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Cholinergic Receptors
Cholinergic Receptors
Cholinergic Receptors are a class of receptors that bind and respond to the neurotransmitter acetylcholine.
These receptors are found throughout the body and play a crucial role in a variety of physiological processes, including muscle contraction, autonomic nervous system function, and cognitive processes.
Cholinergic Receptors can be divided into two main subtypes: muscarinic and nicotinic, each with distinct pharmacological and functional properties.
Understanidng the complex biology of Cholinergic Receptors is essential for the development of new therapies targeting conditions such as Alzheimer's disease, myasthenia gravis, and other neurological and muscular disorders.
Explore the latest research on Cholinergic Receptors with PubCompare.ai's cutting-edg data-driven tools and enhance the reprocibility and accuracy of your studies.
These receptors are found throughout the body and play a crucial role in a variety of physiological processes, including muscle contraction, autonomic nervous system function, and cognitive processes.
Cholinergic Receptors can be divided into two main subtypes: muscarinic and nicotinic, each with distinct pharmacological and functional properties.
Understanidng the complex biology of Cholinergic Receptors is essential for the development of new therapies targeting conditions such as Alzheimer's disease, myasthenia gravis, and other neurological and muscular disorders.
Explore the latest research on Cholinergic Receptors with PubCompare.ai's cutting-edg data-driven tools and enhance the reprocibility and accuracy of your studies.
Most cited protocols related to «Cholinergic Receptors»
Antibodies
Argon
Axon
Cholinergic Receptors
Cross Reactions
Denervation
Dental Plaque
Dyes
Fluorescence
Forceps
Helium Neon Gas Lasers
IgG1
Immunoglobulins
Laser Scanning Microscopy
Light
Mice, House
Microscopy
Muscle Tissue
Nerve Endings
Nerve Tissue
Neurofilaments
Neuromuscular Junction
Submersion
Synapses
Synaptic Vesicles
Synaptophysin
tetramethylrhodamine
Triton X-100
Z 300
Cells were incubated in presence of the M2 selective agonist arecaidine (final concentration 10 and 100 μM) 25 (link) for different times of treatment (24, 48, 72 and 96 hrs). Arecaidine is an alkaloid extracted from areca nut. It displays several different pharmacological effects (e.g. digestant and vermifuge) 30 . The alkaloids of the areca nut bind cholinergic receptors and in particular arecaidine has been demonstrated to have specific agonist property for M2 muscarinic receptor 31 (link). To confirm the involvement of M2 receptor subtype in our experiments, several muscarinic antagonists were used such as: gallamine (M2 antagonist; final concentration 10−6 M), pirenzepine (M1 antagonist; final concentration 10−6 M), 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4-DAMP) (M3 antagonist; final concentration 10−8 M). The concentrations used were comparable with the values of inhibition constant (Ki) reported for rat OLs 5 (link), 6 .
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4-diphenylacetoxy-1,1-dimethylpiperidinium
Alkaloids
Anthelmintics
Areca catechu
arecaidine
Cells
Cholinergic Receptors
Digestants
Gallamine
Iodides
Muscarinic Antagonists
Pirenzepine
Plant Alkaloids
Psychological Inhibition
Receptor, Muscarinic M2
Actins
calponin
Cells
Cholinergic Receptors
Culture Media
Ethics Committees
Fetal Bovine Serum
Fetus
Gestational Age
Homo sapiens
Lung
Myocytes, Smooth Muscle
Phenols
Phenotype
Smooth Muscles
Tissues
The following autoantibodies were tested: anti-thyroid, anti-parietal cell, anti-gliadin, intrinsic factor blocking antibody, anti-islet cell, ANA, anti-cardiolipin, anti-RNP, anti-SSA/SSB, anti-SM, anti-striated, anti-smooth muscle, anti-microsomal, anti-mitochondrial, anti-acetylcholine receptor, anti-GM1, hepatitis B/C, HIV, HTLV-I and CMV. Immunoglobulin and complement levels were also tested.
Anti-GAD antibodies were initially tested in all patients and serially thereafter, in the 32 patients enrolled in the longitudinal protocol, by radioimmunoassay (RIA) using a commercial kit (Kronus, ID). Lumbar puncture was performed in 48 patients but CSF could not be obtained from 5 due to severe lumbar stiffness. CSF was examined for GAD antibodies, total immunoglobulins, oligoclonal bands, IgG index and intrathecal GAD-specific IgG synthesis, as previously described [6 (link), 25 (link), 26 (link)]. Anti-GAD antibodies were also measured in serial CSF’s (first and 2-year visits) in 10 patients by ELISA (Euroimmune, Lubeck). In 50 patients, sera were also tested for anti-glycine receptor and anti-GABAA antibodies using in-house cell-based immunofluorescent assays on live cells (cDNA clones kindly provided by Prof. A. Vincent, Oxford and Prof. J. Dalmau, Barcelona), as described [27 ].
Anti-GAD antibodies were initially tested in all patients and serially thereafter, in the 32 patients enrolled in the longitudinal protocol, by radioimmunoassay (RIA) using a commercial kit (Kronus, ID). Lumbar puncture was performed in 48 patients but CSF could not be obtained from 5 due to severe lumbar stiffness. CSF was examined for GAD antibodies, total immunoglobulins, oligoclonal bands, IgG index and intrathecal GAD-specific IgG synthesis, as previously described [6 (link), 25 (link), 26 (link)]. Anti-GAD antibodies were also measured in serial CSF’s (first and 2-year visits) in 10 patients by ELISA (Euroimmune, Lubeck). In 50 patients, sera were also tested for anti-glycine receptor and anti-GABAA antibodies using in-house cell-based immunofluorescent assays on live cells (cDNA clones kindly provided by Prof. A. Vincent, Oxford and Prof. J. Dalmau, Barcelona), as described [27 ].
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Anabolism
Anti-Antibodies
Antibodies
Antibodies, Blocking
Autoantibodies
Cardiolipins
Cells
Cholinergic Receptors
Clone Cells
DNA, Complementary
Enzyme-Linked Immunosorbent Assay
Gliadin
Glycine Receptors
Hepatitis C virus
Human T-lymphotropic virus 1
Immunofluorescence
Immunoglobulins
Immunoglobulins, Oligoclonal
Intrinsic Factor
Islets of Langerhans
Lumbar Region
Microsomes
Mitochondria
Muscle, Striated
Parietal Cells, Gastric
Patients
Punctures, Lumbar
Serum
Thyroid Gland
Acetylcholine
Blood-Brain Barrier
Cholinergic Receptors
exo-2-(2'-fluoro-5'-pyridinyl)-7-azabicyclo(2.2.1)heptane
Glycopyrrolate
Gray Matter
Hypersensitivity
Muscarinic Antagonists
Nausea
Pharmaceutical Preparations
Physostigmine
Plasma
Positron-Emission Tomography
Radionuclide Imaging
Most recents protocols related to «Cholinergic Receptors»
The administration of scopolamine, an antagonist of muscarinic acetylcholine receptors, causes a temporary blockade of receptors, impaired cognitive functions and cerebral metabolism, which is considered to be a reliable model of AD (Buccafusco, 2009 ). Scopolamine aqueous solution was prepared by dissolving weighed sample in water for injection. A solution of scopolamine was injected intraperitoneally at a dose of 1.5 mg/kg/5 mL once 30 min before testing of the passive avoidancereflex (only on the first day - the day of training).
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Cholinergic Receptors
Cognition
Metabolism
Muscarinic Antagonists
Scopolamine
The administration of scopolamine, an antagonist of muscarinic acetylcholine receptors, causes a temporary blockade of these receptors that impaired cognitive functions (Buccafusco, 2009 ).
For 8 days, animals received oraly latrepirdine polymorphs according to group affiliation (Table 3 ). Polymorph preparations of latrepirdine at a dose of 10 mg/kg were administered to experimental animal groups (groups 3–8) once a day for 7 days. The groups 1 and 2 were administered once a day with an equivalent amount of corn oil.
To study cognitive-enhancing nootropic effect of the polymorphs the passive avoidance (PA) test was performed as described by Burwell et al. (Burwell et al., 2004 (link)). The PA apparatus (Neurobotics, Moscow, Russia) consisting of two compartments (light and dark chambers) separated by sliding guillotine door was used. PA consisted of an acquisition trial on the first (training) day and a retention trial 24 h later. On the seventh day of corn oil or the test polymorph administration, the animals were placed for 5 min in the PA unit to familiarize themselves with the space in order to avoid the stress caused by the new environment. The next day (eighth day) the training phase of PA test was started. 60 min before the start of training, corn oil or the test polymorph was administered, as per the group design. The experimental groups (2–8) were injected intraperitoneally with scopolamine at a dose of 1.5 mg/kg 30 min before training. During the training phase of PA test each rat was placed in the lighted chamber. After 10 s, the door was opened, and latency to enter the dark chamber was recorded. An animal was considered to have entered the dark chamber when all fours paws were beyond the guillotine door. After entry, the door was closed. After 2 s had elapsed, a foot shock stimulus was delivered. The shock level and duration were set at 1 mA for 2 s. The rat was immediately removed back to its home cage. Twenty-4 hours later (ninth day), a retention test consisted of placing the rat back into the lighted chamber, waiting 10 s, opening the door, and the latent period (LP) of the first entry into the dark chamber was recorded. If a rat did not enter the chamber in 180 s, the trial was terminated, and the rat was removed to the home cage.
The most effective polymorph was determined.
For 8 days, animals received oraly latrepirdine polymorphs according to group affiliation (
To study cognitive-enhancing nootropic effect of the polymorphs the passive avoidance (PA) test was performed as described by Burwell et al. (Burwell et al., 2004 (link)). The PA apparatus (Neurobotics, Moscow, Russia) consisting of two compartments (light and dark chambers) separated by sliding guillotine door was used. PA consisted of an acquisition trial on the first (training) day and a retention trial 24 h later. On the seventh day of corn oil or the test polymorph administration, the animals were placed for 5 min in the PA unit to familiarize themselves with the space in order to avoid the stress caused by the new environment. The next day (eighth day) the training phase of PA test was started. 60 min before the start of training, corn oil or the test polymorph was administered, as per the group design. The experimental groups (2–8) were injected intraperitoneally with scopolamine at a dose of 1.5 mg/kg 30 min before training. During the training phase of PA test each rat was placed in the lighted chamber. After 10 s, the door was opened, and latency to enter the dark chamber was recorded. An animal was considered to have entered the dark chamber when all fours paws were beyond the guillotine door. After entry, the door was closed. After 2 s had elapsed, a foot shock stimulus was delivered. The shock level and duration were set at 1 mA for 2 s. The rat was immediately removed back to its home cage. Twenty-4 hours later (ninth day), a retention test consisted of placing the rat back into the lighted chamber, waiting 10 s, opening the door, and the latent period (LP) of the first entry into the dark chamber was recorded. If a rat did not enter the chamber in 180 s, the trial was terminated, and the rat was removed to the home cage.
The most effective polymorph was determined.
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Animals
Animals, Laboratory
Cholinergic Receptors
Cognition
Corn oil
Foot
latrepirdine
Muscarinic Antagonists
Neutrophil
Nootropic Agents
Retention (Psychology)
Scopolamine
Shock
Whole-mount preparations were postfixed in 4% PFA following perfusion of each mouse. Anti–neurofilament heavy chain (anti–NF-H) (1:2,000, AB5539, MilliporeSigma) and anti–synaptic vesicle 2 (anti-SV2) (1:200, YE269, Life Technologies) primary antibodies, followed by donkey anti–chicken Alexa Fluor 488 (1:400, 703-545-155, Jackson ImmunoResearch) and goat anti–rabbit Alexa Fluor 488 (1:200, 111-545-003, Jackson ImmunoResearch) secondary antibodies, were used to label the axon and synaptic terminal. Acetylcholine receptors were labeled with Alexa Fluor 594–conjugated α-bungarotoxin (1:200, B13423, Life Technologies). Representative images were obtained using a laser scanning confocal microscope at 40× magnification (Leica TCS SP8, Leica Microsystems Inc). NMJ analyses was performed in a blinded manner on at least 3 randomly selected fields of view per muscle at 40× magnification. Images were analyzed based on the end plate overlap with the synaptic terminal. End plates with missing overlapping terminal were considered fully denervated, end plates with partial overlap were considered partially denervated, and end plates with complete overlap were considered fully innervated.
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Alexa594
alexa fluor 488
alpha-Bungarotoxin
Antibodies
Axon
Chickens
Cholinergic Receptors
Equus asinus
Goat
Microscopy, Confocal
Mus
Muscle Tissue
Neurofilaments
Perfusion
Presynaptic Terminals
Rabbits
Synaptic Vesicles
We assessed axon extension after acute injury and the formation of neuromuscular junctions (NMJ) at 8 weeks in Thy1-GFP rats. Rats were anesthetized with 5% isoflurane, and maintained under anesthesia with 1–2% isoflurane. Analgesia was provided by Meloxicam (2 mg/kg) pre-operatively and 24 h post-operatively. The sciatic nerve was exposed and a 10-mm silicone conduit placed between the transected nerve ends and sutured with single 10/0 sutures to create an 8 mm defect. The conduits were either filled with 0.7% agarose hydrogel, or three different concentrations of rat-specific IL10 (1 µg/mL, 3 µg/mL, 7 µg/mL, recombinant rat IL10, Peprotech, part #400-19) with 0.7% agarose as a carrier. The muscle and skin were re-apposed using 6-0 Ethilon sutures. Body temperature was maintained by an electrical heating pad placed below rat within the surgical field; body temperature and heating pad temperature were monitored to maintain physiologic body temperature. All surgeons were blinded to treatment groups during surgical procedures and tissue harvests.
To determine axon extension after injury, five groups of animals (IL10 at 1, 3, or 7 µg/mL in 0.7% agarose, unloaded agarose or empty conduit, n = 6–8 animals/group, male and female) were allowed to recover for 21 days. Animals were then anesthetized and euthanized (pentobarbital (250 mg/mL, 4 mL/kg), and the regenerative nerve bridge was harvested. Bridges were placed in a well with PBS and imaged using confocal microscope (Zeiss LSM510 confocal). One spectral window for the emission profile of GFP (488 nm) and the entire extension of the regenerative bridge was imaged using tiled, Z stack images. Axonal outgrowth from the distal stump was quantified by evaluating axonal regenerative profiles extending through contiguous regions of interest (ROI) at 250-µm intervals from the distal end of the proximal stump using BitPlane (Imaris) and calculating GFP + volumes for each ROI. Differences between groups were determined by evaluating GFP + volume and the interaction between dose and contiguous ROI in a mixed-effect model, in the same group of animals.
To determine the effect of exogenous IL10 on neuromuscular junction formation, two groups of animals (n = 8/group) underwent sciatic transection and a silicone conduit repair (10 mm) filled with 3 µg/mL IL10 in 0.7% agarose or agarose only (negative control). Animals were euthanized at 8 weeks NMJ formation in the extensor digitorum longus (EDL) muscle was assessed for terminal axons (green) innervating postsynaptic acetylcholine receptors (AChRs), labeled with rhodamine-ɑ-bungarotoxin (red) conjugated to Alexa Fluor-59454 (link). Briefly, the EDL muscles were harvested bilaterally for whole-mount confocal microscopy. The muscles were dissected into four separate muscle bellies to create thinner samples. The muscles were placed on Pyrex resin-coated dishes and stained with rhodamine alpha-bungarotoxin conjugated to Alexa Fluor-594 (2.5 µg/mL; Thermo Fischer Scientific, CA) at room temperature for 30 min to label the acetylcholine receptors in the postsynaptic membrane. The muscles were rinsed with phosphate-buffered saline and mounted under a coverslip for confocal microscopy. The concentration of alpha-bungarotoxin conjugate was validated using a dose curve in untreated GFP rats. The muscles were imaged using a Zeiss LSM510 confocal microscope. Two spectral windows using the Zeiss Zen image software were used: one using the emission profile of Alexa Fluor-594 (590 nm) and the emission profile of GFP (488 nm). To evaluate the thicker muscle samples, four equidistant z-series (stack) were taken across the muscle sample to acquire images of a minimum of 100 motor end plates. The observer was blinded to the treatment group at the time of acquisition of imaging and during image analysis. The images were used to count the number of innervated and non-innervated motor end plates; innervation was determined by the extension of a GFP-expressing axon to a positively labeled motor end plate. The proportion of innervated NMJ was standardized to each contralateral control.
To determine axon extension after injury, five groups of animals (IL10 at 1, 3, or 7 µg/mL in 0.7% agarose, unloaded agarose or empty conduit, n = 6–8 animals/group, male and female) were allowed to recover for 21 days. Animals were then anesthetized and euthanized (pentobarbital (250 mg/mL, 4 mL/kg), and the regenerative nerve bridge was harvested. Bridges were placed in a well with PBS and imaged using confocal microscope (Zeiss LSM510 confocal). One spectral window for the emission profile of GFP (488 nm) and the entire extension of the regenerative bridge was imaged using tiled, Z stack images. Axonal outgrowth from the distal stump was quantified by evaluating axonal regenerative profiles extending through contiguous regions of interest (ROI) at 250-µm intervals from the distal end of the proximal stump using BitPlane (Imaris) and calculating GFP + volumes for each ROI. Differences between groups were determined by evaluating GFP + volume and the interaction between dose and contiguous ROI in a mixed-effect model, in the same group of animals.
To determine the effect of exogenous IL10 on neuromuscular junction formation, two groups of animals (n = 8/group) underwent sciatic transection and a silicone conduit repair (10 mm) filled with 3 µg/mL IL10 in 0.7% agarose or agarose only (negative control). Animals were euthanized at 8 weeks NMJ formation in the extensor digitorum longus (EDL) muscle was assessed for terminal axons (green) innervating postsynaptic acetylcholine receptors (AChRs), labeled with rhodamine-ɑ-bungarotoxin (red) conjugated to Alexa Fluor-59454 (link). Briefly, the EDL muscles were harvested bilaterally for whole-mount confocal microscopy. The muscles were dissected into four separate muscle bellies to create thinner samples. The muscles were placed on Pyrex resin-coated dishes and stained with rhodamine alpha-bungarotoxin conjugated to Alexa Fluor-594 (2.5 µg/mL; Thermo Fischer Scientific, CA) at room temperature for 30 min to label the acetylcholine receptors in the postsynaptic membrane. The muscles were rinsed with phosphate-buffered saline and mounted under a coverslip for confocal microscopy. The concentration of alpha-bungarotoxin conjugate was validated using a dose curve in untreated GFP rats. The muscles were imaged using a Zeiss LSM510 confocal microscope. Two spectral windows using the Zeiss Zen image software were used: one using the emission profile of Alexa Fluor-594 (590 nm) and the emission profile of GFP (488 nm). To evaluate the thicker muscle samples, four equidistant z-series (stack) were taken across the muscle sample to acquire images of a minimum of 100 motor end plates. The observer was blinded to the treatment group at the time of acquisition of imaging and during image analysis. The images were used to count the number of innervated and non-innervated motor end plates; innervation was determined by the extension of a GFP-expressing axon to a positively labeled motor end plate. The proportion of innervated NMJ was standardized to each contralateral control.
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Alexa594
alpha-Bungarotoxin
Amputation Stumps
Anesthesia
Animals
Axon
Bungarotoxins
Cholinergic Receptors
Electricity
Ethilon
Females
Hyperostosis, Diffuse Idiopathic Skeletal
IL10 protein, human
Injuries
Isoflurane
Males
Management, Pain
Meloxicam
Microscopy, Confocal
Motor Endplate
Muscle Tissue
Nerve Endings
Nervousness
Neuromuscular Junction
Neuronal Outgrowth
Operative Surgical Procedures
PEGDMA Hydrogel
Pentobarbital
Phosphates
physiology
Rattus norvegicus
Regeneration
Resins, Plant
Rhodamine
rhodamine-alpha-bungarotoxin
Saline Solution
Sciatic Nerve
Sepharose
Silicones
Skin
Surgeons
Sutures
Tissue, Membrane
Tissue Harvesting
The primary efficacy end point for this study was the percent of patients achieving a 50% or greater reduction in CS dose at week 39 from baseline (week 0). Secondary efficacy end points measured from baseline (week 0) to week 39 were the percent reduction in CS daily dose and the time to the first episode of MG worsening (as defined above).
Exploratory end points related to CS therapy included the following: percent of patients achieving a ≥75% reduction in CS dose at week 39, percent of patients achieving a CS dose ≤7.5 mg (prednisone equivalent) at week 39, percent of patients CS-free at week 39, change in fasting serum glucose at week 39 vs baseline, percent of patients with fasting glucose ≤125 mg/dL at week 39 vs baseline, and a change in hemoglobin A1c at week 39 compared with baseline (week 0).
Exploratory end points related to MG were as follows: percent of patients experiencing an MC or worsening of MG requiring hospitalization through week 39 and week 39 through week 45, number of episodes of MG worsening from baseline (week 0) to week 39, changes in a 15-item MG-Quality of Life Instrument (MG-QOL 15) at weeks 39, 42, and 45 compared with baseline (week 0), changes in MG-Activities of Daily Living (MG-ADL) score at weeks 39, 42, and 45 from baseline (week 0), and changes from baseline (week 0) in the activity (binding, blocking, and modulating) of anti-acetylcholine receptor antibodies at week 39 (Covance Central Laboratory, Indianapolis, IN). In addition, the change in serum IgG levels from baseline (week 0) was measured at weeks 9, 24, and 39.
The guide for CS taper was the QMG score.17 (link) A 3-point improvement in the QMG score reflects a clinically significant improvement.19 (link) Study patients taking cholinesterase inhibitors were instructed not to take these medications for 12 hours before QMG testing. The MG-QOL 15 is a measure of mobility, symptoms, general contentment, and emotional well-being as assessed by the patient.20 (link)- (link)22 (link) The MG-ADL score is designed to assess the effects of MG on usual daily activities. A 2-point improvement in MG-ADL was designated as clinically significant.23 (link) The MG Composite scale has been recommended by the MGFA as a quantitative measure for patients with generalized MG.24 (link),25 (link) A 3-point improvement in the MG Composite was correlated with clinical improvement and meaningful improvement to patients.26 (link)
Exploratory end points related to CS therapy included the following: percent of patients achieving a ≥75% reduction in CS dose at week 39, percent of patients achieving a CS dose ≤7.5 mg (prednisone equivalent) at week 39, percent of patients CS-free at week 39, change in fasting serum glucose at week 39 vs baseline, percent of patients with fasting glucose ≤125 mg/dL at week 39 vs baseline, and a change in hemoglobin A1c at week 39 compared with baseline (week 0).
Exploratory end points related to MG were as follows: percent of patients experiencing an MC or worsening of MG requiring hospitalization through week 39 and week 39 through week 45, number of episodes of MG worsening from baseline (week 0) to week 39, changes in a 15-item MG-Quality of Life Instrument (MG-QOL 15) at weeks 39, 42, and 45 compared with baseline (week 0), changes in MG-Activities of Daily Living (MG-ADL) score at weeks 39, 42, and 45 from baseline (week 0), and changes from baseline (week 0) in the activity (binding, blocking, and modulating) of anti-acetylcholine receptor antibodies at week 39 (Covance Central Laboratory, Indianapolis, IN). In addition, the change in serum IgG levels from baseline (week 0) was measured at weeks 9, 24, and 39.
The guide for CS taper was the QMG score.17 (link) A 3-point improvement in the QMG score reflects a clinically significant improvement.19 (link) Study patients taking cholinesterase inhibitors were instructed not to take these medications for 12 hours before QMG testing. The MG-QOL 15 is a measure of mobility, symptoms, general contentment, and emotional well-being as assessed by the patient.20 (link)- (link)22 (link) The MG-ADL score is designed to assess the effects of MG on usual daily activities. A 2-point improvement in MG-ADL was designated as clinically significant.23 (link) The MG Composite scale has been recommended by the MGFA as a quantitative measure for patients with generalized MG.24 (link),25 (link) A 3-point improvement in the MG Composite was correlated with clinical improvement and meaningful improvement to patients.26 (link)
Anti-Antibodies
Cholinergic Receptors
Cholinesterase Inhibitors
Drug Tapering
Emotions
Glucose
Hemoglobin A, Glycosylated
Hospitalization
Patients
Pharmaceutical Preparations
Prednisone
Range of Motion, Articular
Serum
Therapeutics
Top products related to «Cholinergic Receptors»
Sourced in United States
The α-BTX is a laboratory instrument designed for the detection and quantification of alpha-bungarotoxin, a neurotoxin commonly used in the study of nicotinic acetylcholine receptors. The core function of the α-BTX is to provide accurate and reliable measurements of this specific molecule in research samples.
Sourced in United States
The Acetylcholine receptor is a type of receptor protein found in the cell membranes of certain tissues, including muscle, nerve, and gland cells. It functions as a binding site for the neurotransmitter acetylcholine, which is involved in the transmission of signals between neurons and target cells.
Sourced in United States
Anti-synaptophysin is an antibody used in immunohistochemistry and western blotting to detect the presence of the synaptophysin protein. Synaptophysin is a marker for synaptic vesicles and is commonly used to identify neurons and neuroendocrine cells in tissue samples.
Sourced in Japan
Alexa Fluor® 594 conjugated α‐bungarotoxin is a fluorescent labeling reagent. It is a conjugate of the Alexa Fluor® 594 dye and the α-bungarotoxin protein, which binds selectively to nicotinic acetylcholine receptors.
The SMI-312R is a lab equipment product that serves as a high-precision spectrophotometer. It is designed to accurately measure the absorption and transmission of light through samples across a wide range of wavelengths.
Sourced in Sweden, United States
The Biacore 3000 is a label-free interaction analysis system that allows real-time monitoring of biomolecular interactions. It is designed to provide quantitative data on affinity, kinetics, and specificity of molecular interactions.
The CMS chip is a lab equipment product from Cytiva. It is designed to enable the controlled manipulation and analysis of cells and cellular samples. The core function of the CMS chip is to provide a microfluidic platform for cell culture, cell separation, and cell-based assays.
The T1175 is a laboratory instrument designed for use in scientific research and analysis. It is a compact and precise device that performs a specific core function.
Sourced in United States, Germany, United Kingdom, Japan, China, Canada, Italy, Australia, France, Switzerland, Spain, Belgium, Denmark, Panama, Poland, Singapore, Austria, Morocco, Netherlands, Sweden, Argentina, India, Finland, Pakistan, Cameroon, New Zealand
DAPI is a fluorescent dye used in microscopy and flow cytometry to stain cell nuclei. It binds strongly to the minor groove of double-stranded DNA, emitting blue fluorescence when excited by ultraviolet light.
More about "Cholinergic Receptors"
Cholinergic receptors, also known as acetylcholine receptors, are a class of receptors that bind and respond to the neurotransmitter acetylcholine.
These receptors are found throughout the body and play a crucial role in a variety of physiological processes, including muscle contraction, autonomic nervous system function, and cognitive processes.
Cholinergic receptors can be divided into two main subtypes: muscarinic and nicotinic, each with distinct pharmacological and functional properties.
Muscarinic cholinergic receptors (mAChRs) are a type of G protein-coupled receptor (GPCR) that are activated by the agonist muscarine, as well as by the endogenous neurotransmitter acetylcholine.
Muscarinic receptors are involved in a wide range of physiological functions, such as the regulation of heart rate, gastrointestinal motility, and bladder contraction.
Nicotinic cholinergic receptors (nAChRs), on the other hand, are ligand-gated ion channels that are activated by the agonist nicotine, as well as by acetylcholine.
Nicotinic receptors are found in the neuromuscular junction, autonomic ganglia, and the central nervous system, where they play a role in the transmission of electrical signals.
Understanding the complex biology of cholinergic receptors is essential for the development of new therapies targeting conditions such as Alzheimer's disease, myasthenia gravis, and other neurological and muscular disorders.
Researchers often utilize tools like α-BTX (α-Bungarotoxin), Alexa Fluor® 594 conjugated α‐bungarotoxin, and SMI-312R to study the localization and function of these receptors.
Additionally, advanced techniques like Biacore 3000 and CMS chip technology can be used to analyze the binding kinetics and affinity of cholinergic receptor ligands, while DAPI (4′,6-diamidino-2-phenylindole) can be used to visualize cell nuclei in immunofluorescence experiments.
The incorporation of these techniques, along with the exploration of related terms like T1175, can enhance the reproducibility and accuracy of studies focused on cholinergic receptors.
These receptors are found throughout the body and play a crucial role in a variety of physiological processes, including muscle contraction, autonomic nervous system function, and cognitive processes.
Cholinergic receptors can be divided into two main subtypes: muscarinic and nicotinic, each with distinct pharmacological and functional properties.
Muscarinic cholinergic receptors (mAChRs) are a type of G protein-coupled receptor (GPCR) that are activated by the agonist muscarine, as well as by the endogenous neurotransmitter acetylcholine.
Muscarinic receptors are involved in a wide range of physiological functions, such as the regulation of heart rate, gastrointestinal motility, and bladder contraction.
Nicotinic cholinergic receptors (nAChRs), on the other hand, are ligand-gated ion channels that are activated by the agonist nicotine, as well as by acetylcholine.
Nicotinic receptors are found in the neuromuscular junction, autonomic ganglia, and the central nervous system, where they play a role in the transmission of electrical signals.
Understanding the complex biology of cholinergic receptors is essential for the development of new therapies targeting conditions such as Alzheimer's disease, myasthenia gravis, and other neurological and muscular disorders.
Researchers often utilize tools like α-BTX (α-Bungarotoxin), Alexa Fluor® 594 conjugated α‐bungarotoxin, and SMI-312R to study the localization and function of these receptors.
Additionally, advanced techniques like Biacore 3000 and CMS chip technology can be used to analyze the binding kinetics and affinity of cholinergic receptor ligands, while DAPI (4′,6-diamidino-2-phenylindole) can be used to visualize cell nuclei in immunofluorescence experiments.
The incorporation of these techniques, along with the exploration of related terms like T1175, can enhance the reproducibility and accuracy of studies focused on cholinergic receptors.