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Benserazide

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Benserazide is a pharmaceutical compound used as a component in the treatment of Parkinson's disease. It acts as a decarboxylase inhibitor, which helps to maintain higher levels of levodopa, the primary drug used to treat Parkinson's symptoms. Benserazide is typically administered in combination with levodopa.

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Lab products found in correlation

L dopa, by Merck Group (25 mentions) L dopa methyl ester, by Merck Group (7 mentions) 6 ohda, by Merck Group (5 mentions) Levodopa, by Merck Group (5 mentions) Carbidopa, by Merck Group (3 mentions) Riluzole, by Merck Group (3 mentions) Skf81297, by Bio-Techne (3 mentions) Ascorbic acid, by Merck Group (2 mentions) Desipramine, by Merck Group (2 mentions) L dopa methyl ester hydrochloride, by Merck Group (2 mentions) L dopa benserazide, by Merck Group (2 mentions) Apomorphine, by Merck Group (2 mentions) Haloperidol, by Merck Group (2 mentions) Desipramine hydrochloride, by Merck Group (2 mentions) Guanfacine hydrochloride, by Merck Group (2 mentions) Tamoxifen, by Merck Group (2 mentions) 6 hydroxydopamine, by Merck Group (2 mentions) Pargyline, by Merck Group (2 mentions) Sigma d1507, by Merck Group (2 mentions) Ethovision 3, by Noldus (1 mentions)

64 protocols using benserazide

1

Pharmacological Modulation of L-Dopa

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L-Dopa and benserazide were purchased from Sigma-Aldrich (Spain), and MTEP was purchased from Abcam (UK). All drugs were freshly prepared in 0.9% saline before use. L-Dopa (Sigma-Aldrich) plus benserazide (Sigma-Aldrich) was administrated once daily. MTEP (3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]-pyridine, Abcam, UK) preceded the L-Dopa cocktail 20 minutes earlier once daily for 2 weeks.
Lin J.Y., Liu Z.G., Xie C.L., Song L, & Yan A.J. (2017). Antidyskinetic Treatment with MTEP Affects Multiple Molecular Pathways in the Parkinsonian Striatum. Parkinson's Disease, 2017, 5798734.
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2

Chronic L-DOPA Treatment Protocols

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l-DOPA (Sigma Aldrich, Milan, Italy) was injected accordingly to the following protocols: (1) daily injection of 3 (day 1–3), 6 (day 4–6) or 12 (day 7–9) mg/kg in combination with benserazide (Sigma-Aldrich) (12 mg/kg) in the 9 days protocol; (2) twice a week 12 mg/kg with 12 mg/kg benserazide in the maintenance protocol of 4 and 7 weeks and in the reversal protocol of 4 weeks (experimental design 1, 4, and 5, respectively). Mice not treated with l-DOPA received an equivalent volume of Saline. Both drugs were injected i.p. in a total volume of 10 mL/kg body weight.
Behavioral analysis, in vivo microdialysis and postmortem examination were performed as described in refs 28 (link),33 (link)–36 (link).
Bido S., Solari N., Indrigo M., D’Antoni A., Brambilla R., Morari M, & Fasano S. (2015). Differential involvement of Ras-GRF1 and Ras-GRF2 in L-DOPA-induced dyskinesia. Annals of Clinical and Translational Neurology, 2(6), 662-678.
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3

Investigating Depressive-like Behavior and NE Levels after 6-OHDA-induced LC Neuronal Loss

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To determine if the depressive-like behavior observed 3 weeks after LC neuronal loss induced by 6-OHDA (5 μg/μl) was due to reduced NE concentrations, L- 1-3-4-dihydroxyphenylalanine (DOPA) (3 mg/kg, sc) + benserazide (15 mg/kg, sc) (Sigma-Aldrich, St. Louis, MO) or L-threo-3,4-dihydroxyphenylserine (DOPS) (500 mg/kg, sc) + benserazide (0.25 mg/kg, sc) were administered to animals approximately 6 hr before the FST (Figure 1C). Control animals for the L-DOPA or DOPS group received the appropriate dose of benserazide alone. L-DOPA is the precursor to NE (and DA) and is considered the gold standard of treatment for Parkinson’s disease (Cotzias et al., 1969 (link)). DOPS is converted to NE by aromatic L-amino acid decarboxylase, which is present in all biogenic amine neurons. The doses of L-DOPA + benserazide and DOPS + benserazide, and time of exposure were chosen based on previously published work (Thomas et al., 1998 (link); Francardo et al., 2011 (link)). As described above, the animals were killed after the FST, the brains were removed and the hippocampus (HP; bilaterally), frontal cortex (FC) and the hindbrain portion containing the LC region were dissected free, and the degree of LC neuronal loss was determined by TH-IH. Catecholamine concentrations were determined in the HP and FC.
Szot P., Franklin A., Miguelez C., Wang Y., Vidaurrazaga I., Ugedo L., Sikkema C., Wilkinson C.W, & Raskind M.A. (2015). Depressive-like behavior observed with a minimal loss of locus coeruleus (LC) neurons following administration of 6-hydroxydopamine is associated with electrophysiological changes and reversed with precursors of norepinephrine. Neuropharmacology, 101, 76-86.
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4

Assessing Parkinson's-like Motor Deficits in Mice

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The modified constant speed rotarod assay was performed as previously described.29 (link), 36 (link) After a training period when each mouse attained stable baseline levels of performance staying at 15 r.p.m. for 60 s, mice received several trials at 15, 25, 35 and 44 r.p.m. rotation speed with 60-s maximum trial length and 5-min intervals between individual trials. Two maximal values per speed per day were used to calculate the average, which was used for subsequent statistical analyses.
For the open field test, mice were placed individually into an open arena and monitored for 5 min via video camera. The resulting data were analyzed using the image processing system EthoVision 3.0 (Noldus Information Technology, Wageningen, Netherlands) and Any-maze 4.82 (Stoelting Co., Wood Dale, IL, USA). For each sample, the system recorded position, object area and the status of defined events to calculate the traveled distance.
To follow the effects of L-3,4-dihydroxyphenylalanine (l-DOPA) on locomotor performance, 17 weeks post Tam (wpT) injection control and Dicerfl/fl/DATCreERT2 mice were tested in the modified rotarod assay before and immediately after an intraperitoneal injection of 20 mg/kg l-DOPA (Sigma-Aldrich) complemented with 12 mg/kg benserazide (Sigma-Aldrich).
Chmielarz P., Konovalova J., Najam S.S., Alter H., Piepponen T.P., Erfle H., Sonntag K.C., Schütz G., Vinnikov I.A, & Domanskyi A. (2017). Dicer and microRNAs protect adult dopamine neurons. Cell Death & Disease, 8(5), e2813-.
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5

Parkinsonian Rat Model: L-DOPA and Ropinirole

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L-DOPA (L-3,4-dihydroxyphenylalanine methyl ester hydrochloride, Sigma Aldrich AB, Sweden) was always co-administered s.c. with a fixed dose of the peripheral DOPA-decarboxylase inhibitor benserazide (benserazide hydrochloride, 12 mg/kg; Sigma Aldrich AB, Stockholm, Sweden). Ropinirole (Hello Bio, Bristol, UK) was dissolved separately in saline solution and injected s.c., with or without L-DOPA (see treatment groups at 1.2). The selected doses of L-DOPA (6 mg/kg) and ropinirole (0.5 mg/kg) are commonly used in parkinsonian rat models and have been previously shown to produce an equivalent improvement in forelimb hypokinesia in MFB-lesioned rats [8 (link)]. The combination of L-DOPA 3 mg/kg and ropinirole 0.5 mg/kg has been previously shown to have anti-akinetic and dyskinetic effects similar to L-DOPA 6 mg/kg [8 (link)].
Elabi O.F., Espa E., Skovgård K., Fanni S, & Cenci M.A. (2023). Ropinirole Cotreatment Prevents Perivascular Glial Recruitment in a Rat Model of L-DOPA-Induced Dyskinesia. Cells, 12(14), 1859.
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6

Mouse Model of Parkinson's Disease

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Mice were anesthetized with isoflurane and placed in a stereotaxic apparatus (Kopf Instruments, CA, USA). As previously described (Solís et al., 2017 (link)), the animals received unilateral injections of either 2 × 2 μL of 6-hydroxydopamine hydrobromide (6-OHDA) (20 mmol/L containing .02% ascorbic acid; Sigma-Aldrich, Spain) or saline solution (0.9% NaCl) into the dorsal striatum at the following coordinates: (mm from bregma/dura) anteroposterior, +0.65; lateral, -2.0; and dorsoventral, -4.0 and -3.5. Desipramine (20 mg/kg, i.p.; Sigma-Aldrich, Spain) was injected 30 min before the intrastriatal injections of 6-OHDA to avoid destroying noradrenergic neurons. Two to three weeks after the lesion procedures, mice were treated daily with benserazide (10 mg/kg, i.p.; Sigma-Aldrich, Spain) and l-DOPA (20 mg/kg, i.p.; Sigma-Aldrich, Spain) for 2 wk. benserazide and l-DOPA were freshly prepared before use and injected in a volume of 10 mL/kg.
Solís O., García-Montes J.R., Garcia-Sanz P., Herranz A.S., Asensio M.J., Kang G., Hiroi N, & Moratalla R. (2017). Human COMT over-expression confers a heightened susceptibility to dyskinesia in mice. Neurobiology of disease, 102, 133-139.
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7

Rodent Model of L-DOPA-Induced Dyskinesia

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Approximately 6 weeks after the 6-OHDA lesion, rats in the high-dose 7-d L-DOPA priming group (n=6) were treated daily with L-DOPA (12 mg/kg) + benserazide (15 mg/kg, s.c., Sigma-Aldrich) for 7 d (i.e., during L-DOPA priming) (Fig. 2A–D). Rats in the low-dose 21-d L-DOPA priming group were treated daily with L-DOPA (7 mg/kg, i.p.) + benserazide (14 mg/kg) for 3 weeks, as previously published (Bartlett et al., 2016 (link)) (Fig. 1C). Rats in the 21-d group received maintenance doses of L-DOPA (7 mg/kg + 15 mg/kg benserazide) following the 21-d priming period (two doses per week, every 2–3 days for the remainder of the experiment). L-DOPA-induced AIMs were scored by an experimentally blinded investigator on a scale from 0 to 4, and cumulative limb, axial, and orolingual (LAO) scores for all LID rats across all sessions are presented in Fig. 3B as previously published (Bartlett et al., 2016 (link)). After the 21-d priming period, rats that met behavioral criteria (n=7) proceeded to surgical implantation, and were given maintenance injections of L-DOPA (7 mg/kg) every 2–3 days to maintain stable dyskinesia (Bartlett et al., 2016 (link)). This contrasts with the 7-d priming group that was implanted prior to L-DOPA exposure. Neural recordings began one week following implantation.
Ye T., Bartlett M.J., Sherman S.J., Falk T, & Cowen S.L. (2021). Spectral Signatures of L-DOPA-Induced Dyskinesia Depend on L-DOPA Dose and are Suppressed by Ketamine. Experimental neurology, 340, 113670.
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8

6-OHDA Lesion Preparation and Levodopa Treatment

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6-OHDA (Sigma Aldrich) was prepared at 5 mg/mL in normal saline. Levodopa was prepared (0.5 mg/mL Sigma Aldrich) with benserazide (0.25 mg/mL, Sigma Aldrich) in normal saline and always administered at 5 mg/kg.
Schor J.S., Gonzalez Montalvo I., Spratt P.W., Brakaj R.J., Stansil J.A., Twedell E.L., Bender K.J, & Nelson A.B. (2022). Therapeutic deep brain stimulation disrupts movement-related subthalamic nucleus activity in parkinsonian mice. eLife, 11, e75253.
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9

6-OHDA Neurotoxicology Protocol

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6-Hydroxydopamine hydrobromide (6-OHDA), d-amphetamine sulfate (Amph), L-3,4-dihydroxyphenilalanine methyl ester hydrochloride (L-DOPA), and benserazide were purchased from Sigma-Aldrich. 6-OHDA was freshly prepared in physiological saline solution plus 0.02% ascorbic acid. The other drugs were freshly prepared in physiological saline solution only.
Ingallinesi M., Galet B., Pegon J., Faucon Biguet N., Do Thi A., Millan M.J., Mannoury la Cour C, & Meloni R. (2019). Knock-Down of GPR88 in the Dorsal Striatum Alters the Response of Medium Spiny Neurons to the Loss of Dopamine Input and L-3-4-Dyhydroxyphenylalanine. Frontiers in Pharmacology, 10, 1233.
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10

Cultivation of Escherichia coli Strains

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Escherichia coli DH5a or BL21 were routinely grown aerobically in Luria-Broth (LB) at 37 °C degrees with continuous agitation. Other strains listed in Supplementary Table 6 were grown anaerobically (10% H2, 10% CO2, 80% N2) in a Don Whitley Scientific DG250 Workstation (LA Biosystems, Waalwijk, The Netherlands) at 37 °C in an enriched beef broth based on SHIME medium37 (link) (Supplementary Table 7). Bacteria were inoculated from −80 °C stocks and grown overnight. Before the experiment, cultures were diluted 1:100 in fresh medium from overnight cultures. Levodopa (D9628, Sigma, The Netherlands), carbidopa (C1335, Sigma), benserazide (B7283, Sigma), or methyldopa (857416, Sigma) were supplemented during the lag or stationary phase depending on the experiment. Growth was followed by measuring the optical density (OD) at 600 nM in a spectrophotometer (UV1600PC, VWR International, Leuven, Belgium).
van Kessel S.P., Frye A.K., El-Gendy A.O., Castejon M., Keshavarzian A., van Dijk G, & El Aidy S. (2019). Gut bacterial tyrosine decarboxylases restrict levels of levodopa in the treatment of Parkinson’s disease. Nature Communications, 10, 310.
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