation7 (link).
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Publication 2023
Adult Contraceptives, Oral Placebos Positron-Emission Tomography Raclopride SLC6A3 protein, human Striatum, Corpus
The participants underwent simultaneous PET/MRI imaging in a 3 T Biograph mMR scanner (Siemens; Medical Solutions, Erlangen, Germany). All studies were initiated at noon to minimize confounds from circadian variability. Venous catheters were placed in the left dorsal hand vein for radiotracer injection, and in the right dorsal hand vein for intravenous injection of medications. Heart rate (HR), systolic and diastolic blood pressures (BPs) were continuously monitored throughout the study with an Expression MR400 patient monitor (Philips, Netherlands). Thirty minutes before tracer injection, either 60 mg of MP or placebo was administered p.o. The participant was then positioned in the scanner. Earplugs were used to minimize scanner noise and padding was used to minimize head motion. A T1 weighted dual-echo image was collected for attenuation correction using an ultrashort-TE (UTE) sequence (1923 (link) matrix, 1.56 mm isotropic resolution, TR = 11.94 ms, TE = 0.07 and 2.46 ms), and T1-weighted 3D magnetization-prepared gradient-echo (MPRAGE; TR/TI/TE = 2200/1000/4.25 ms; FA = 9°, 1 mm isotropic resolution) was used to map brain structure. List mode PET emission data were acquired continuously for 90 min and initiated immediately after a manual bolus injection of [11C]raclopride (dose = 15.7 ± 1.9 mCi; duration 5–10 s). Thirty minutes after tracer injection, either 0.25 mg/kg MP or placebo were manually injected i.v. as a ~30-s bolus. The participants were instructed to remain as still as possible and to relax and keep their eyes open during scanning.
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Publication 2023
Brain Catheters Earplugs ECHO protocol Eye Head Patient Monitoring Pharmaceutical Preparations Placebos Pressure, Diastolic Raclopride Rate, Heart Systole Veins
The analyses were performed using the participants randomized by computer to an intervention and an active control group of the PHIBRA study (n = 30 per group), a 6-month aerobic exercise intervention [33 (link)]. One participant from the active control group dropped out before the follow-up, and one did not have a T1-weighted image from MRI. Thus, the effective sample was 30 for the aerobic exercise intervention group, and 28 for the active control group. Between test sessions, individuals assigned to the aerobic group engaged in walking, jogging, cycling, or using cross-trainers to improve aerobic capacity, whereas the active control group performed stretching and toning to improve muscle strength, flexibility, and balance. The training was completed three times a week in separate group sessions, with individualized instruction aimed at maximizing VO2 improvements. Notably, both groups increased significantly in aerobic fitness over the study period [33 (link)], and were comparable for lesions volume and various cardiovascular risk factors (Supplementary Table 1). In the present work, the whole sample (regardless of intervention type) was divided according to lesion severity grade (see descriptives in Table 1). Participants underwent brain imaging with MRI, and PET/CT scans with 11C-raclopride, at two occasions separated by approximately 7 months. Exclusion criteria included engagement in regular physical activity, neurological and psychiatric disorders, previous head trauma, diabetes, and medications that can affect brain and cognitive functioning. Further exclusion criteria consisted of a Mini Mental State Examination (MMSE) score <27; and MRI-incompatible factors. All structural MRI images were screened for structural abnormalities by a neuroradiologist.

Descriptives for mild- and moderate-to-high lesion severity groups, as dichotomized by grades 0–1 and 2–3 according to the Fazekas lesion grading scale.

Mild lesion severity (Fazekas grade 0 or 1)Moderate- to-high lesions severity (Fazekas grade 2 or 3)
N3523
Aerobic intervention vs. control group (%)63% vs. 37%35% vs. 65%*
Age68.9 ± 2.568.7 ± 3.2
Sex46% men44% men
Education14.3 ± 3.812.6 ± 4.5
MMSE29.1 ± 1.029.3 ± 0.9
Total lesion volume (ml)1.5 ± 1.57.1 ± 5.3*
CVD risk profiles (%)23.0 ± 9.722.3 ± 9.9
Systolic blood pressure143.8 ± 20.2148.9 ± 13.6
Diastolic blood pressure81.0 ± 9.285.9 ± 7.2*
BMI26.3 ± 3.526.4 ± 3.2
Fat (%)36.7 ± 6.937.3 ± 8.3
VO2 peak21.4 ± 3.619.6 ± 4.0
VO2 peak change5.2 ± 3.95.2 ± 3.3

Significant group differences (p < 0.05) are shown with an asterisk.

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Publication 2023
BLOOD Brain Congenital Abnormality Craniocerebral Trauma Diabetes Mellitus Exercise, Aerobic Mental Disorders Mini Mental State Examination Muscle Strength Pharmaceutical Preparations Raclopride Radionuclide Imaging Scan, CT PET

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Raclopride is a selective dopamine D2 receptor antagonist used in research applications. It is commonly utilized in various scientific studies, including neuroimaging and pharmacological investigations.
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SCH23390 is a laboratory reagent used for scientific research. It is a specific antagonist of the D1 dopamine receptor, and is commonly used as a tool compound in neuroscience and biochemistry studies. The core function of SCH23390 is to selectively bind to and block the activity of the D1 dopamine receptor in in vitro and in vivo experimental settings.
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Raclopride is a selective dopamine D2 receptor antagonist. It is commonly used as a research tool in neuroscience studies.
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[3H]-raclopride is a radioligand used for the in vitro and in vivo quantification of dopamine D2 receptors. It has a high affinity and selectivity for the dopamine D2 receptor.
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(+)-Butaclamol is a synthetic chemical compound used as a laboratory tool. It serves as a dopamine receptor antagonist, which means it can bind to and block the activity of dopamine receptors in experimental settings. The core function of (+)-butaclamol is to facilitate the study of dopamine receptor-related processes in research environments.
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R(+)-SCH-23390 hydrochloride is a chemical compound that functions as a selective dopamine D1 receptor antagonist. It is commonly used as a research tool in pharmacological studies to investigate the role of dopamine D1 receptors in various biological processes.
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S(−)-raclopride (+)-tartrate salt is a chemical compound used in research applications. It is a selective D2 dopamine receptor antagonist. The product is available in powder form.
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Quinpirole hydrochloride is a chemical compound commonly used in laboratory research. It functions as a dopamine D2 receptor agonist, which means it can activate and stimulate the D2 subtype of dopamine receptors. This compound is often utilized in experimental studies involving the dopaminergic system and its role in various physiological and behavioral processes.
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Raclopride tartrate is a selective dopamine D2 receptor antagonist. It is used as a research tool in neuroscience studies to investigate the role of dopamine receptors in various physiological and behavioral processes.

More about "Raclopride"

Raclopride is a selective and high-affinity dopamine D2 receptor ligand that has been extensively utilized in positron emission tomography (PET) imaging studies to investigate the role of dopamine in various neurological and psychiatric disorders.
This radiolabeled compound, also known as [11C]raclopride, provides a quantitative measure of D2 receptor availability, allowing researchers to elucidate the underlying neurochemical mechanisms involved in conditions such as Parkinson's disease, schizophrenia, and addiction.
In addition to raclopride, other related compounds like SCH23390, [3H]-raclopride, (+)-butaclamol, R(+)-SCH-23390 hydrochloride, S(−)-raclopride (+)-tartrate salt, and Quinpirole hydrochloride have also been employed in dopamine receptor research.
The selection of appropriate experimental protocols is crucial for ensuring the reproducibility and accuracy of these Raclopride-based studies.
PubCompare.ai's innovative AI-driven platform offers a unique solution by helping researchers identify the most effective Raclopride protocols from the vast body of literature, preprints, and patents.
This tool streamlines the research process, optimizing for reproducibility and accuracy, and enhances the outcomes of Raclopride-related investigations.
Experiene the power of AI-driven analysis to elevate your Raclopride studies and advance our understanding of the dopaminergic system.