Unilateral 6-OHDA lesions were performed on 190–305 g rats, as described previously (Magill et al., 2001 (link)). Twenty-five min before the injection of 6-OHDA, all animals received a bolus of desipramine (25 mg/kg, i.p.; Sigma) to minimize the uptake of 6-OHDA by noradrenergic neurons (Schwarting and Huston, 1996a (link)). Anesthesia was induced and maintained with isoflurane (as above). The neurotoxin 6-OHDA (hydrochloride salt; Sigma) was dissolved immediately before use in ice-cold 0.9% w/v NaCl solution containing 0.02% w/v ascorbate to a final concentration of 4 mg/ml. Then 3 μl of 6-OHDA solution was injected into the region adjacent to the medial substantia nigra (4.5 mm posterior and 1.2 mm lateral of bregma, and 7.9 mm ventral to the dura) (Paxinos and Watson, 1986 ). The extent of the dopamine neuron lesion was assessed 14 or 15 d after 6-OHDA injection by challenge with apomorphine (0.05 mg/kg, s.c.; Sigma) (Schwarting and Huston, 1996b (link)). The lesion was considered successful in those animals that made ≥80 net contraversive rotations in 20 min. Note that the emergence of exaggerated β oscillations after 6-OHDA lesions is not dependent on apomorphine (Sharott et al., 2005 (link)). Electrophysiological recordings were performed ipsilateral to 6-OHDA lesions in anesthetized rats 21–45 d after surgery, when pathophysiological changes in the basal ganglia are likely to have leveled out near their maxima (Vila et al., 2000 (link)).
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Desipramine
Desipramine
Desipramine is a tricyclic antidepressant medication commonly used to treat depression and other mood disorders.
It works by inhibiting the reuptake of norepinephrine and serotonin in the brain, which can help alleviate symptoms of depression.
Desipramine may also be used off-label to treat conditions such as neuropathic pain, fibromyalgia, and attention-deficit/hyperactivity disorder (ADHD).
Reasearchers can use PubComapre.ai to optimize their Desipramine studies by locating relevant protocols from literature, preprints, and patents, then using AI-driven comparisons to identify the best protocols and products.
This can improve reproducibility and accuracy in Desipramine research.
It works by inhibiting the reuptake of norepinephrine and serotonin in the brain, which can help alleviate symptoms of depression.
Desipramine may also be used off-label to treat conditions such as neuropathic pain, fibromyalgia, and attention-deficit/hyperactivity disorder (ADHD).
Reasearchers can use PubComapre.ai to optimize their Desipramine studies by locating relevant protocols from literature, preprints, and patents, then using AI-driven comparisons to identify the best protocols and products.
This can improve reproducibility and accuracy in Desipramine research.
Most cited protocols related to «Desipramine»
Anesthesia
Animals
Apomorphine
Basal Ganglia
Cold Temperature
Desipramine
Dopaminergic Neurons
Dura Mater
Isoflurane
Neurotoxins
Noradrenergic Neurons
Normal Saline
Operative Surgical Procedures
Oxidopamine
Rattus
Sodium Chloride
Substantia Nigra
We performed a comprehensive analysis of the collected DNMs (Supplementary Figure S1 ). ANNOVAR (70 (link)) was used to perform comprehensive annotation of the DNMs based on definitions of transcripts from RefSeq, UCSC known Gene, and Ensembl Gene. Based on the functional effects, DNMs were classified into the following different types: (i) LoF variants, including frameshift indels, splicing, stopgain, and stoploss variants, (ii) deleterious missense variants (Dmis), (iii) tolerant missense variants (Tmis), (iv) synonymous variants (Syn), (v) non-frameshift indels (NF) variants and (vi) noncoding variants. The pathogenesis of the missense variants were predicted using ReVe, which was recently developed by our group (71 (link)). Missense variants with a ReVe score higher than 0.7 were considered Dmis. The LoF and Dmis variants were referred to as putative functional (Pfun) variants.
The transmitted and de novo association (TADA) model (72 (link)) was used to calculate the P-value and false discovery rate (FDR) for each gene with Pfun variants in each disorder (Supplementary Table S2 ). The TADA parameters for each disorder, including the background gene-level de novo mutation rate (GDNMR) of each gene, the fraction of risk genes among all human genes (π), the fold-enrichment (λ) and the relative risk (γ) were evaluated. The GDNMR was sourced from a previous study based on the trinucleotide model and several adjusted factors (73 (link)). The fraction of risk genes was evaluated by maximum likelihood estimation based on the number of Pfun DNMs and the number of genes with multiple Pfun DNMs, as described in previous studies (3 (link),4 (link),74 (link)). The fold-enrichment of LoF and Dmis were calculated by comparing the number of normalized LoF and Dmis variants in each case with the control. As previous studies, we normalized the number of LoF and Dmis using the number of de novo synonymous mutations in each case and the control. Finally, we calculated the relative risk of LoF and Dmis using the equation: π(γ − 1) = λ − 1. For some disorders with >500 samples, including ASD, CHD, UDD, ID, EE, SCZ and Tourette Disorder (TD), the parameters of the TADA model were re-evaluated (74 (link)). For other diseases with inadequate sample sizes, we used parameters estimated from all the integrated DNMs. Two strategies were used to prioritize candidate genes. In the first strategy, we performed TADA to calculate the FDR of each gene for each disorder. In the second strategy, we combined DNMs of each gene in all disorders and calculated the FDR. Genes with different FDR levels in either of the two prioritization strategies were classified using the following criteria, respectively: High confidence [0, 0.0001], Strong [0.0001, 0.001], Suggestive [0.001, 0.01], Positive [0.01, 0.05], Possible [0.05, 0.1] and Minor evidence [0.1, 0.2].
The transmitted and de novo association (TADA) model (72 (link)) was used to calculate the P-value and false discovery rate (FDR) for each gene with Pfun variants in each disorder (
Candidate Gene Identification
Desipramine
Frameshift Mutation
Genes
Gilles de la Tourette Syndrome
INDEL Mutation
Missense Mutation
pathogenesis
Silent Mutation
Adult
Anterior segment mesenchymal dysgenesis
Chlorpromazine
Desipramine
Imipramine
International Normalized Ratio
Lipids
Monoxide, Carbon
olipudase alfa
Patients
Pharmaceutical Preparations
Platelet Counts, Blood
Spleen
Therapeutics
Transplant, Organ
Treatment Protocols
The study consisted of 272 patients (66% female, 34% male; mean age: 38±10) with MDD and 264 healthy control individuals (60% female, 40% male; average age: 36±11). MDD was defined as a DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition) diagnosis of current, unipolar major depressive episode and a 21-item Hamilton Depression Rating Scale (HAM-D21) score of ⩾18 with item number 1 (depressed mood) rated ⩾2. All MDD patients were screened for the pharmacogenetic study of antidepressant treatment response as previously described.7 All MDD patients had comprehensive psychiatric and medical assessments in their primary language, on the basis of diagnostic and ratings instruments that had been fully validated in English and in Spanish. Exclusion criteria included active medical illnesses that could be etiologically related to the ongoing depressive episode, current or active suicidal ideation with a plan and strong intent, pregnancy, lactation, current use of medications with significant central nervous system activity, which interfere with electroencephalogram (EEG) activity (for example, benzodiazepines) or any other antidepressant treatment within the 2 weeks before enrollment, illicit drug use and/or alcohol abuse in the last 3 months or current enrollment in psychotherapy. All MDD patients were Mexican-Americans and had at least three grandparents born in Mexico.
All patients had an initial comprehensive psychiatric and medical assessment and, if enrolled in the pharmacogenetic study of antidepressant treatment response, had weekly structured follow-up assessments for 9 weeks. The study consisted of two phases: a 1-week single-blind placebo lead-in phase to minimize the impact of placebo responders followed, if subjects continued to meet the inclusion criteria after phase 1, by random assignment to one of the two treatment groups: fluoxetine 10–40 mg per day or desipramine 50–200 mg per day, administered in a double-blind manner for 8 weeks. Our primary clinical outcome measure was HAM-D21 score and clinical remission on antidepressants was defined as having a final (week 8) HAM-D21 score <8. In addition, the relative response change was also computed as the difference in HAM-D21 score between pre- and post-treatment divided by the pretreatment HAM-D21 score.
Age-, gender- and ethnicity-matched healthy control individuals were recruited from the same Mexican-American community in Los Angeles by the same bilingual clinical research team. Controls for our genomic studies were in general good health but were not screened for medical or psychiatric illness.
All patients had an initial comprehensive psychiatric and medical assessment and, if enrolled in the pharmacogenetic study of antidepressant treatment response, had weekly structured follow-up assessments for 9 weeks. The study consisted of two phases: a 1-week single-blind placebo lead-in phase to minimize the impact of placebo responders followed, if subjects continued to meet the inclusion criteria after phase 1, by random assignment to one of the two treatment groups: fluoxetine 10–40 mg per day or desipramine 50–200 mg per day, administered in a double-blind manner for 8 weeks. Our primary clinical outcome measure was HAM-D21 score and clinical remission on antidepressants was defined as having a final (week 8) HAM-D21 score <8. In addition, the relative response change was also computed as the difference in HAM-D21 score between pre- and post-treatment divided by the pretreatment HAM-D21 score.
Age-, gender- and ethnicity-matched healthy control individuals were recruited from the same Mexican-American community in Los Angeles by the same bilingual clinical research team. Controls for our genomic studies were in general good health but were not screened for medical or psychiatric illness.
Abuse, Alcohol
Antidepressive Agents
Benzodiazepines
Breast Feeding
Central Nervous System
Childbirth
Desipramine
Diagnosis
Electroencephalography
Ethnicity
Fluoxetine
Gender
Genome
Grandparent
Hispanic or Latino
Illicit Drugs
Males
Mental Disorders
Mexican Americans
Mood
Patients
Pharmaceutical Preparations
Pharmacogenomic Analysis
Placebos
Pregnancy
Psychotherapy
Unipolar Depression
Visually Impaired Persons
Woman
To stimulate endogenous release of norepinephrine, all rats were infused for 15 min with tyramine (1.26 μmol/min/kg, 217 μl/min/kg, Berg, 2005 (link)). The control group (PBS + tyramine) was injected with PBS 10 min prior to the tyramine-infusion. To identify responses caused by the tyramine-induced reverse transport through NET, rats were injected i.p. with the NET inhibitor desipramine hydrochloride (44 μmol/kg) 5 h prior to the experiment (Miralles et al., 2002 (link); Berg et al., 2012 (link)), and pre-treated with PBS 10 min before tyramine during the experiment (desipramine + PBS + tyramine). To test if the tyramine-evoked rise in BP elicited baroreceptor activation and reflex vagal inhibition of HR, another group was pre-treated with the muscarinic receptor antagonist atropine sulfate (2.9 μmol, Berg, 2002 (link)) 20 min before tyramine (atropine + tyramine). To analyze the influence of α2AR, rats were pre-treated with the non-selective α2AR antagonist L-659,066, which does not penetrate the blood-brain barrier (Clineschmidt et al., 1988 (link); 4.4 μmol/kg, 10 min before tyramine, Berg et al., 2012 (link); L-659,066 + tyramine), or with the non-selective, α2AR-agonist clonidine, which easily penetrates the blood-brain barrier (151 nmol/kg, 15 min prior to tyramine, Berg et al., 2012 (link)). Clonidine was injected 10 min after a sham-injection with PBS (PBS + clonidine + tyramine) or L-659,066 as above (L-659,066 + clonidine + tyramine) to differentiate between involvement of CNS and peripheral α2AR. In a time-control group, the rats were pre-treated with PBS and subsequently infused with PBS instead of tyramine (PBS + PBS). The number of rats per group is shown in Table 1 .
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Atropine
Blood-Brain Barrier
Clonidine
Desipramine
Hydrochloride, Desipramine
L 659066
Muscarinic Antagonists
Norepinephrine
Pneumogastric Nerve
Pressoreceptors
Psychological Inhibition
Rattus norvegicus
Reflex
Sulfate, Atropine
Tyramine
Most recents protocols related to «Desipramine»
In both two cohorts, we targeted the variants in the coding region of the DNM1L gene (NM_001278466 ). The variants with a missing rate of >5% and deviations from Hardy–Weinberg equilibrium in controls (p < 0.05) were removed using PLINK v1.90. We annotated the gene regions (hg19 RefSeq), amino acid changes, and allele frequency of each variant in the Genomic Aggregation Database (gnomAD) and Exon Aggregation Consortium (ExAC) by ANNOVAR. Next, the functional impact of each nonsynonymous variant was predicted by ReVe (threshold, 0.7).
We categorized the variants according to the minor allele frequency (MAF) as common variants (MAF > 0.01) and rare variants (MAF < 0.01). Furthermore, we re-extracted the rare variants with MAF below 0.001 and performed gene analysis of rare variants with MAF below 0.01 and 0.001, respectively. According to predicted functions, all the rare nonsynonymous variants were classified into three variant groups: missense, potentially damaging missense (Dmis, ReVe score > 0.7), and loss of function variants (LoF stop gain/loss, frameshift, and splice site), and the sum of Dmis and LoF. After adjusting the abovementioned covariates in two cohorts, sequence kernel association test-optimal (SKAT-O) was applied to each cohort to assess the combined effect of rare variants and each variants group. Fisher's exact test was also done for common variants to validate the significant relationship between the common variants of DNM1L and PD. Moreover, logistic regression analysis based on an allele model was also performed by PLINK v1.90, and a p-value of < 0.05 was considered suggestive significant.
We categorized the variants according to the minor allele frequency (MAF) as common variants (MAF > 0.01) and rare variants (MAF < 0.01). Furthermore, we re-extracted the rare variants with MAF below 0.001 and performed gene analysis of rare variants with MAF below 0.01 and 0.001, respectively. According to predicted functions, all the rare nonsynonymous variants were classified into three variant groups: missense, potentially damaging missense (Dmis, ReVe score > 0.7), and loss of function variants (LoF stop gain/loss, frameshift, and splice site), and the sum of Dmis and LoF. After adjusting the abovementioned covariates in two cohorts, sequence kernel association test-optimal (SKAT-O) was applied to each cohort to assess the combined effect of rare variants and each variants group. Fisher's exact test was also done for common variants to validate the significant relationship between the common variants of DNM1L and PD. Moreover, logistic regression analysis based on an allele model was also performed by PLINK v1.90, and a p-value of < 0.05 was considered suggestive significant.
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Alleles
Amino Acids
Desipramine
DNM1L protein, human
Exons
Frameshift Mutation
Genes
Genetic Diversity
Genome
The SN and cortex of WT mice 4 weeks after saline, DSP-4 or Desipramine + DSP-4 treatments were dissected and snap-frozen in liquid nitrogen. Then, samples were sonicated on ice by probe sonication on setting 3 with a 30% duty cycle in ice-cold 0.1 M PCA containing 0.1 mM EDTA. Samples were centrifuged at 10,000×g for 10 min at 4 °C. Then, supernatants were transferred into fresh 0.22 µM PVDF microcentrifuge filter tubes. NE and serotonin concentrations were determined by reverse-phase high-performance liquid chromatography (HPLC) with electrochemical detection (HPLC-ED). For HPLC, an ESA 5600A CoulArray detection system, equipped with an ESA Model 584 pump and an ESA 542 refrigerated autosampler was used. Separations were performed at 26 °C using an MD-150 × 3.2 mm C18 column. The mobile phase consisted of 1.6 mM 1-octane sulfonic acid sodium, 75 mM NaH2PO4, 0.025% triethylamine, and 8% acetonitrile at pH 3.0. The samples were eluted isocratically at 0.4 mL/min and detected using a 6210 electrochemical cell (ESA, Bedford, MA) equipped with a 5020-guard cell. Guard cell potential was set at 600 mV, while analytical cell potentials were − 175, 150, 350 and 425 mV. The total run time for each run is 40 min. The analytes were identified by the matching criteria of retention time to known standards (Sigma Chemical Co., St. Louis MO). NE and serotonin were quantified by comparing peak areas to those of standards on the dominant sensor. Data were normalized by protein concentration in each brain sample.
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acetonitrile
Brain
Cells
Cold Temperature
Cortex, Cerebral
Desipramine
DSP 4
Edetic Acid
Freezing
High-Performance Liquid Chromatographies
Mus
Nitrogen
octane
polyvinylidene fluoride
Proteins
Retention (Psychology)
Saline Solution
Serotonin
Sodium
Sulfonic Acids
triethylamine
N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSP-4) was prepared in saline solution and injected IP in a single dose of 50 mg/kg (2958; Tocris). This dose was selected based on previous studies showing tissue NE depletion in the brain [19 (link)]. Three days after DSP-4 treatment, stereotaxic injection of 6OHDA or rAAV2–hα-SYN injection was performed as described above. To block the norepinephrine transporter (NET), we use Desipramine (D3900; Sigma). A single dose of Desipramine (25 mg/kg in saline solution) was delivered IP 45 min prior to DSP-4 treatment. Propranolol was delivered IP daily at 10 mg/kg in saline solution (0624; Tocris). Propranolol treatment started 45 min after stereotaxic injection of rAAV2–hα-SYN injection and was given once a day until the end of the experiment. Xamoterol (3 mg/kg; IP) (24,267; Cayman) and Clenbuterol (10 mg/kg; IP) (C5423, Sigma) daily treatment was performed beginning 45 min after stereotaxic injection of rAAV2–hα-SYN injection for 4 weeks until the end of the experiment. All drugs used here were dissolved fresh using saline solution the day of treatment and saline solution was used as vehicle control in all experimental conditions. Clenbuterol and xamoterol doses were selected based on previous studies related to CNS pathologies [16 (link), 20 (link)].
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Brain
Caimans
Cardiac Arrest
Clenbuterol
Desipramine
DSP 4
Pharmaceutical Preparations
Propranolol
Saline Solution
SLC6A2 protein, human
Tissues
Xamoterol
On the day of surgery, 6-hydroxydopamine hydrobromide (6-OHDA; Millipore Sigma #162957, Darmstadt, Germany) and desipramine hydrochloride (Millipore Sigma #D3900) were freshly made and stored on ice away from light. 6-OHDA was prepared at 2 mg/ml in 0.03% ascorbic acid (AA) and desipramine at 4 mg/ml in 0.9% saline. Mice were anesthetized under 4.0% isoflurane at 400 ml/min, and surgical levels of isoflurane (1.5–3.0%) were maintained at approximately 120 ml/min (SomnoSuite, Kent Scientific, Torrington, CT, USA). Desipramine (25 mg/kg) was injected intraperitoneally (IP) to protect norepinephrine terminals against 6-OHDA25 ,26 . An incision was made along midline and bilateral craniotomies drilled above the VTA (AP −3.3, ML +/−1.1). Mice were randomly assigned to four different groups: (1) midbrain vehicle injections treated with dimethyl sulfoxide (DMSO; Vehicle DMSO); (2) VTA dopamine depletion treated with DMSO (6-OHDA DMSO); (3) VTA dopamine depletion treated with terazosin (6-OHDA terazosin); and (4) midbrain vehicle injections treated with terazosin (Vehicle terazosin). The vehicle group received microinjections of 0.5 μl 0.03% AA bilaterally, and the dopamine depletion groups received equal volumes of 6-OHDA prepared in AA (AP −3.3, ML +/−1.1, DV −4.6 at 10° laterally). Vehicle or 6-OHDA was infused over 10 min (0.05 µl/min; Legato 130 Syringe Pump, kd Scientific, Holliston, MA , USA), with a 5-minute wait period before removing the needle. After the incision was closed, mice were moved to a clean cage with ad lib access to food and either DMSO- or terazosin-treated water (described below). All mice recovered for one week before transitioning back to the interval timing switch task for approximately 3–4 weeks of post-surgical behavioral training.
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Ascorbic Acid
Craniotomy
Desipramine
Dopamine
Food
Hydrochloride, Desipramine
Isoflurane
Light
Mesencephalon
Mice, House
Microinjections
Needles
Norepinephrine
Normal Saline
Operative Surgical Procedures
Oxidopamine
Oxidopamine Hydrobromide
Sulfoxide, Dimethyl
Surgery, Day
Syringes
Terazosin
The unilateral 6-OHDA lesions of the MFB in rats were carried out as previously described (Carvalho et al., 2013 (link)). Rats were anesthetized with sodium pentobarbital (40 mg/kg, i.p.) followed by the injection of desipramine (25 mg/kg, i.p.) to protect noradrenergic neurons. Then the rats were placed on a stereotaxic frame (SN-2N; Narishige, Tokyo, Japan) and 6-OHDA (12 μg/4 μl) was injected into the left MFB (AP –4.4 mm, ML –1.2 mm, DV –7.8 mm; Paxinos and Watson, 1998 ). After the injection, the glass pipette was left in place for 5 min to allow diffusion. Two weeks later, rats were subcutaneously injected with apomorphine (0.05 mg/kg, s.c.) to verify the effectiveness of 6-OHDA lesion (Wang et al., 2009 (link)) and those showing more than 20 contralateral turns per 5 min were selected for further experiments. All rats used in the following experiments turned consistently toward right of >30 turns per 5 min.
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Apomorphine
Desipramine
Diffusion
Noradrenergic Neurons
Oxidopamine
Pentobarbital Sodium
Rattus
Reading Frames
Top products related to «Desipramine»
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Desipramine is a chemical compound used in laboratory settings. It is a tricyclic antidepressant drug that can be utilized for various research and testing purposes. The core function of Desipramine is to serve as a reference standard or a research tool in analytical and pharmacological studies.
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6-OHDA is a chemical compound used as a laboratory tool in neuroscience research. It has the molecular formula C₈H₁₁NO₂. 6-OHDA is primarily employed as a neurotoxin to induce selective degeneration of dopaminergic and noradrenergic neurons in animal models, enabling the study of Parkinson's disease and related neurological disorders.
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Fluoxetine is a chemical compound used in laboratory settings. It is a selective serotonin reuptake inhibitor (SSRI) that affects the neurotransmitter serotonin in the brain. Fluoxetine is commonly used in research applications, but its specific core function is to modulate serotonin levels.
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Desipramine hydrochloride is a chemical compound used in laboratory settings. It is a crystalline solid that is soluble in water and organic solvents. The primary function of desipramine hydrochloride is as a reagent for various analytical and research applications, but a detailed description of its specific intended uses is not available.
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Pargyline is a monoamine oxidase inhibitor (MAOI) that is used as a laboratory reagent. It acts by inhibiting the enzyme monoamine oxidase, which is involved in the metabolism of neurotransmitters such as serotonin, norepinephrine, and dopamine.
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Imipramine is a pharmaceutical product manufactured by Merck Group for use in laboratory settings. It is a tricyclic antidepressant medication that affects the balance of certain natural substances in the brain. The core function of Imipramine is to serve as a research tool for studying the mechanisms and effects of tricyclic antidepressants in controlled laboratory environments.
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Apomorphine is a laboratory equipment product manufactured by Merck Group. It is a chemical compound used in various research and analytical applications. Apomorphine serves as a core function in specific laboratory procedures and experiments.
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The SpectraMax M3 is a multimode microplate reader that can measure absorbance, fluorescence, and luminescence. It is designed to provide accurate and reliable data for a variety of assays in life science research and drug discovery applications.
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Benserazide hydrochloride is a chemical compound used as a laboratory reagent. It is a white, crystalline powder that is soluble in water. Benserazide hydrochloride is primarily used as an analytical standard and in research applications.
Sourced in United States
6-OHDA hydrochloride is a laboratory chemical used for research purposes. It is a potent neurotoxin that selectively damages dopaminergic and noradrenergic neurons. The compound is commonly used in experimental models to induce Parkinson's-like symptoms in animals.
More about "Desipramine"
Desipramine is a tricyclic antidepressant medication commonly used to treat depression and other mood disorders.
It works by inhibiting the reuptake of norepinephrine and serotonin in the brain, which can help alleviate symptoms of depression.
Desipramine hydrochloride is the salt form of desipramine and may be used interchangeably.
Desipramine may also be used off-label to treat other conditions such as neuropathic pain, fibromyalgia, and attention-deficit/hyperactivity disorder (ADHD).
Researchers can use PubCompare.ai to optimize their desipramine studies by locating relevant protocols from literature, preprints, and patents, then using AI-driven comparisons to identify the best protocols and products.
This can improve reproducibility and accuracy in desipramine research.
In addition to desipramine, other related compounds like 6-OHDA (6-hydroxydopamine), fluoxetine, pargyline, imipramine, and apomorphine may also be of interest for depression, Parkinson's disease, and other neurological conditions.
Analytical tools like SpectraMax M3 can be used to study the effects of these compounds.
Benserazide hydrochloride is another compound that may be used in combination with desipramine or other medications.
Researchers can utilize PubCompare.ai to find the best protocols and optimize their studies on desipramine and related compounds, improving the reproducibility and accuracy of their findings.
It works by inhibiting the reuptake of norepinephrine and serotonin in the brain, which can help alleviate symptoms of depression.
Desipramine hydrochloride is the salt form of desipramine and may be used interchangeably.
Desipramine may also be used off-label to treat other conditions such as neuropathic pain, fibromyalgia, and attention-deficit/hyperactivity disorder (ADHD).
Researchers can use PubCompare.ai to optimize their desipramine studies by locating relevant protocols from literature, preprints, and patents, then using AI-driven comparisons to identify the best protocols and products.
This can improve reproducibility and accuracy in desipramine research.
In addition to desipramine, other related compounds like 6-OHDA (6-hydroxydopamine), fluoxetine, pargyline, imipramine, and apomorphine may also be of interest for depression, Parkinson's disease, and other neurological conditions.
Analytical tools like SpectraMax M3 can be used to study the effects of these compounds.
Benserazide hydrochloride is another compound that may be used in combination with desipramine or other medications.
Researchers can utilize PubCompare.ai to find the best protocols and optimize their studies on desipramine and related compounds, improving the reproducibility and accuracy of their findings.