A high-affinity muscarinic antagonist commonly used as a tool in animal and tissue studies.
One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for MUSCARINE over NICOTINE. There are several subtypes (usually M1, M2, M3....) that are characterized by their cellular actions, pharmacology, and molecular biology.
Quinuclidines are organic compounds consisting of a tricyclic structure with a three-membered ring fused to a piperidine ring, often used as building blocks in the synthesis of pharmaceuticals and bioactive molecules.
Benzilates are organic compounds that contain the structure of benzil, characterized by two benzoyl groups (-COPh) bonded to a central carbon atom, and can be esters of benzilic acid with various alcohols.
Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology.
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
An analog of benzilylcholine mustard. It is an alkylating nitrogen mustard analog that binds specifically and irreversibly to cholinergic muscarinic receptors and is used as an affinity label to isolate and study the receptors.
A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.
A non-hydrolyzed muscarinic agonist used as a research tool.
Drugs that mimic the effects of parasympathetic nervous system activity. Included here are drugs that directly stimulate muscarinic receptors and drugs that potentiate cholinergic activity, usually by slowing the breakdown of acetylcholine (CHOLINESTERASE INHIBITORS). Drugs that stimulate both sympathetic and parasympathetic postganglionic neurons (GANGLIONIC STIMULANTS) are not included here.
A muscarinic antagonist used to study binding characteristics of muscarinic cholinergic receptors.
Agents that inhibit the actions of the parasympathetic nervous system. The major group of drugs used therapeutically for this purpose is the MUSCARINIC ANTAGONISTS.
Drugs that bind to and activate muscarinic cholinergic receptors (RECEPTORS, MUSCARINIC). Muscarinic agonists are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder and the eye. They may also be used to reduce heart rate.
An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as CIMETIDINE and RANITIDINE. It is generally well tolerated by patients.
An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
Tritium is an isotope of hydrogen (specifically, hydrogen-3) that contains one proton and two neutrons in its nucleus, making it radioactive with a half-life of about 12.3 years, and is used in various applications including nuclear research, illumination, and dating techniques due to its low energy beta decay.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
The rate dynamics in chemical or physical systems.

Roles of threonine 192 and asparagine 382 in agonist and antagonist interactions with M1 muscarinic receptors. (1/244)

Conserved amino acids, such as Thr in transmembrane domains (TM) V and Asn in TM VI of muscarinic receptors, may be important in agonist binding and/or receptor activation. In order to determine the functional roles of Thr192 and Asn382 in human M1 receptors in ligand binding and receptor activation processes, we created and characterized mutant receptors with Thr192 or Asn382 substituted by Ala. HM1 wild-type (WT) and mutant receptors [HM1(Thr192Ala) and HM1(Asn382Ala)] were stably expressed in A9 L cells. The Kd values for 3H-(R)-QNB and Ki values for other classical muscarinic antagonists were similar at HM1(WT) and HM1(Thr192Ala) mutant receptors, yet higher at HM1(Asn382Ala) mutant receptors. Carbachol exhibited lower potency and efficacy in stimulating PI hydrolysis via HM1(Thr192Ala) mutant receptors, and intermediate agonist activity at the HM1(Asn382Ala) mutant receptors. The Asn382 residue in TM VI but not the Thr192 residue in TM V of the human M1 receptor appears to participate directly in antagonist binding. Both Thr192 and Asn382 residues are involved differentially in agonist binding and/or receptor activation processes, yet the Asn382 residue is less important than Thr192 in agonist activation of M1 receptors. Molecular modelling studies indicate that substitution of Thr192 or Asn382 results in the loss of hydrogen-bond interactions and changes in the agonist binding mode associated with an increase in hydrophobic interactions between ligand and receptor.  (+info)

Functional comparison of muscarinic partial agonists at muscarinic receptor subtypes hM1, hM2, hM3, hM4 and hM5 using microphysiometry. (2/244)

1. This study describes the pharmacological comparison of the muscarinic partial agonists sabcomeline, xanomeline and milameline at human cloned muscarinic receptor subtypes (hM1-5). 2. Radioligand binding studies at the hM1-5 muscarinic receptor subtypes were compared with functional studies using microphysiometry using carbachol as the standard full agonist. 3. In binding assays none of the compounds studied displayed preferential affinity for the M1,3,4 or M5 subtypes although carbachol was less potent at hM1 than hM3,4,5. 4. In functional studies, all of the compounds studied displayed similar levels of efficacy across the muscarinic receptors with the exception of M3, where there was a large apparent receptor reserve and the compounds behaved essentially as full agonists. 5. Sabcomeline was the most potent agonist in functional studies but also showed the lowest efficacy. In terms of potency, xanomeline showed some selectivity for M1 over M2 receptors and milameline showed some selectivity for M2 over M1 receptors. 6. These results show the value of microphysiometry in being able to compare receptor pharmacology across subtypes irrespective of the signal transduction pathway. 7. None of the partial agonists showed functional selectivity for M1 receptors, or indeed any muscarinic receptor, in the present study.  (+info)

Effects of mitoxantrone on action potential and membrane currents in isolated cardiac myocytes. (3/244)

1. The effects of mitoxantrone (MTO), an anticancer drug, on the membrane electrical properties of cardiac myocytes were investigated using the whole-cell clamp technique. 2. In isolated guinea-pig ventricular myocytes, 30 microM MTO induced a time-dependent prolongation of action potential duration (APD) which was occasionally accompanied by early afterdepolarizations. APD prolongation was preserved in the presence of 10 microM tetrodotoxin and showed reverse rate-dependence. 3. Both the inward rectifier K+ current (I(KI)) and the delayed rectifier K+ current (I(K)) of guinea-pig ventricular myocytes were significantly depressed by 30 microM MTO. The rapidly activating component of I(k) (I(Kr)) seemed to be preferentially blocked by MTO. The transient outward current was not affected by MTO in rat ventricular myocytes. 4. Thirty microM MTO had no direct effect on the L-type Ca2+ current (I(Ca(L))), but reversed the inhibitory effect of 1 microM carbamylcholine but not the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (1 microM) on I(Ca(L)) enhanced by 50 nM isoprenaline in guinea-pig ventricular myocytes. In guinea-pig atrial mycotyes, 30 microM MTO inhibited by 93% the muscarinic receptor gated K+ current (I(K,ACh)) evoked by 1 microM carbamylcholine, whereas I(K,ACh) elicited by 100 microM GTPgammaS, a nonhydrolysable GTP analogue, was only decreased by 12%. 5. The specific binding of [3H]QNB, a muscarinic receptor ligand, to human atrial membranes was concentration-dependently displaced by MTO (1-1000 microM). 6. In conclusion, MTO blocks cardiac muscarinic receptors and prolongs APD by inhibition of I(KI) and I(Kr). The occasionally observed early afterdepolarizations may signify a potential cardiac hazard of the drug.  (+info)

Alterations of muscarinic acetylcholine receptor subtypes in diffuse lewy body disease: relation to Alzheimer's disease. (4/244)

OBJECTIVES: Dementia associated with Lewy bodies in cortical and subcortical areas is classified as dementia of the non-Alzheimer type and termed diffuse Lewy body disease (DLBD). The generic term "dementia with Lewy bodies (DLB)" was proposed in the international workshop on Lewy body dementia to include the similar disorders presenting Lewy bodies. In DLB, a lower level of choline acetyltransferase (ChAT) activity in the neocortex was found compared with that in Alzheimer's disease. The purpose of the present study was to determine the total amount of muscarinic acetylcholine receptors (mAChRs) and relative proportion of each subtype (m1-m4) of mAChRs in the frontal and temporal cortex of seven DLBD and 11 Alzheimer's disease necropsied brains. METHODS: A [(3)H]quinuclidinyl benzilate (QNB) binding assay and an immunoprecipitation assay using subtype-specific antibodies were performed. Each antibody was raised against fusion proteins containing peptides corresponding to the third intracellular (i3) loops of the respective mAChR subtype. RESULTS: The total amounts of mAChRs were significantly lower in the preparations of temporal cortices from DLBD and Alzheimer's disease than in those from dead controls (seven cases). In both diseases, the proportion of the m3 receptor in the frontal cortex was significantly increased and that of the m4 receptor in the temporal cortex was significantly decreased compared with the control specimens. The proportions of the m1 and m2 subtypes were significantly different in the temporal cortex. The proportion of the m1 receptor was significantly greater in the DLBD brains, whereas that of the m2 receptor was significantly greater in the Alzheimer's disease brains than in the controls. CONCLUSIONS: The m1 receptor is the major subtype in the cerebral cortex, and m2 is known to be present at presynaptic terminals. The higher proportions of m1 in DLBD and m2 in Alzheimer's disease suggest that the manner of degeneration in the cholinergic system is different between the diseases. It is hypothesised that a severe depletion of presynaptic cholinergic projective neurons causes the upregulation of m1 receptor in the temporal cortex in DLBD.  (+info)

Alanine-scanning mutagenesis of transmembrane domain 6 of the M(1) muscarinic acetylcholine receptor suggests that Tyr381 plays key roles in receptor function. (5/244)

Transmembrane domain 6 of the muscarinic acetylcholine (ACh) receptors is important in ligand binding and in the conformational transitions of the receptor but the roles of individual residues are poorly understood. We have carried out a systematic alanine-scanning mutagenesis study on residues Tyr381 to Val387 within the binding domain of the M(1) muscarinic ACh receptor. The seven mutations were then analyzed to define the effects on receptor expression, agonist and antagonist binding, and signaling efficacy. Tyr381Ala produced a 40-fold reduction in ACh affinity and a 50-fold reduction in ACh-signaling efficacy. Leu386Ala had similar but smaller effects. Asn382Ala caused the largest inhibition of antagonist binding. The roles of the hydroxyl group and benzene ring of Tyr381 were probed further by comparative analysis of the Tyr381Phe and Tyr381Ala mutants using three series of ligands: ACh analogs, azanorbornane- and quinuclidine-based ligands, and atropine analogs. These data suggested that the hydroxyl group of Tyr381 is primarily involved in forming hydrogen bond interactions with the oxygen atoms present in the side chain of ACh. We propose that this interaction is established in the ground state and preserved in the activated state of the receptor. In contrast, the Tyr381 benzene ring may form a cation-pi interaction with the positively charged head group of ACh that contributes to the activated state of the receptor but not the ground state. However, the hydroxyl group and benzene ring of Tyr381 both participate in interactions with azanorbornane- and quinuclidine-based ligands and atropine analogs in the ground state as well as the activated state of the receptor.  (+info)

Changes in rat brain cholinesterase activity and muscarinic receptor density during and after repeated oral exposure to chlorpyrifos in early postnatal development. (6/244)

The effects of repeated oral exposures to the organophosphorus insecticide chlorpyrifos (CPS) on brain muscarinic receptor densities, together with cholinesterase (ChE) activity, were studied in early postnatal rats. Initially, the effects on esterases from lactational exposure to CPS were investigated in young rats by administering CPS (100, 150, or 200 mg/kg subcutaneously in corn oil) to dams 1 day postpartum, yielding a significant body burden of CPS in the dams for possible excretion in the milk. Brain ChE inhibition in pups was less severe than in dams, whereas liver carboxylesterase (CbxE) inhibition in pups was at the same level as in dams. Because of the limited brain ChE inhibition obtained following lactation, pups were exposed to CPS directly by gavage, using 3 dosing regimens to yield a dose response. The rats were gavaged with CPS in corn oil on alternate days from postnatal day (PND) 1 through PND 21. Rats in the low-dosage group received 11 treatments at 3 mg/kg, those in the medium-dosage group received 3 treatments at 3 mg/kg and 8 at 6 mg/kg, and those in the high dosage group received 3 treatments at 3 mg/kg, 4 at 6 mg/kg, and 4 at 12 mg/kg. ChE activity in brain homogenates were inhibited significantly by 29% and 63% in the low- and high-dosage groups, respectively, on PND 22 and by 17% in the high dosage group on PND 40. Muscarinic receptor densities in brain synaptosomes were reduced using 3H-N-methylscopolamine (NMS) and 3H-quinuclidinyl benzilate (QNB) as ligands, with the effects more prominent from 3H-NMS. Densities of both ligands recovered to the control level several days after terminating treatment. The results indicate that pups are apparently exposed to only limited amounts of chlorpyrifos and/or its oxon through the milk when dams are exposed to extremely high chlorpyrifos levels. In addition, repeated direct oral exposures of early postnatal rats to CPS will result in persistent brain ChE inhibition and will transiently reduce muscarinic receptor density.  (+info)

Urothelium-derived inhibitory factor(s) influences on detrusor muscle contractility in vitro. (7/244)

The function of the bladder urothelium in modulating contractile responses of the underlying detrusor smooth muscle to muscarinic stimulation has been examined in the pig bladder. Saturation curves for [3H]-QNB binding demonstrated a greater muscarinic receptor density in the urothelium than in the detrusor smooth muscle. The presence of an intact urothelium on isolated bladder strips inhibited contractions induced by carbachol but not KCl. Contractions of a urothelium-denuded muscle strip were inhibited in the presence of a second bladder strip with an intact urothelium, but not if the second strip was denuded. The urothelium-induced inhibition of contractions was not prevented in the presence of L-NOARG, methylene blue, indomethacin, propranolol, suramin, TEA or apamin. The data suggest the presence of a diffusable, urothelium-derived inhibitory factor, which could not be identified but appears to be neither nitric oxide, a cyclo-oxygenase product, a catecholamine, adenosine, GABA nor an EDHF sensitive to apamin.  (+info)

Evidence for a tandem two-site model of ligand binding to muscarinic acetylcholine receptors. (8/244)

After short preincubations with N-[(3)H]methylscopolamine ([(3)H]NMS) or R(-)-[(3)H]quinuclidinyl benzilate ([(3)H]QNB), radioligand dissociation from muscarinic M(1) receptors in Chinese hamster ovary cell membranes was fast, monoexponential, and independent of the concentration of unlabeled NMS or QNB added to reveal dissociation. After long preincubations, the dissociation was slow, not monoexponential, and inversely related to the concentration of the unlabeled ligand. Apparently, the unlabeled ligand becomes able to associate with the receptor simultaneously with the already bound radioligand if the preincubation lasts for a long period, and to hinder radioligand dissociation. When the membranes were preincubated with [(3)H]NMS and then exposed to benzilylcholine mustard (covalently binding specific ligand), [(3)H]NMS dissociation was blocked in wild-type receptors, but not in mutated (D99N) M(1) receptors. Covalently binding [(3)H]propylbenzilylcholine mustard detected substantially more binding sites than [(3)H]NMS. The observations support a model in which the receptor binding domain has two tandemly arranged subsites for classical ligands, a peripheral one and a central one. Ligands bind to the peripheral subsite first (binding with lower affinity) and translocate to the central subsite (binding with higher affinity). The peripheral subsite of M(1) receptors may include Asp-99. Experimental data on [(3)H]NMS and [(3)H]QNB association and dissociation perfectly agree with the predictions of the tandem two-site model.  (+info)

Quinuclidinyl benzilate is a synthetic chemical compound that acts as a potent anticholinergic drug. Its chemical formula is C18H26N2O2. It is an odorless, white crystalline powder that is slightly soluble in water and more soluble in organic solvents.

Quinuclidinyl benzilate is a deliriant drug, which means it can cause delirium, confusion, hallucinations, and other altered mental states. It works by blocking the action of acetylcholine, a neurotransmitter in the brain that is involved in memory, attention, and perception.

This compound has been used in research as a tool to study the nervous system and has also been explored for its potential use as a chemical weapon. It is classified as a Schedule II controlled substance in the United States due to its high potential for abuse and the risk of severe psychological harm.

Muscarinic receptors are a type of G protein-coupled receptor (GPCR) that bind to the neurotransmitter acetylcholine. They are found in various organ systems, including the nervous system, cardiovascular system, and respiratory system. Muscarinic receptors are activated by muscarine, a type of alkaloid found in certain mushrooms, and are classified into five subtypes (M1-M5) based on their pharmacological properties and signaling pathways.

Muscarinic receptors play an essential role in regulating various physiological functions, such as heart rate, smooth muscle contraction, glandular secretion, and cognitive processes. Activation of M1, M3, and M5 muscarinic receptors leads to the activation of phospholipase C (PLC) and the production of inositol trisphosphate (IP3) and diacylglycerol (DAG), which increase intracellular calcium levels and activate protein kinase C (PKC). Activation of M2 and M4 muscarinic receptors inhibits adenylyl cyclase, reducing the production of cAMP and modulating ion channel activity.

In summary, muscarinic receptors are a type of GPCR that binds to acetylcholine and regulates various physiological functions in different organ systems. They are classified into five subtypes based on their pharmacological properties and signaling pathways.

Quinuclidines are a class of organic compounds that contain a unique cage-like structure consisting of a tetrahydrofuran ring fused to a piperidine ring. The name "quinuclidine" is derived from the Latin word "quinque," meaning five, and "clidis," meaning key or bar, which refers to the five-membered ring system that forms the core of these compounds.

Quinuclidines have a variety of biological activities and are used in pharmaceuticals as well as agrochemicals. Some quinuclidine derivatives have been found to exhibit anti-inflammatory, antiviral, and anticancer properties. They can also act as inhibitors of various enzymes and receptors, making them useful tools for studying biological systems and developing new drugs.

It is worth noting that quinuclidines are not typically used in medical diagnosis or treatment, but rather serve as building blocks for the development of new pharmaceutical compounds.

I could not find a medical definition for "Benzilates" as it is not a recognized term in medicine or pharmacology. It seems that you may have made a typographical error, and the correct term you are looking for might be "benzoylates." Benzoylates refer to salts or esters of benzoic acid, which have various uses including as preservatives and pharmaceutical ingredients.

If you meant something else by "Benzilates," please provide more context so I can give a more accurate response.

Cholinergic receptors are a type of receptor in the body that are activated by the neurotransmitter acetylcholine. Acetylcholine is a chemical that nerve cells use to communicate with each other and with muscles. There are two main types of cholinergic receptors: muscarinic and nicotinic.

Muscarinic receptors are found in the heart, smooth muscle, glands, and the central nervous system. They are activated by muscarine, a type of alkaloid found in certain mushrooms. When muscarinic receptors are activated, they can cause changes in heart rate, blood pressure, and other bodily functions.

Nicotinic receptors are found in the nervous system and at the junction between nerves and muscles (the neuromuscular junction). They are activated by nicotine, a type of alkaloid found in tobacco plants. When nicotinic receptors are activated, they can cause the release of neurotransmitters and the contraction of muscles.

Cholinergic receptors play an important role in many physiological processes, including learning, memory, and movement. They are also targets for drugs used to treat a variety of medical conditions, such as Alzheimer's disease, Parkinson's disease, and myasthenia gravis (a disorder that causes muscle weakness).

Muscarinic antagonists, also known as muscarinic receptor antagonists or parasympatholytics, are a class of drugs that block the action of acetylcholine at muscarinic receptors. Acetylcholine is a neurotransmitter that plays an important role in the parasympathetic nervous system, which helps to regulate various bodily functions such as heart rate, digestion, and respiration.

Muscarinic antagonists work by binding to muscarinic receptors, which are found in various organs throughout the body, including the eyes, lungs, heart, and gastrointestinal tract. By blocking the action of acetylcholine at these receptors, muscarinic antagonists can produce a range of effects depending on the specific receptor subtype that is affected.

For example, muscarinic antagonists may be used to treat conditions such as chronic obstructive pulmonary disease (COPD) and asthma by relaxing the smooth muscle in the airways and reducing bronchoconstriction. They may also be used to treat conditions such as urinary incontinence or overactive bladder by reducing bladder contractions.

Some common muscarinic antagonists include atropine, scopolamine, ipratropium, and tiotropium. It's important to note that these drugs can have significant side effects, including dry mouth, blurred vision, constipation, and confusion, especially when used in high doses or for prolonged periods of time.

Propylbenzilylcholine mustard is not a medical term, but it is a chemical compound that has been used in research and development. It's a type of muscarinic receptor agonist, which means it binds to and activates muscarinic acetylcholine receptors, a type of receptor found in the nervous system.

In a medical context, this compound may be used in research to study the functions of the muscarinic receptors or to develop new medications that target these receptors. However, it is not currently used as a medication in clinical practice.

It's important to note that Propylbenzilylcholine mustard is also known as a "receptor agonist" and has been used in research as a tool to stimulate muscarinic receptors. It's not a drug, but a compound used in laboratory settings for scientific studies.

Carbachol is a cholinergic agonist, which means it stimulates the parasympathetic nervous system by mimicking the action of acetylcholine, a neurotransmitter that is involved in transmitting signals between nerves and muscles. Carbachol binds to both muscarinic and nicotinic receptors, but its effects are more pronounced on muscarinic receptors.

Carbachol is used in medical treatments to produce miosis (pupil constriction), lower intraocular pressure, and stimulate gastrointestinal motility. It can also be used as a diagnostic tool to test for certain conditions such as Hirschsprung's disease.

Like any medication, carbachol can have side effects, including sweating, salivation, nausea, vomiting, diarrhea, bradycardia (slow heart rate), and bronchoconstriction (narrowing of the airways in the lungs). It should be used with caution and under the supervision of a healthcare professional.

Oxotremorine is a muscarinic receptor agonist, which means it binds to and activates muscarinic acetylcholine receptors. These receptors are found in the central and peripheral nervous system and are involved in various physiological functions, including cognition, motivation, reward, motor control, and sensory processing.

Oxotremorine is primarily used in research settings to study the role of muscarinic receptors in different physiological processes and diseases. It has been shown to produce effects similar to those caused by natural neurotransmitter acetylcholine, such as increased salivation, sweating, and gastrointestinal motility.

In addition, oxotremorine has been investigated for its potential therapeutic use in the treatment of various neurological disorders, including Alzheimer's disease, Parkinson's disease, and schizophrenia. However, its clinical use is limited due to its side effects, such as nausea, vomiting, diarrhea, and abdominal cramps.

Parasympathomimetics are substances or drugs that mimic the actions of the parasympathetic nervous system. The parasympathetic nervous system is one of the two branches of the autonomic nervous system, which regulates involuntary physiological functions. It is responsible for the "rest and digest" response, and its neurotransmitter is acetylcholine.

Parasympathomimetic drugs work by either directly stimulating muscarinic receptors or increasing the availability of acetylcholine in the synaptic cleft. These drugs can have various effects on different organs, depending on the specific receptors they target. Some common effects include decreasing heart rate and contractility, reducing respiratory rate, constricting pupils, increasing glandular secretions (such as saliva and sweat), stimulating digestion, and promoting urination and defecation.

Examples of parasympathomimetic drugs include pilocarpine, which is used to treat dry mouth and glaucoma; bethanechol, which is used to treat urinary retention and neurogenic bladder; and neostigmine, which is used to treat myasthenia gravis and reverse the effects of non-depolarizing muscle relaxants.

N-Methylscopolamine is a anticholinergic drug, which means it blocks the action of acetylcholine, a neurotransmitter in the body. It is a derivative of scopolamine and is used to treat various conditions such as gastrointestinal disorders (such as gastritis, peptic ulcer), Parkinson's disease, motion sickness, and to reduce saliva production during surgical or diagnostic procedures.

It works by blocking the muscarinic receptors in the nervous system, which leads to a decrease in the secretion of fluids (such as saliva, sweat, stomach acid) and decreased muscle contractions in the gastrointestinal tract. N-Methylscopolamine can also cause side effects such as dizziness, dry mouth, blurred vision, and difficulty urinating.

Parasympatholytics are a type of medication that blocks the action of the parasympathetic nervous system. The parasympathetic nervous system is responsible for the body's rest and digest response, which includes slowing the heart rate, increasing intestinal and glandular activity, and promoting urination and defecation.

Parasympatholytics work by selectively binding to muscarinic receptors, which are found in various organs throughout the body, including the heart, lungs, and digestive system. By blocking these receptors, parasympatholytics can cause a range of effects, such as an increased heart rate, decreased glandular secretions, and reduced intestinal motility.

Some common examples of parasympatholytics include atropine, scopolamine, and ipratropium. These medications are often used to treat conditions such as bradycardia (slow heart rate), excessive salivation, and gastrointestinal cramping or diarrhea. However, because they can have significant side effects, parasympatholytics are typically used only when necessary and under the close supervision of a healthcare provider.

Muscarinic agonists are a type of medication that binds to and activates muscarinic acetylcholine receptors, which are found in various organ systems throughout the body. These receptors are activated naturally by the neurotransmitter acetylcholine, and when muscarinic agonists bind to them, they mimic the effects of acetylcholine.

Muscarinic agonists can have a range of effects on different organ systems, depending on which receptors they activate. For example, they may cause bronchodilation (opening up of the airways) in the respiratory system, decreased heart rate and blood pressure in the cardiovascular system, increased glandular secretions in the gastrointestinal and salivary systems, and relaxation of smooth muscle in the urinary and reproductive systems.

Some examples of muscarinic agonists include pilocarpine, which is used to treat dry mouth and glaucoma, and bethanechol, which is used to treat urinary retention. It's important to note that muscarinic agonists can also have side effects, such as sweating, nausea, vomiting, and diarrhea, due to their activation of receptors in various organ systems.

Pirenzepine is a medication that belongs to a class of drugs called anticholinergics or parasympatholytics. It works by blocking the action of acetylcholine, a neurotransmitter in the body, on certain types of muscarinic receptors.

Pirenzepine is primarily used to treat peptic ulcers and gastroesophageal reflux disease (GERD) by reducing the production of stomach acid. It may also be used to manage symptoms of irritable bowel syndrome, such as abdominal pain and diarrhea.

The medication is available in the form of tablets or gel for topical application. Side effects of pirenzepine may include dry mouth, blurred vision, constipation, dizziness, and difficulty urinating. It should be used with caution in people with glaucoma, benign prostatic hyperplasia, or other conditions that may be exacerbated by anticholinergic drugs.

It is important to note that this definition is for informational purposes only and should not be taken as medical advice. Always consult with a healthcare professional before starting any new medication.

Atropine is an anticholinergic drug that blocks the action of the neurotransmitter acetylcholine in the central and peripheral nervous system. It is derived from the belladonna alkaloids, which are found in plants such as deadly nightshade (Atropa belladonna), Jimson weed (Datura stramonium), and Duboisia spp.

In clinical medicine, atropine is used to reduce secretions, increase heart rate, and dilate the pupils. It is often used before surgery to dry up secretions in the mouth, throat, and lungs, and to reduce salivation during the procedure. Atropine is also used to treat certain types of nerve agent and pesticide poisoning, as well as to manage bradycardia (slow heart rate) and hypotension (low blood pressure) caused by beta-blockers or calcium channel blockers.

Atropine can have several side effects, including dry mouth, blurred vision, dizziness, confusion, and difficulty urinating. In high doses, it can cause delirium, hallucinations, and seizures. Atropine should be used with caution in patients with glaucoma, prostatic hypertrophy, or other conditions that may be exacerbated by its anticholinergic effects.

A radioligand assay is a type of in vitro binding assay used in molecular biology and pharmacology to measure the affinity and quantity of a ligand (such as a drug or hormone) to its specific receptor. In this technique, a small amount of a radioactively labeled ligand, also known as a radioligand, is introduced to a sample containing the receptor of interest. The radioligand binds competitively with other unlabeled ligands present in the sample for the same binding site on the receptor. After allowing sufficient time for binding, the reaction is stopped, and the amount of bound radioligand is measured using a technique such as scintillation counting. The data obtained from this assay can be used to determine the dissociation constant (Kd) and maximum binding capacity (Bmax) of the receptor-ligand interaction, which are important parameters in understanding the pharmacological properties of drugs and other ligands.

"Competitive binding" is a term used in pharmacology and biochemistry to describe the behavior of two or more molecules (ligands) competing for the same binding site on a target protein or receptor. In this context, "binding" refers to the physical interaction between a ligand and its target.

When a ligand binds to a receptor, it can alter the receptor's function, either activating or inhibiting it. If multiple ligands compete for the same binding site, they will compete to bind to the receptor. The ability of each ligand to bind to the receptor is influenced by its affinity for the receptor, which is a measure of how strongly and specifically the ligand binds to the receptor.

In competitive binding, if one ligand is present in high concentrations, it can prevent other ligands with lower affinity from binding to the receptor. This is because the higher-affinity ligand will have a greater probability of occupying the binding site and blocking access to the other ligands. The competition between ligands can be described mathematically using equations such as the Langmuir isotherm, which describes the relationship between the concentration of ligand and the fraction of receptors that are occupied by the ligand.

Competitive binding is an important concept in drug development, as it can be used to predict how different drugs will interact with their targets and how they may affect each other's activity. By understanding the competitive binding properties of a drug, researchers can optimize its dosage and delivery to maximize its therapeutic effect while minimizing unwanted side effects.

Tritium is not a medical term, but it is a term used in the field of nuclear physics and chemistry. Tritium (symbol: T or 3H) is a radioactive isotope of hydrogen with two neutrons and one proton in its nucleus. It is also known as heavy hydrogen or superheavy hydrogen.

Tritium has a half-life of about 12.3 years, which means that it decays by emitting a low-energy beta particle (an electron) to become helium-3. Due to its radioactive nature and relatively short half-life, tritium is used in various applications, including nuclear weapons, fusion reactors, luminous paints, and medical research.

In the context of medicine, tritium may be used as a radioactive tracer in some scientific studies or medical research, but it is not a term commonly used to describe a medical condition or treatment.

Acetylcholine is a neurotransmitter, a type of chemical messenger that transmits signals across a chemical synapse from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell. It is involved in both peripheral and central nervous system functions.

In the peripheral nervous system, acetylcholine acts as a neurotransmitter at the neuromuscular junction, where it transmits signals from motor neurons to activate muscles. Acetylcholine also acts as a neurotransmitter in the autonomic nervous system, where it is involved in both the sympathetic and parasympathetic systems.

In the central nervous system, acetylcholine plays a role in learning, memory, attention, and arousal. Disruptions in cholinergic neurotransmission have been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, and myasthenia gravis.

Acetylcholine is synthesized from choline and acetyl-CoA by the enzyme choline acetyltransferase and is stored in vesicles at the presynaptic terminal of the neuron. When a nerve impulse arrives, the vesicles fuse with the presynaptic membrane, releasing acetylcholine into the synapse. The acetylcholine then binds to receptors on the postsynaptic membrane, triggering a response in the target cell. Acetylcholine is subsequently degraded by the enzyme acetylcholinesterase, which terminates its action and allows for signal transduction to be repeated.

"Inbred strains of rats" are genetically identical rodents that have been produced through many generations of brother-sister mating. This results in a high degree of homozygosity, where the genes at any particular locus in the genome are identical in all members of the strain.

Inbred strains of rats are widely used in biomedical research because they provide a consistent and reproducible genetic background for studying various biological phenomena, including the effects of drugs, environmental factors, and genetic mutations on health and disease. Additionally, inbred strains can be used to create genetically modified models of human diseases by introducing specific mutations into their genomes.

Some commonly used inbred strains of rats include the Wistar Kyoto (WKY), Sprague-Dawley (SD), and Fischer 344 (F344) rat strains. Each strain has its own unique genetic characteristics, making them suitable for different types of research.

I must clarify that the term "Guinea Pigs" is not typically used in medical definitions. However, in colloquial or informal language, it may refer to people who are used as the first to try out a new medical treatment or drug. This is known as being a "test subject" or "in a clinical trial."

In the field of scientific research, particularly in studies involving animals, guinea pigs are small rodents that are often used as experimental subjects due to their size, cost-effectiveness, and ease of handling. They are not actually pigs from Guinea, despite their name's origins being unclear. However, they do not exactly fit the description of being used in human medical experiments.

The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:

1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.

The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.

The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.

The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.

Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

... (QNB) (IUPAC name 1-azabicyclo[2.2.2]octan-3-yl hydroxy(diphenyl)acetate; US Army code EA-2277; NATO ... Erowid-BZ Vault eMedicine-3-Quinuclidinyl Benzilate Poisoning Possible Abuse of BZ by Insurgents in Iraq, Defense Tech blog, ... 3-Quinuclidinyl esters, Chemical weapons of the United States, Swiss inventions, Tertiary alcohols, Benzilate esters). ...
Tests in vitro showed it to have a binding affinity over 1000 times more potent than 3-quinuclidinyl benzilate. CS-27349 EA- ... Ball JC (2015). "Dual Use Research of Concern: Derivatives of 3-Quinuclidinyl Benzilate". Military Medical Science Letters. 84 ... 3-Quinuclidinyl thiochromane-4-carboxylate is a research compound which is one of the most potent muscarinic antagonists known ... 3-Quinuclidinyl esters, All stub articles, Pharmacology stubs). ...
It has 37% of the potency of the related compound 3-quinuclidinyl benzilate (BZ) in producing peripheral effects, but 85% of ... Ball JC (2015). "Dual Use Research of Concern: Derivatives of 3-Quinuclidinyl Benzilate". Military Medical Science Letters. 84 ... CS-27349, or L-2-α-tropinyl benzilate, is an experimental incapacitating agent. It acts as an antagonist to muscarinic ...
... is an anticholinergic drug related to the chemical warfare agent 3-Quinuclidinyl benzilate. N-Ethyl-3-piperidyl benzilate is ... N-methyl-3-piperidyl benzilate 3-Quinuclidinyl benzilate Ditran Lebovits, Binyamin Z.; VISOTSKY HM; OSTFELD AM (1960). "LSD and ... ethyl-3-piperidyl benzilate and (+)N-[11C]propyl-3-piperidyl benzilate for muscarinic cholinergic receptors: a PET study with ... Both the N-methyl and N-ethyl analogues of 3-piperidyl benzilate are, however, Schedule I controlled drugs. Radiolabelled ...
In addition to LSD, the Army also tested quinuclidinyl benzilate, a hallucinogen code-named BZ. (Note 37) Many of these tests ...
Sedatives or hypnotics that alter higher cognitive function include ethanol, scopolamine, 3-quinuclidinyl benzilate, potent ... These include ethanol, scopolamine, 3-quinuclidinyl benzilate, midazolam, flunitrazepam, sodium thiopental, and amobarbital, ...
N-Methyl-3-piperidyl benzilate N-Ethyl-3-piperidyl benzilate 3-Quinuclidinyl benzilate EA-3167 Franke S, Franz P, Warnke W ( ... Ditran (JB-329) is an anticholinergic drug mixture, related to the chemical warfare agent 3-Quinuclidinyl benzilate (QNB). ... The ditran mixture is more potent as an anticholinergic than the piperidyl benzilate drugs such as N-methyl-3-piperidyl ... but most modern research using these kinds of anticholinergic drugs uses N-methyl-3-piperidyl benzilate due to its wider ...
... ketanserin and quinuclidinyl benzilate in the rat brain]". Eksperimental'naia i Klinicheskaia Farmakologiia (in Russian). 56 (1 ...
Each bomblet held about 6 ounces (170 g) of the incapacitating agent BZ, also known as 3-Quinuclidinyl benzilate. The bomblets ...
The bomblets each held about 6 ounces (170 g) of the incapacitating agent BZ, also known as 3-Quinuclidinyl benzilate. The M43 ...
It is used in manufacture of the incapacitating agent 3-quinuclidinyl benzilate (BZ) which is regulated by the Chemical Weapons ... "Nerve Agent Precursors: Benzilic acid and Methyl Benzilate", Factsheets on Chemical and Biological Warfare Agents, Chemical ...
EA-3167 N-methyl-3-piperidyl benzilate N-ethyl-3-piperidyl benzilate 3-Quinuclidinyl benzilate Ditran Commission on Life ... related to the chemical warfare agent 3-Quinuclidinyl benzilate (QNB). It was developed under contract to Edgewood Arsenal ...
Britain was also investigating the possible use of LSD and the chemical BZ (3-quinuclidinyl benzilate) as nonlethal battlefield ...
Edgewood Arsenal human experiments N-Methyl-3-piperidyl benzilate N-Ethyl-3-piperidyl benzilate 3-Quinuclidinyl benzilate ... related to the chemical warfare agent 3-quinuclidinyl benzilate (QNB). It was developed under contract to Edgewood Arsenal ... 3-Quinuclidinyl esters, Acetate esters, Tertiary alcohols, Phenylcyclopentylglycolate esters, All stub articles, Hallucinogen ...
N-ethyl-3-piperidyl benzilate 3-Quinuclidinyl benzilate Ditran Takahashi K, Murakami M, Miura S, Iida H, Kanno I, Uemura K ( ... is an anticholinergic drug related to the chemical warfare agent 3-quinuclidinyl benzilate. N-methyl-3-piperidyl benzilate is ... Both the N-methyl and N-ethyl analogues of 3-piperidyl benzilate are, however, Schedule I controlled drugs. Radiolabelled ... methyl-3-piperidyl benzilate as a potent radioligand for positron emission tomography". Applied Radiation and Isotopes. 50 (3 ...
The use of 3-Quinuclidinyl benzilate or Agent BZ was alleged in Operation White Wing by journalist Pierre Darcourt in L'Express ... BZ (3-quinuclidinyl benzillate) The Wednesday Report. Canada's Aerospace and Defence Weekly. retrieved: January 9, 2017 Lee, ...
Arsenal human experiments EA-3167 N-methyl-3-piperidyl benzilate N-ethyl-3-piperidyl benzilate 3-Quinuclidinyl benzilate Ditran ... related to the chemical warfare agent 3-quinuclidinyl benzilate (QNB). It was developed under contract to Edgewood Arsenal ...
EA-3167 N-methyl-3-piperidyl benzilate N-ethyl-3-piperidyl benzilate 3-Quinuclidinyl benzilate Ditran "Possible Long-Term ... related to the chemical warfare agent 3-Quinuclidinyl benzilate (QNB). It was developed under contract to Edgewood Arsenal ...
One of the anticholinergic compounds, 3-quinuclidinyl benzilate, was assigned the NATO code "BZ" and was weaponized beginning ...
3-Quinuclidinyl benzilate) and its precursor in the substance used in the Sergei and Yulia Skripal poisoning case. However, ...
... related to the chemical warfare agent 3-quinuclidinyl benzilate (QNB). It was developed under contract to Edgewood Arsenal ... EA-3167 N-Methyl-3-piperidyl benzilate N-Ethyl-3-piperidyl benzilate Ditran Commission on Life Sciences (1982). Possible Long- ...
One of the anticholinergic compounds, 3-quinuclidinyl benzilate, was assigned the NATO code BZ and was weaponized at the ...
One of the anticholinergic compounds, 3-quinuclidinyl benzilate, was assigned the NATO code BZ and was weaponized at the ...
3-quinuclidinyl benzilate) is a prototype; the indoles, represented by EA 1729 (LSD-25); the cannabinols, or marijuana-like ... compounds; and the sedative, or tranquilizer, group." One of the most significant of these chemicals was 3-quinuclidinyl ...
... as labeled by tritiated quinuclidinyl benzilate, from rat brain. Further details about the binding of MLA to nAChRs were ...
3-Quinuclidinyl benzilate (BZ) Phencyclidine (SN) Lysergic acid diethylamide (LSD) These substances have also been investigated ...
The molecular formula C21H23NO3 may refer to: N-(p-Amylcinnamoyl)anthranilic acid Olopatadine 3-Quinuclidinyl benzilate This ...
CAR-302,282 EA-3167 N-methyl-3-piperidyl benzilate N-ethyl-3-piperidyl benzilate 3-Quinuclidinyl benzilate Ditran Possible Long ... related to the chemical warfare agent 3-Quinuclidinyl benzilate (QNB). It was developed under contract to Edgewood Arsenal ...
Phentermine Pramipexole Prolintane Prolintanone Propylhexedrine Psilocybin Pyrovalerone Quinuclidinyl benzilate (QNB) ...
... quinuclidinyl benzilate MeSH D03.605.869.189 - atropine MeSH D03.605.869.189.297 - atropine derivatives MeSH D03.605.869.189. ...
3-Quinuclidinyl benzilate (QNB) (IUPAC name 1-azabicyclo[2.2.2]octan-3-yl hydroxy(diphenyl)acetate; US Army code EA-2277; NATO ... Erowid-BZ Vault eMedicine-3-Quinuclidinyl Benzilate Poisoning Possible Abuse of BZ by Insurgents in Iraq, Defense Tech blog, ... 3-Quinuclidinyl esters, Chemical weapons of the United States, Swiss inventions, Tertiary alcohols, Benzilate esters). ...
The chemical warfare agent 3-quinuclidinyl benzilate (QNB, BZ) is an anticholinergic agent that affects both the peripheral and ... encoded search term (3-Quinuclidinyl Benzilate Poisoning) and 3-Quinuclidinyl Benzilate Poisoning What to Read Next on Medscape ... 3-Quinuclidinyl Benzilate Poisoning. Updated: Feb 22, 2021 * Author: Christopher P Holstege, MD; Chief Editor: Duane C Caneva, ... Determination of 3-quinuclidinyl benzilate (QNB) and its major metabolites in urine by isotope dilution gas chromatography/mass ...
Determination of 3-quinuclidinyl benzilate (QNB) and its major metabolites in urine by isotope dilution gas chromatography/mass ...
3-Quinuclidinyl Benzilate (BZ). ...
Comment: Quinuclidinyl benzilate is a anticholinergic glycolate that acts as a competitive, non-selective antagonist of ...
In addition to LSD, the Army also tested quinuclidinyl benzilate, a hallucinogen code-named BZ. (Note 37) Many of these tests ...
3-Quinuclidinyl Benzilate (BZ). ...
Quinuclidinyl Benzilate * otenzepad Grants and funding * 1F32HL07691-01 CLN2/HL/NHLBI NIH HHS/United States ...
Quinuclidinyl Benzilate / metabolism * Rats * Rats, Inbred Strains * Receptors, Cholinergic / drug effects* * Receptors, ...
3) BZ: 3-Quinuclidinyl benzilate (*). (6581-06-2). *. B Precursors:. *. (4) Chemicals, except for those listed in Schedule 1, ...
R)-3-quinuclidinyl benzilate. Ne3. N-terminal region of the third extracellular loop. TM. transmembrane domain. R-SAT. receptor ...
3H]quinuclidinyl benzilate. TM. transmembrane domain. ERK1/2. extracellular signal-regulated kinase 1/2. PBS. phosphate- ...
From Hoffmann-La Roche the army obtained its first batch of a drug called quinuclidinyl benzilate (BZ). Clinical studies with ...
From Hoffmann-La Roche the army obtained its first batch of a drug called quinuclidinyl benzilate (BZ). Clinical studies with ...
In radioligand binding experiments using cerebral cortical membranes, PZ inhibited the binding of [3H]quinuclidinyl benzilate ... quinuclidinyl benzilate or [3H]PZ. The reasons for this somewhat selective effect of PBCM are not apparent. ...
BZ: 3-Quinuclidinyl benzilate (*) 2933.39 (16) Chemicals, except for those listed in Schedule 1, containing a phosphorus atom ...
The 16 metal boxes with special markings that suggest they contained BZ (3-Quinuclidinyl benzilate) incapacitating agent as ...
Investigation of the Conditions of Extraction of Ion-Associates of 3-Quinuclidinyl Benzilate with Acidic Dyes. Emil Halámek and ... Ion-associates of 3-quinuclidinyl benzilate (BZ) with thirteen acidic dyes were examined after their extraction into chloroform ...
... methanol in the presence or absence of 3-quinuclidinyl benzilate (3-QNB) [17.5 ng (0.5 mg/kg body weight) for CD-1 mice; 70 ng ... 3-quinuclidinyl benzilate, indicating that a substantial portion of intraperitoneally administered Colivelin passes through the ...
Imaging cholinergic function in vivo in the brain with radioiodinated stereoisomers of quinuclidinyl benzilate. PhD thesis, ...
3H]pirenzepine and (-)-[3H]quinuclidinyl benzilate binding to rat cerebral cortical and cardiac muscarinic cholinergic sites. I ... 3H]pirenzepine and (-)-[3H]quinuclidinyl benzilate binding to rat cerebral cortical and cardiac muscarinic cholinergic sites. ... 3H]Pirenzepine and [3H]quinuclidinyl benzilate binding to brain muscarinic cholinergic receptors. Differences in measured ... quinuclidinyl benzilate [(3H]QNB) and [3H]pirenzepine [(3H]PZ). Recovery of binding sites was approximately 25% of the initial ...
The binding of [3H] quinuclidinyl benzilate ( [3H] QNB) to muscarinic cholinergic receptors in dentate gyrus of rat hippocampal ...
... by spiking a citys water supply and developed a super hallucinogen known as quinuclidinyl benzilate (BZ), which was tested on ...
3-quinuclidinyl benzilate). The experiments have shown that those weapons are not primarily designed not to kill but instead to ...
Synonyms: (-)MQNB , [3H](-)N-methyl-3-quinuclidinyl benzilate , Ro-23773 Compound class: Synthetic organic ...
Inhibition of [3H]- quinuclidinyl benzilate binding to Muscarinic acetylcholine receptor M4 expressed in CHO cell membranes B ... Inhibition of [3H]- quinuclidinyl benzilate binding to human Muscarinic acetylcholine receptor M2 expressed in CHO cell ... Muscarinic receptor M2 in rat heart using [3H]QNB (quinuclidinyl benzylate) radioligand as a M2 non-selective muscarinic ... Binding affinity against Muscarinic receptor M2 in rat brain using [3H]QNB (quinuclidinyl benzylate) radioligand at a ...
Quinuclidinyl benzilate.. hepatitis c antibodies hepatitis c antigens hepatitis c, chronic hepatitis, chronic hepatitis, ...
3-Quinuclidinyl benzilate. 6923-22-4................................. Monocrotophos*. 7439-92-1 ...
  • 3 H]Pirenzepine and (-)-[ 3 H]quinuclidinyl benzilate binding to rat cerebral cortical and cardiac muscarinic cholinergic sites. (arizona.edu)
  • The chemical warfare agent 3-quinuclidinyl benzilate (QNB, BZ) is an anticholinergic agent that affects both the peripheral and central nervous systems (CNS). (medscape.com)
  • Quinuclidinyl benzilate is a anticholinergic glycolate that acts as a competitive, non-selective antagonist of muscarinic receptors in cardiac muscle, smooth muscle, exocrine glands and at postsynaptic receptors in neurons. (guidetomalariapharmacology.org)
  • One anticholinergic chemical-warfare agent is 3-quinuclidinyl benzilate, North Atlantic Treaty Organization (NATO) code BZ. (msdmanuals.com)
  • The binding of [3H] quinuclidinyl benzilate ( [3H] QNB) to muscarinic cholinergic receptors in dentate gyrus of rat hippocampal formation was analyzed by membrane binding assay and in vitro autoradiography. (duke.edu)
  • Binding of the potent muscarinic antagonist [ 3 H]quinuclidinyl benzilate ( 3 H-QNB) showed that the cochlea has sites with the pharmacological specificity of muscarinic cholinergic receptors. (northwestern.edu)
  • The deliriant drugs atropine , scopolamine (both found in Datura) and diphenhydramine all act as antagonists upon muscarinic acetylcholine receptors, as does the chemical incapacitating agent 3-Quinuclidinyl benzilate, better known as BZ. (psychonautwiki.org)
  • In the absence of PZ, treatment of cerebral cortical membranes with 20 nM PBCM at 4 degrees C for 50 min resulted in a 69% reduction in the density of M1 binding sites and a 55% reduction in the density of M2 binding sites with no change in the equilibrium dissociation constants of the radioligands [3H]quinuclidinyl benzilate or [3H]PZ. (aspetjournals.org)
  • In radioligand binding experiments using cerebral cortical membranes, PZ inhibited the binding of [3H]quinuclidinyl benzilate in a biphasic manner. (aspetjournals.org)
  • In addition, intraperitoneally administered Colivelin suppresses memory impairment caused by a muscarinic acetylcholine receptor antagonist, 3-quinuclidinyl benzilate, indicating that a substantial portion of intraperitoneally administered Colivelin passes through the blood-brain barrier and suppresses functional memory deficit. (jneurosci.org)
  • Neither compound was effective in displacing [3H]quinuclidinyl benzilate (QNB) used to label the entire muscarinic receptor population. (cdc.gov)
  • The 16 metal boxes with special markings that suggest they contained BZ (3-Quinuclidinyl benzilate) incapacitating agent as well as CS (chlorobenzylidenemalononitrile) and CR (dibenzoxazepine) harassing 'riot-control' agents, were accompanied by the "citizens of foreign nations," he also alleged. (rt.com)
  • Chemical calmative weapons such as BZ (3-quinuclidinyl benzilate, a compound related to scopolamine) were developed during the Cold War. (globalresearch.ca)
  • Neither compound was effective in displacing [3H]quinuclidinyl benzilate (QNB) used to label the entire muscarinic receptor population. (cdc.gov)
  • The data demonstrate that perinatal choline supplementation causes (a) long-term facilitative effects on working and reference memory components of a 12-arm radial maze task, and (b) alternations of muscarinic receptor density as indexed by [3H]quinuclidinyl benzilate (QNB) binding and choline acetyltransferase (ChAT) levels in the hippocampus and frontal cortex of adult rats. (nih.gov)
  • Using N-(2-[18F]fluoroethyl)-4-piperidyl benzilate ([18F]FEPB), a moderate affinity (Ki = 1.7 nmol/L) nonsubtype-selective muscarinic receptor antagonist, the authors examined the sensitivity of equilibrium in vivo radioligand binding in rat brain with changes in endogenous acetylcholine levels produced by treatments with acetylcholinesterase inhibitors. (lookformedical.com)
  • A binding assay employing tritiated quinuclidinyl benzilate permits us to investigate properties of receptor binding sites and to measure receptor levels in cultured neuroblastoma and hybrid cells under systematically varied conditions. (nih.gov)
  • Determination of 3-quinuclidinyl benzilate (QNB) and its major metabolites in urine by isotope dilution gas chromatography/mass spectrometry. (medscape.com)
  • 3 H]Quinuclidinyl benzilate specific binding analysis showed that the equilibrium dissociation constant (K D ) did not differ between control and MSG, indicating that affinity is not affected by obesity induced by MSG. (bvsalud.org)
  • In vitro and in vivo metabolism of 3-quinuclidinyl benzilate by high-resolution mass spectrometry. (medscape.com)
  • Acetylcholinesterase inhibition increases in vivo N-(2-[18F]fluoroethyl)-4-piperidyl benzilate binding to muscarinic acetylcholine receptors. (lookformedical.com)
  • One anticholinergic chemical-warfare agent is 3-quinuclidinyl benzilate, North Atlantic Treaty Organization (NATO) code BZ. (msdmanuals.com)
  • 125I] 3-quinuclidinyl 4-iodobenzilate: a high affinity, high specific activity radioligand for the M1 and M2-acetylcholine receptors. (medscape.com)
  • Fusek J, Dlabkova A, Misik J. Psychotomimetic Agent BZ (3-Quinuclidinyl Benzilate). (medscape.com)
  • Psychodelic Agent 3 - Quinuclidinyl Benzilate (BZ). (medscape.com)