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Journal articles on the topic 'M1 mAChRs'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Dasari, Sameera, and Allan T. Gulledge. "M1 and M4 Receptors Modulate Hippocampal Pyramidal Neurons." Journal of Neurophysiology 105, no. 2 (2011): 779–92. http://dx.doi.org/10.1152/jn.00686.2010.

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Acetylcholine (ACh), acting at muscarinic ACh receptors (mAChRs), modulates the excitability and synaptic connectivity of hippocampal pyramidal neurons. CA1 pyramidal neurons respond to transient (“phasic”) mAChR activation with biphasic responses in which inhibition is followed by excitation, whereas prolonged (“tonic”) mAChR activation increases CA1 neuron excitability. Both phasic and tonic mAChR activation excites pyramidal neurons in the CA3 region, yet ACh suppresses glutamate release at the CA3-to-CA1 synapse (the Schaffer–collateral pathway). Using mice genetically lacking specific mAC

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2

Kullmann, F. Aura, D. Artim, J. Beckel, S. Barrick, W. C. de Groat, and L. A. Birder. "Heterogeneity of muscarinic receptor-mediated Ca2+ responses in cultured urothelial cells from rat." American Journal of Physiology-Renal Physiology 294, no. 4 (2008): F971—F981. http://dx.doi.org/10.1152/ajprenal.00313.2007.

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Muscarinic receptors (mAChRs) have been identified in the urothelium, a tissue that may be involved in bladder sensory mechanisms. This study investigates the expression and function of mAChRs using cultured urothelial cells from the rat. RT-PCR established the expression of all five mAChR subtypes. Muscarinic agonists acetylcholine (ACh; 10 μM), muscarine (Musc; 20 μM), and oxotremorine methiodide (OxoM; 0.001–20 μM) elicited transient repeatable increases in the intracellular calcium concentration ([Ca2+]i) in ∼50% of cells. These effects were blocked by the mAChR antagonist atropine methyl

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Kohlmeier, Kristi A., Masaru Ishibashi, Jürgen Wess, Martha E. Bickford, and Christopher S. Leonard. "Knockouts reveal overlapping functions of M2 and M4 muscarinic receptors and evidence for a local glutamatergic circuit within the laterodorsal tegmental nucleus." Journal of Neurophysiology 108, no. 10 (2012): 2751–66. http://dx.doi.org/10.1152/jn.01120.2011.

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Cholinergic neurons in the laterodorsal tegmental (LDT) and peduncolopontine tegmental (PPT) nuclei regulate reward, arousal, and sensory gating via major projections to midbrain dopamine regions, the thalamus, and pontine targets. Muscarinic acetylcholine receptors (mAChRs) on LDT neurons produce a membrane hyperpolarization and inhibit spike-evoked Ca2+ transients. Pharmacological studies suggest M2 mAChRs are involved, but the role of these and other localized mAChRs (M1--M4) has not been definitively tested. To identify the underlying receptors and to circumvent the limited receptor select

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Zlatopolskiy, Boris D., Felix Neumaier, Till Rüngeler, Birte Drewes, Niklas Kolks, and Bernd Neumaier. "Preparation of a First 18F-Labeled Agonist for M1 Muscarinic Acetylcholine Receptors." Molecules 25, no. 12 (2020): 2880. http://dx.doi.org/10.3390/molecules25122880.

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M1 muscarinic acetylcholine receptors (mAChRs) are abundant in postsynaptic nerve terminals of all forebrain regions and have been implicated in the cognitive decline associated with Alzheimer’s disease and other CNS pathologies. Consequently, major efforts have been spent in the development of subtype-selective positron emission tomography (PET) tracers for mAChRs resulting in the development of several 11C-labeled probes. However, protocols for the preparation of 18F-labeled mAChR-ligands have not been published so far. Here, we describe a straightforward procedure for the preparation of an

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5

Smith, Richard S., and Ricardo C. Araneda. "Cholinergic Modulation of Neuronal Excitability in the Accessory Olfactory Bulb." Journal of Neurophysiology 104, no. 6 (2010): 2963–74. http://dx.doi.org/10.1152/jn.00446.2010.

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The accessory olfactory bulb (AOB), the first relay of chemosensory information in the Vomeronasal system, receives extensive cholinergic innervation from the basal forebrain. Cholinergic modulation of neuronal activity in the olfactory bulb has been hypothesized to play an important role in olfactory processing; however, little is known about the cellular actions of acetylcholine (ACh) within the AOB. Here using in vitro slice preparation, we show that muscarinic acetylcholine receptor (mAChR) activation increases neuronal excitability of granule and mitral/tufted cells (GCs and MCs) in the A

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6

Maeda, Shoji, Jun Xu, Francois Marie N. Kadji, et al. "Structure and selectivity engineering of the M1 muscarinic receptor toxin complex." Science 369, no. 6500 (2020): 161–67. http://dx.doi.org/10.1126/science.aax2517.

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Muscarinic toxins (MTs) are natural toxins produced by mamba snakes that primarily bind to muscarinic acetylcholine receptors (MAChRs) and modulate their function. Despite their similar primary and tertiary structures, MTs show distinct binding selectivity toward different MAChRs. The molecular details of how MTs distinguish MAChRs are not well understood. Here, we present the crystal structure of M1AChR in complex with MT7, a subtype-selective anti-M1AChR snake venom toxin. The structure reveals the molecular basis of the extreme subtype specificity of MT7 for M1AChR and the mechanism by whic

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7

Yang, Danqing, Robert Günter, Guanxiao Qi, Gabriele Radnikow, and Dirk Feldmeyer. "Muscarinic and Nicotinic Modulation of Neocortical Layer 6A Synaptic Microcircuits Is Cooperative and Cell-Specific." Cerebral Cortex 30, no. 6 (2019): 3528–42. http://dx.doi.org/10.1093/cercor/bhz324.

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Abstract Acetylcholine (ACh) is known to regulate cortical activity during different behavioral states, for example, wakefulness and attention. Here we show a differential expression of muscarinic ACh receptors (mAChRs) and nicotinic ACh receptors (nAChRs) in different layer 6A (L6A) pyramidal cell (PC) types of somatosensory cortex. At low concentrations, ACh induced a persistent hyperpolarization in corticocortical (CC) but a depolarization in corticothalamic (CT) L6A PCs via M 4 and M1 mAChRs, respectively. At ~ 1 mM, ACh depolarized exclusively CT PCs via α4β2 subunit-containing nAChRs wit

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8

van Koppen, C. J. "Multiple pathways for the dynamin-regulated internalization of muscarinic acetylcholine receptors." Biochemical Society Transactions 29, no. 4 (2001): 505–8. http://dx.doi.org/10.1042/bst0290505.

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An important regulatory pathway of G-protein-coupled receptors (GPCRs) is the internalization of receptors into the cell interior. To unravel the molecular mechanisms by which GPCRs are internalized, we have studied the internalization of various members of the family of muscarinic acetylcholine receptors (mAChRs). Using the transient expression system of HEK-293 cells, we showed that the M1, M3 and M4 mAChRs are internalized into clathrin-coated vesicles and recycle back to the plasma membrane. This internalization pathway is dependent on the concerted action of β-arrestin, c-Src and the GTPa

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9

Yang, Jyh-Jeen, Yu-Ting Wang, Pi-Cheng Cheng, Yeh-Jung Kuo, and Rong-Chi Huang. "Cholinergic Modulation of Neuronal Excitability in the Rat Suprachiasmatic Nucleus." Journal of Neurophysiology 103, no. 3 (2010): 1397–409. http://dx.doi.org/10.1152/jn.00877.2009.

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The central cholinergic system regulates both the circadian clock and sleep-wake cycle and may participate in the feedback control of vigilance states on neural excitability in the suprachiasmatic nucleus (SCN) that houses the circadian clock. Here we investigate the mechanisms for cholinergic modulation of SCN neuron excitability. Cell-attached recordings indicate that the nonspecific cholinergic agonist carbachol (CCh) inhibited 55% and excited 21% SCN neurons, leaving 24% nonresponsive. Similar response proportions were produced by two muscarinic receptor [muscarinic acetylcholine receptor

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10

Yang, Qing, Andrew D. Sumner, Henry L. Puhl, and Victor Ruiz-Velasco. "M1 and M2 Muscarinic Acetylcholine Receptor Subtypes Mediate Ca2+ Channel Current Inhibition in Rat Sympathetic Stellate Ganglion Neurons." Journal of Neurophysiology 96, no. 5 (2006): 2479–87. http://dx.doi.org/10.1152/jn.00093.2006.

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Muscarinic acetylcholine receptors (mAChRs) are known to mediate the acetylcholine inhibition of Ca2+ channels in central and peripheral neurons. Stellate ganglion (SG) neurons provide the main sympathetic input to the heart and contribute to the regulation of heart rate and myocardial contractility. Little information is available regarding mAChR regulation of Ca2+ channels in SG neurons. The purpose of this study was to identify the mAChR subtypes that modulate Ca2+ channel currents in rat SG neurons innervating heart muscle. Accordingly, the modulation of Ca2+ channel currents by the muscar

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11

Ozenil, Marius, Jonas Aronow, Daniela Piljak, et al. "Synthesis, Biological, and Computational Evaluation of Antagonistic, Chiral Hydrobenzoin Esters of Arecaidine Targeting mAChR M1." Pharmaceuticals 13, no. 12 (2020): 437. http://dx.doi.org/10.3390/ph13120437.

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Muscarinic acetylcholine receptors (mAChRs) are a pivotal constituent of the central and peripheral nervous system. Yet, therapeutic and diagnostic applications thereof are hampered by the lack of subtype selective ligands. Within this work, we synthesized and chemically characterized three different stereoisomers of hydrobenzoin esters of arecaidine by NMR, HR-MS, chiral chromatography, and HPLC-logP. All compounds are structurally eligible for carbon-11 labeling and show appropriate stability in Dulbecco’s phosphate-buffered saline (DPBS) and F12 cell culture medium. A competitive radioligan

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12

McCoy, Portia, Thomas T. Norton, and Lori L. McMahon. "Layer 2/3 Synapses in Monocular and Binocular Regions of Tree Shrew Visual Cortex Express mAChR-Dependent Long-Term Depression and Long-Term Potentiation." Journal of Neurophysiology 100, no. 1 (2008): 336–45. http://dx.doi.org/10.1152/jn.01134.2007.

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Acetylcholine is an important modulator of synaptic efficacy and is required for learning and memory tasks involving the visual cortex. In rodent visual cortex, activation of muscarinic acetylcholine receptors (mAChRs) induces a persistent long-term depression (LTD) of transmission at synapses recorded in layer 2/3 of acute slices. Although the rodent studies expand our knowledge of how the cholinergic system modulates synaptic function underlying learning and memory, they are not easily extrapolated to more complex visual systems. Here we used tree shrews for their similarities to primates, i

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13

Ma, Lei, Matthew A. Seager, Marion Wittmann, et al. "Selective activation of the M1 muscarinic acetylcholine receptor achieved by allosteric potentiation." Proceedings of the National Academy of Sciences 106, no. 37 (2009): 15950–55. http://dx.doi.org/10.1073/pnas.0900903106.

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The forebrain cholinergic system promotes higher brain function in part by signaling through the M1 muscarinic acetylcholine receptor (mAChR). During Alzheimer's disease (AD), these cholinergic neurons degenerate, therefore selectively activating M1 receptors could improve cognitive function in these patients while avoiding unwanted peripheral responses associated with non-selective muscarinic agonists. We describe here benzyl quinolone carboxylic acid (BQCA), a highly selective allosteric potentiator of the M1 mAChR. BQCA reduces the concentration of ACh required to activate M1 up to 129-fold

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14

Mallios, V. J., R. Lydic, and H. A. Baghdoyan. "Muscarinic receptor subtypes are differentially distributed across brain stem respiratory nuclei." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 6 (1995): L941—L949. http://dx.doi.org/10.1152/ajplung.1995.268.6.l941.

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Cholinergic mechanisms are known to play a key role in the regulation of breathing, but the distribution of muscarinic receptor (mAChR) subtypes has not been localized within brain stem respiratory nuclei. This study examined the hypothesis that mAChR subtypes are heterogeneously distributed across brain stem nuclei that control breathing. With the use of in vitro receptor autoradiography, the results provide the first selective labeling and quantitative mapping of M1, M2, and M3 mAChR subtypes in cat brain stem regions known to regulate breathing. Among brain stem nuclei known to contain resp

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15

Ogura, Tatsuya, Steven A. Szebenyi, Kurt Krosnowski, Aaron Sathyanesan, Jacqueline Jackson, and Weihong Lin. "Cholinergic microvillous cells in the mouse main olfactory epithelium and effect of acetylcholine on olfactory sensory neurons and supporting cells." Journal of Neurophysiology 106, no. 3 (2011): 1274–87. http://dx.doi.org/10.1152/jn.00186.2011.

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The mammalian olfactory epithelium is made up of ciliated olfactory sensory neurons (OSNs), supporting cells, basal cells, and microvillous cells. Previously, we reported that a population of nonneuronal microvillous cells expresses transient receptor potential channel M5 (TRPM5). Using transgenic mice and immunocytochemical labeling, we identify that these cells are cholinergic, expressing the signature markers of choline acetyltransferase (ChAT) and the vesicular acetylcholine transporter. This result suggests that acetylcholine (ACh) can be synthesized and released locally to modulate activ

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16

Mohamadi, Ali, Marco Martari, Cindy D. Holladay, John A. Phillips, Primus E. Mullis, and Roberto Salvatori. "Mutation Analysis of the Muscarinic Cholinergic Receptor Genes in Isolated Growth Hormone Deficiency Type IB." Journal of Clinical Endocrinology & Metabolism 94, no. 7 (2009): 2565–70. http://dx.doi.org/10.1210/jc.2009-0512.

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Background: Isolated GH deficiency (IGHD) is familial in 5–30% of patients. The most frequent form (IGHD-IB) has autosomal recessive inheritance, and it is known that it can be caused by mutations in the GHRH receptor (GHRHR) gene or in the GH gene. However, most forms of IGHD-IB have an unknown genetic cause. In normal subjects, muscarinic cholinergic stimulation causes an increase in pituitary GH release, whereas its blockade has the opposite effect, suggesting that a muscarinic acetylcholine receptor (mAchR) is involved in stimulating GH secretion. Five types of mAchR (M1–M5) exist. A trans

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17

Fukushima, Kazuyuki, Kazuto Yamazaki, Norimasa Miyamoto, and Kohei Sawada. "Functional Characterization of Acetylcholine Receptors Expressed in Human Neurons Differentiated from Hippocampal Neural Stem/Progenitor Cells." Journal of Biomolecular Screening 21, no. 10 (2016): 1065–74. http://dx.doi.org/10.1177/1087057116665567.

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Neurotransmission mediated by acetylcholine receptors (AChRs) plays an important role in learning and memory functions in the hippocampus. Impairment of the cholinergic system contributes to Alzheimer’s disease (AD), indicating the importance of AChRs as drug targets for AD. To improve the success rates for AD drug development, human cell models that mimic the target brain region are important. Therefore, we characterized the functional expression of nicotinic and muscarinic AChRs (nAChRs and mAChRs, respectively) in human hippocampal neurons differentiated from hippocampal neural stem/progeni

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18

von der Kammer, Heinz, Cüneyt Demiralay, Barbara Andresen, Claudia Albrecht, Manuel Mayhaus, and Roger M. Nitsch. "Regulation of gene expression by muscarinic acetylcholine receptors." Biochemical Society Symposia 67 (February 1, 2001): 131–40. http://dx.doi.org/10.1042/bss0670131.

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In the brain, muscarinic acetylcholine receptors (mAChRs) are involved in higher cognitive functions including synaptic plasticity and memory. In Alzheimer's disease (AD) patients the cholinergic nervous system is severely damaged. In order to reinforce the cholinergic system, clinical tests were started to use cholinomimetic drugs to treat AD patients. To identify the genes involved in mAChR signalling, we used a differential display approach and found 11 genes that were readily activated by mAChR with 1 hour of activation. These included the transcription factors Egr-1, Egr-2, Egr-3, c-Jun,

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19

Mans, Robert Alan, Brian A. Warmus, Caroline C. Smith, and Lori L. McMahon. "An acetylcholinesterase inhibitor, eserine, induces long-term depression at CA3-CA1 synapses in the hippocampus of adult rats." Journal of Neurophysiology 112, no. 10 (2014): 2388–97. http://dx.doi.org/10.1152/jn.00048.2014.

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Studies in humans and rodents support a role for muscarinic ACh receptor (mAChR) and nicotinic AChR in learning and memory, and both regulate hippocampal synaptic plasticity using complex and often times opposing mechanisms. Acetylcholinesterase (AChE) inhibitors are commonly prescribed to enhance cholinergic signaling in Alzheimer's disease in hopes of rescuing cognitive function, caused, in part, by degeneration of cholinergic innervation to the hippocampus and cortex. Unfortunately, therapeutic efficacy is moderate and inconsistent, perhaps due to unanticipated mechanisms. M1 mAChRs bidirec

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20

Capece, M. L., and R. Lydic. "cAMP and protein kinase A modulate cholinergic rapid eye movement sleep generation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 4 (1997): R1430—R1440. http://dx.doi.org/10.1152/ajpregu.1997.273.4.r1430.

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Cholinergic neurotransmission in the medial pontine reticular formation (mPRF) modulates rapid eye movement (REM) sleep generation. Microinjection of cholinergic agonists and acetylcholinesterase inhibitors into the mPRF induces a REM sleep-like state, and microdialysis data reveal increased mPRF levels of acetylcholine during REM sleep. Muscarinic cholinergic receptors (mAChRs) participate in REM sleep generation, and data suggest that mAChRs of a non-M1 subtype modulate REM sleep generation. The signal transduction pathway activated by m2 and m4 mAChRs involves a pertussis toxin-sensitive G

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Ma, Ke, Zhi-Hui Yang, Li-Min Yang, Hong-Zhuan Chen, and Yang Lu. "Activation of M1 mAChRs by lesatropane rescues glutamate neurotoxicity in PC12 cells via PKC-mediated phosphorylation of ERK1/2." Bosnian Journal of Basic Medical Sciences 13, no. 3 (2013): 146. http://dx.doi.org/10.17305/bjbms.2013.2346.

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22

Miao, Yinglong, Dahlia Anne Goldfeld, Ee Von Moo, et al. "Accelerated structure-based design of chemically diverse allosteric modulators of a muscarinic G protein-coupled receptor." Proceedings of the National Academy of Sciences 113, no. 38 (2016): E5675—E5684. http://dx.doi.org/10.1073/pnas.1612353113.

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Design of ligands that provide receptor selectivity has emerged as a new paradigm for drug discovery of G protein-coupled receptors, and may, for certain families of receptors, only be achieved via identification of chemically diverse allosteric modulators. Here, the extracellular vestibule of the M2 muscarinic acetylcholine receptor (mAChR) is targeted for structure-based design of allosteric modulators. Accelerated molecular dynamics (aMD) simulations were performed to construct structural ensembles that account for the receptor flexibility. Compounds obtained from the National Cancer Instit

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Smith, Emery, Peter Chase, Colleen M. Niswender, et al. "Application of Parallel Multiparametric Cell-Based FLIPR Detection Assays for the Identification of Modulators of the Muscarinic Acetylcholine Receptor 4 (M4)." Journal of Biomolecular Screening 20, no. 7 (2015): 858–68. http://dx.doi.org/10.1177/1087057115581770.

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Muscarinic acetylcholine receptors (mAChRs) have long been viewed as viable targets for novel therapeutic agents for the treatment of Alzheimer’s disease and other disorders involving impaired cognitive function. In an attempt to identify orthosteric and allosteric modulators of the muscarinic acetylcholine receptor M4 (M4), we developed a homogenous, multiparametric, 1536-well assay to measure M4 receptor agonism, positive allosteric modulation (PAM), and antagonism in a single well. This assay yielded a Z′ of 0.85 ± 0.05 in the agonist, 0.72 ± 0.07 in PAM, and 0.80 ± 0.06 in the antagonist m

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Strang, Christianne E., Ye Long, Konstantin E. Gavrikov, Franklin R. Amthor, and Kent T. Keyser. "Nicotinic and muscarinic acetylcholine receptors shape ganglion cell response properties." Journal of Neurophysiology 113, no. 1 (2015): 203–17. http://dx.doi.org/10.1152/jn.00405.2014.

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The purpose of this study was to evaluate the expression patterns of nicotinic and muscarinic ACh receptors (nAChRs and mAChRs, respectively) in relation to one another and to understand their effects on rabbit retinal ganglion cell response properties. Double-label immunohistochemistry revealed labeled inner-retinal cell bodies and complex patterns of nAChR and mAChR expression in the inner plexiform layer. Specifically, the expression patterns of m1, m4, and m5 muscarinic receptors overlapped with those of non-α7 and α7 nicotinic receptors in presumptive amacrine and ganglion cells. There wa

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Siregar, Petrus, Gilbert Audira, Ling-Yi Feng, et al. "Pharmaceutical Assessment Suggests Locomotion Hyperactivity in Zebrafish Triggered by Arecoline Might Be Associated with Multiple Muscarinic Acetylcholine Receptors Activation." Toxins 13, no. 4 (2021): 259. http://dx.doi.org/10.3390/toxins13040259.

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Arecoline is one of the nicotinic acid-based alkaloids, which is found in the betel nut. In addition to its function as a muscarinic agonist, arecoline exhibits several adverse effects, such as inducing growth retardation and causing developmental defects in animal embryos, including zebrafish, chicken, and mice. In this study, we aimed to study the potential adverse effects of waterborne arecoline exposure on zebrafish larvae locomotor activity and investigate the possible mechanism of the arecoline effects in zebrafish behavior. The zebrafish behavior analysis, together with molecular dockin

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Marshall-Gradisnik, Sonya, Peter Smith, Bernd Nilius, and Donald R. Staines. "Examination of Single Nucleotide Polymorphisms in Acetylcholine Receptors in Chronic Fatigue Syndrome Patients." Immunology and Immunogenetics Insights 7 (January 2015): III.S25105. http://dx.doi.org/10.4137/iii.s25105.

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Objective Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a disorder characterized by debilitating fatigue accompanied by pain and impairments in memory, cognition, and concentration. Acetylcholine (ACh) has a plethora of roles in neuronal and neuromuscular transmission. There are two types of ACh receptors, muscarinic and nicotinic, comprising 17 different subunits of the nicotinic ACh receptor (nAChR) and five different subtypes of the muscarinic receptor (mAChR) that have been identified in humans. The purpose of this study was to determine the role of ACh receptor (nAChRs an

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McCutchen, Eve, Cary L. Scheiderer, Lynn E. Dobrunz, and Lori L. McMahon. "Coexistence of Muscarinic Long-Term Depression With Electrically Induced Long-Term Potentiation and Depression at CA3–CA1 Synapses." Journal of Neurophysiology 96, no. 6 (2006): 3114–21. http://dx.doi.org/10.1152/jn.00144.2006.

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Our laboratory recently characterized a form of long-term depression (LTD) at CA3–CA1 synapses mediated by M1 muscarinic receptors (mAChRs), termed muscarinic LTD (mLTD). mLTD is both activity and NMDAR dependent, characteristics shared by forms of synaptic plasticity thought to be relevant to learning and memory, including long-term potentiation (LTP) induced by high-frequency stimulation (HFS-LTP) and long-term depression induced by low-frequency stimulation (LFS-LTD). However, it remains unclear whether mLTD can occur sequentially with these electrically induced forms of hippocampal plastic

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Lee, Choongheon, J. Chris Holt, and Timothy A. Jones. "Effect of M-current modulation on mammalian vestibular responses to transient head motion." Journal of Neurophysiology 118, no. 6 (2017): 2991–3006. http://dx.doi.org/10.1152/jn.00384.2017.

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The precise role and mechanisms underlying efferent modulation of peripheral vestibular afferent function are not well understood in mammals. Clarifying the details of efferent action may lead to new strategies for clinical management of debilitating disturbances in vestibular and balance function. Recent evidence in turtle indicates that efferent modulation of M-currents is likely one mechanism for modifying afferent discharge. M-currents depend in part on KCNQ potassium conductances (Kv7), which can be adjusted through efferent activation of M1, M3, and/or M5 muscarinic acetylcholine recepto

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González-García, B., ME Olave, E. Ramos-Martínez, C. González-Horta, M. Levario-Carrillo, and B. Sánchez-Ramírez. "Decrease of muscarinic cholinergic receptors expression in placenta from rats exposed to methyl parathion." Human & Experimental Toxicology 27, no. 3 (2008): 241–46. http://dx.doi.org/10.1177/0960327108091863.

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Placental transfer of methyl parathion (MP), an organophosphate pesticide, could involve effects on cholinergic system. To analyze whether placental cholinergic system is altered by prenatal exposure to MP, expression of muscarinic cholinergic receptors (M1 and M2 subtypes; mAChR) was determined in pregnant rats exposed to MP at 0.0, 1.0, 1.5, and 2.0 mg/kg. An immunohistochemical analysis for M1 and M2 mAChR was performed, and the density of the mAChR signal was measured by image analysis. M1 and M2 mAChR were found in the trophoblast present in the labyrinth, with an 18% predominance of M2 o

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Reina, S., L. Sterin-Borda, B. Orman, and E. Borda. "Autoantibodies against Submandibular Gland Muscarinic Cholinoceptor Subtypes in Primary Sjögren Syndrome." European Journal of Inflammation 3, no. 3 (2005): 135–41. http://dx.doi.org/10.1177/1721727x0500300305.

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Sjögren Syndrome (SS) is a chronic autoimmune disease characterized by parasympathetic exocrine gland dysfunction. Here, the involvement of submandibular gland muscarinic acetylcholine receptor (mAChR) M4 subtype is proposed as an IgG target together with M1 and M3 mAChR subtypes. The Kd values were total membranes 0.20 ± 0.017 nM; acini membranes 0.33 ± 0.023 nM and duct membranes 0.22 ± 0.040 nM and Bmax values were total, 1038 ± 24, acini, 1359 ± 28 and ducts, 593 ± 30. The rank order of Bmax was: acini > total > ducts, indicating that acini express the highest number of binding sites

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Nissen, Christoph, Ann E. Power, Eric A. Nofzinger, et al. "M1 Muscarinic Acetylcholine Receptor Agonism Alters Sleep without Affecting Memory Consolidation." Journal of Cognitive Neuroscience 18, no. 11 (2006): 1799–807. http://dx.doi.org/10.1162/jocn.2006.18.11.1799.

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Preclinical studies have implicated cholinergic neurotransmission, specifically M1 muscarinic acetylcholine receptor (mAChR) activation, in sleep-associated memory consolidation. In the present study, we investigated the effects of administering the direct M1 mAChR agonist RS-86 on pre-post sleep memory consolidation. Twenty healthy human participants were tested in a declarative word-list task and a procedural mirror-tracing task. RS-86 significantly reduced rapid eye movement (REM) sleep latency and slow wave sleep (SWS) duration in comparison with placebo. Presleep acquisition and postsleep

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Shmuel, Miriam, Efrat Nodel-Berner, Tehila Hyman, Alexander Rouvinski, and Yoram Altschuler. "Caveolin 2 Regulates Endocytosis and Trafficking of the M1 Muscarinic Receptor in MDCK Epithelial Cells." Molecular Biology of the Cell 18, no. 5 (2007): 1570–85. http://dx.doi.org/10.1091/mbc.e06-07-0618.

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Clathrin and caveolins are known for their involvement in the internalization of numerous receptors. Here we show that in polarized epithelial Madin-Darby canine kidney cells, both the clathrin machinery and caveolins are involved in the endocytosis and delivery to the plasma membrane (PM) of the M1 muscarinic acetylcholine receptor (mAChR). We initially localized this receptor to the lateral membrane, where it accumulates proximal to the tight junctions. From there it is internalized through the clathrin-mediated pathway. In addition, the receptor may associate on the PM with caveolin (cav) 2

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Elhusseiny, Ahmed, Zvi Cohen, André Olivier, Danica B. Stanimirović, and Edith Hamel. "Functional Acetylcholine Muscarinic Receptor Subtypes in Human Brain Microcirculation: Identification and Cellular Localization." Journal of Cerebral Blood Flow & Metabolism 19, no. 7 (1999): 794–802. http://dx.doi.org/10.1097/00004647-199907000-00010.

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Acetylcholine is an important regulator of local cerebral blood flow. There is, however, limited information available on the possible sites of action of this neurotransmitter on brain intraparenchymal microvessels. In this study, a combination of molecular and functional approaches was used to identify which of the five muscarinic acetylcholine receptors (mAChR) are present in human brain microvessels and their intimately associated astroglial cells. Microvessel and capillary fractions isolated from human cerebral cortex were found by reverse transcriptase-polymerase chain reaction to express

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Michelle Lewis, L., Douglas Sheffler, Richard Williams, et al. "Synthesis and SAR of selective muscarinic acetylcholine receptor subtype 1 (M1 mAChR) antagonists." Bioorganic & Medicinal Chemistry Letters 18, no. 3 (2008): 885–90. http://dx.doi.org/10.1016/j.bmcl.2007.12.051.

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Sheffler, Douglas J., Christian Sevel, Uyen Le, et al. "Further exploration of M1 allosteric agonists: Subtle structural changes abolish M1 allosteric agonism and result in pan-mAChR orthosteric antagonism." Bioorganic & Medicinal Chemistry Letters 23, no. 1 (2013): 223–27. http://dx.doi.org/10.1016/j.bmcl.2012.10.132.

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Egamino, J., V. K. Sharma, J. Wojtczak, and S. S. Sheu. "M1 mAChR signaling in carbachol induced positive inotropy in cultured neonatal rat ventricular myocytes." Life Sciences 64, no. 6-7 (1999): 576. http://dx.doi.org/10.1016/s0024-3205(99)90507-6.

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Cyrillo, Joslaine Noely dos Santos Gonçalves, Maurício Mello de Alencar, Alexander George Razook, Maria Eugênia Zerlotti Mercadante, and Leopoldo Andrade de Figueiredo. "Modelagem e estimação de parâmetros genéticos e fenotípicos para pesos do nascimento à seleção (378 dias) de machos Nelore." Revista Brasileira de Zootecnia 33, no. 6 (2004): 1405–15. http://dx.doi.org/10.1590/s1516-35982004000600007.

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Parâmetros genéticos para pesos (17.942 observações), obtidos em intervalos de 60 dias, do nascimento ao momento da seleção (378 dias de idade), de 2.582 animais machos da raça Nelore, foram estimados em análises univariadas pelo método da máxima verossimilhança restrita. Os modelos de análise incluíram os efeitos fixos de grupo de contemporâneos, mês de nascimento, idade da mãe e idade na pesagem como covariável. Três modelos diferindo nos efeitos aleatórios foram testados: o modelo1 (M1) ajustou para os efeitos genéticos aditivos direto e materno e de ambiente permanente materno; no modelo 2

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Shen, J. B., B. Jiang, and A. J. Pappano. "M1 mAChR does not regulate L-type calcium current when carbachol increases ventricular myocyte contractions." Life Sciences 64, no. 6-7 (1999): 577. http://dx.doi.org/10.1016/s0024-3205(99)90509-x.

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Mou, Liping, and Darrell A. Jackson. "Transient Hypoxia Differentially Decreases GRK2 Protein Levels in CHO Cells Stably Expressing the m1 mAChR." Biochemical and Biophysical Research Communications 286, no. 5 (2001): 848–51. http://dx.doi.org/10.1006/bbrc.2001.5487.

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Jackson, Liping Mou and Darrell A. "Transient Hypoxia Differentially Decreases GRK2 Protein Levels in CHO Cells Stably Expressing the m1 mAChR." Biochemical and Biophysical Research Communications 288, no. 2 (2001): 489–90. http://dx.doi.org/10.1006/bbrc.2001.5771.

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Fujii, Seiji, Ginko Yamazoe, Masayuki Itoh, Yoshihiro Kubo, and Osamu Saitoh. "Spinophilin inhibits the binding of RGS8 to M1-mAChR but enhances the regulatory function of RGS8." Biochemical and Biophysical Research Communications 377, no. 1 (2008): 200–204. http://dx.doi.org/10.1016/j.bbrc.2008.09.096.

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Douglas, Christopher L., Helen A. Baghdoyan, and Ralph Lydic. "Postsynaptic Muscarinic M1 Receptors Activate Prefrontal Cortical EEG of C57BL/6J Mouse." Journal of Neurophysiology 88, no. 6 (2002): 3003–9. http://dx.doi.org/10.1152/jn.00318.2002.

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Recent pharmacological studies exploring the functional roles of muscarinic cholinergic receptor (mAChR) subtypes in prefrontal cortex of C57BL/6J (B6) mouse have provided evidence for a presynaptic M2 autoreceptor. The B6 mouse was chosen for these studies because it is a genetically well-characterized model that also provides the genomic background for many genetically modified mice. In addition to increasing ACh release, one functional consequence of pharmacologically blocking the cortical M2 autoreceptor is activation of the contralateral prefrontal cortical EEG. To date, the mechanisms th

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Yu, Ping, Wen-Pei Dong, Ya-Bin Tang, Hong-Zhuan Chen, Yong-Yao Cui, and Xiao-Lan Bian. "Huperzine A lowers intraocular pressure via the M3 mAChR and provides retinal neuroprotection via the M1 mAChR: a promising agent for the treatment of glaucoma." Annals of Translational Medicine 9, no. 4 (2021): 332. http://dx.doi.org/10.21037/atm-20-8093.

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Jörg, Manuela, Emma T. van der Westhuizen, Elham Khajehali, et al. "6-Phenylpyrimidin-4-ones as Positive Allosteric Modulators at the M1 mAChR: The Determinants of Allosteric Activity." ACS Chemical Neuroscience 10, no. 3 (2018): 1099–114. http://dx.doi.org/10.1021/acschemneuro.8b00613.

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Vasconcellos, Leonardo de Souza, Luiz Ronaldo Alberti, Juliana Ribeiro Romeiro, and Andy Petroianu. "Influência da icterícia colestática na variação ponderal em modelo experimental." Revista do Colégio Brasileiro de Cirurgiões 39, no. 6 (2012): 502–8. http://dx.doi.org/10.1590/s0100-69912012000600010.

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OBJETIVO: Avaliar a influência da icterícia colestática na variação ponderal. MÉTODOS: Foram utilizados 64 ratos adultos, distribuídos em seis grupos: F1 (n=6) - fêmeas normais, F2 (n=6) - fêmeas laparotomizadas, F3 (n=20) - fêmeas ictéricas, M1 (n=6) - machos normais, M2 (n=6) - machos laparotomizados, M3 (n=20) - machos ictéricos. A icterícia foi obtida com ligadura e secção do ducto biliopancreático. Os pesos dos animais foram registrados semanalmente, durante sete semanas. No 14º dia de experimento, dosaram-se as bilirrubinas séricas e os hormônios gonadais. Após a sétima semana, realizou-

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Bridges, Thomas M., J. Phillip Kennedy, Meredith J. Noetzel, et al. "Chemical lead optimization of a pan Gq mAChR M1, M3, M5 positive allosteric modulator (PAM) lead. Part II: Development of a potent and highly selective M1 PAM." Bioorganic & Medicinal Chemistry Letters 20, no. 6 (2010): 1972–75. http://dx.doi.org/10.1016/j.bmcl.2010.01.109.

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Kim, Beom Keun, Haong-Yen Phi Tran, Eun-Joo Shin, et al. "IL-6 attenuates trimethyltin-induced cognitive dysfunction via activation of JAK2/STAT3, M1 mAChR and ERK signaling network." Cellular Signalling 25, no. 6 (2013): 1348–60. http://dx.doi.org/10.1016/j.cellsig.2013.02.017.

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Sharma, Naveen, Eun-Joo Shin, Nam Hun Kim, et al. "Far-infrared Ray-mediated Antioxidant Potentials are Important for Attenuating Psychotoxic Disorders." Current Neuropharmacology 17, no. 10 (2019): 990–1002. http://dx.doi.org/10.2174/1570159x17666190228114318.

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Far-infrared ray (FIR) is an electromagnetic wave that produces various health benefits against pathophysiological conditions, such as diabetes mellitus, renocardiovascular disorders, stress, and depression etc. However, the therapeutic application on the FIR-mediated protective potentials remains to be further extended. To achieve better understanding on FIR-mediated therapeutic potentials, we summarized additional findings in the present study that exposure to FIR ameliorates stressful condition, memory impairments, drug dependence, and mitochondrial dysfunction in the central nervous system

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Yang, C. M., J. M. Farley, and T. M. Dwyer. "Muscarinic stimulation of submucosal glands in swine trachea." Journal of Applied Physiology 64, no. 1 (1988): 200–209. http://dx.doi.org/10.1152/jappl.1988.64.1.200.

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The properties of muscarinic acetylcholine receptors (mAChR) on tracheal explants and isolated submucosal gland cells were determined using [3H]quinuclidinyl benzilate ([3H]QNB) and N-[3H]methylscopolamine ([3H]NMS) as ligands. Analysis of competitive displacement of ([3H]NMS binding by pirenzepine demonstrated the presence of M1- (27 +/- 2%) and M2G- (73 +/- 2%) receptors on isolated tracheal submucosal gland cells (TSGC's) in control. Daily administration of diisopropylfluorophosphate (DFP) inhibited cholinesterase activity by greater than 95%. After 7 days of DFP treatment, [3H]QNB binding

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BERRA, ALEJANDRO, SABRINA GANZINELLI, MARIO SARAVIA, ENRI BORDA, and LEONOR STERIN-BORDA. "Inducible nitric oxide synthase subserves cholinergic vasodilation in retina." Visual Neuroscience 22, no. 3 (2005): 371–77. http://dx.doi.org/10.1017/s0952523805223118.

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In this paper, we investigate the role of muscarinic acetylcholine receptor (mAChR) activity in the regulation of inducible (i) nitric oxide synthase (iNOS) expression and activity. The signaling pathway involved is also examined. These experiments also provide a link between mAChR activation and the nitric oxide (NO)-dependent regulation of retinal vascular diameter. The diameter of the retinal vessels at a distance of 1 disc diameter from the center of the optic disc was measured in rats using digital retinal photography, and both iNOS-mRNA gene expression and NOS were specifically measured

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