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Готові списки джерел за темами / Nicotinic acetylcholine receptors α7 / Статті в журналах

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Статті в журналах з теми "Nicotinic acetylcholine receptors α7"

Автор: Grafiati

Опубліковано: 3 червня 2025

Оновлено: 31 липня 2025

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1

Lavezzi, Anna. "Toxic Effect of Cigarette Smoke on Brainstem Nicotinic Receptor Expression: Primary Cause of Sudden Unexplained Perinatal Death." Toxics 6, no. 4 (2018): 63. http://dx.doi.org/10.3390/toxics6040063.

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Among the neurotoxicants contained in tobacco smoke, if absorbed during pregnancy, nicotine significantly affects α7-nicotinic acetylcholine receptors, which play essential roles in the development of the brainstem regions receiving cholinergic projections in perinatal life. Immunohistochemical procedures for analysing formalin-fixed and paraffin-embedded brainstem samples from 68 fetuses and early newborns, with smoking and non-smoking mothers, who died of known and unknown causes, were carried out in order to determine if nicotine had activated the α7-nicotinic acetylcholine receptors. High

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2

Wongtrakool, Cherry, Susanne Roser-Page, Hilda N. Rivera та Jesse Roman. "Nicotine alters lung branching morphogenesis through the α7 nicotinic acetylcholine receptor". American Journal of Physiology-Lung Cellular and Molecular Physiology 293, № 3 (2007): L611—L618. http://dx.doi.org/10.1152/ajplung.00038.2007.

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There is abundant epidemiological data linking prenatal environmental tobacco smoke with childhood asthma and wheezing, but the underlying molecular and physiological mechanisms that occur in utero to explain this link remain unelucidated. Several studies suggest that nicotine, which traverses the placenta, is a causative agent. Therefore, we studied the effects of nicotine on lung branching morphogenesis using embryonic murine lung explants. We found that the expression of α7 nicotinic acetylcholine receptors, which mediate many of the biological effects of nicotine, is highest in pseudogland

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3

Beckel, Jonathan M., Anthony Kanai, Sun-Ju Lee, William C. de Groat, and Lori A. Birder. "Expression of functional nicotinic acetylcholine receptors in rat urinary bladder epithelial cells." American Journal of Physiology-Renal Physiology 290, no. 1 (2006): F103—F110. http://dx.doi.org/10.1152/ajprenal.00098.2005.

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Although nicotinic acetylcholine receptors in both the central and peripheral nervous systems play a prominent role in the control of urinary bladder function, little is known regarding expression or function of nicotinic receptors in the bladder epithelium, or urothelium. Nicotinic receptors have been described in epithelial cells lining the upper gastrointestinal tract, respiratory tract, and the skin. Thus the present study examined the expression and functionality of nicotinic receptors in the urothelium, as well as the effects of stimulation of nicotinic receptors on the micturition refle

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4

MANEU, VICTORIA, GUILLERMO GERONA, LAURA FERNÁNDEZ, NICOLÁS CUENCA, and PEDRO LAX. "Evidence of alpha 7 nicotinic acetylcholine receptor expression in retinal pigment epithelial cells." Visual Neuroscience 27, no. 5-6 (2010): 139–47. http://dx.doi.org/10.1017/s0952523810000246.

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AbstractSome evidence suggests that retinal pigment epithelium (RPE) can express nicotinic acetylcholine receptors (nAChRs) as described for other epithelial cells, where nAChRs have been involved in processes such as cell development, cell death, cell migration, and angiogenesis. This study is designed to determine the expression and activity of α7 nAChRs in RPE cells. Reverse transcriptase (RT)-PCR was performed to test the expression of nicotinic α7 subunit in bovine RPE cells. Protein expression was determined by Western blot and by immunocytochemistry. Expression of nicotinic α7 subunits

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5

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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6

Hawkins, Brian T., Richard D. Egleton, and Thomas P. Davis. "Modulation of cerebral microvascular permeability by endothelial nicotinic acetylcholine receptors." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (2005): H212—H219. http://dx.doi.org/10.1152/ajpheart.01210.2004.

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Nicotine increases the permeability of the blood-brain barrier in vivo. This implies a possible role for nicotinic acetylcholine receptors in the regulation of cerebral microvascular permeability. Expression of nicotinic acetylcholine receptor subunits in cerebral microvessels was investigated with immunofluorescence microscopy. Positive immunoreactivity was found for receptor subunits α3, α5, α7, and β2, but not subunits α4, β3, or β4. Blood-brain barrier permeability was assessed via in situ brain perfusion with [14C]sucrose. Nicotine increased the rate of sucrose entry into the brain from 0

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7

Panchal, Jayharsh L. "Dual Signaling Modes of Alpha7 Nicotinic Acetylcholine Receptors (α7 nAChRs)". Annals of Experimental and Molecular Biology 1, № 1 (2018): 1–2. http://dx.doi.org/10.23880/aemb-16000102.

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This themed section of the Annals of Experimental and Molecular Biology is the product of an article that is focusing on metabotropic signaling of an ionotropic channel alpha7 nicotinic ACh receptors (α7 nAChRs). The article talks about how α7 nAChR, being an ion channel, can function in a metabotropic-signaling mode via Gprotein coupling followed by Gαq-PLC-IP3-Ca2+ release

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8

Christophe, Elodie, Aline Roebuck, Jochen F. Staiger, Daniel J. Lavery, Serge Charpak, and Etienne Audinat. "Two Types of Nicotinic Receptors Mediate an Excitation of Neocortical Layer I Interneurons." Journal of Neurophysiology 88, no. 3 (2002): 1318–27. http://dx.doi.org/10.1152/jn.2002.88.3.1318.

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Nicotinic acetylcholine receptors are widely expressed in the neocortex but their functional roles remain largely unknown. Here we investigated the effect of nicotinic receptor activation on interneurons of layer I, which contains a high density of cholinergic fiber terminals. Ninety-seven of 101 neurons recorded in whole cell configuration in rat acute slices were excited by local pressure application of nicotinic agonists, acetylcholine (500 μM), 1,1-dimethyl-4-phenyl-piperazinium (500 μM) or choline (10 mM). Biocytin labeling confirmed that our sample included different morphological types

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9

Pinheiro, Nathalia M., Rosana Banzato, Iolanda Tibério та ін. "Acute Lung Injury in Cholinergic-Deficient Mice Supports Anti-Inflammatory Role of α7 Nicotinic Acetylcholine Receptor". International Journal of Molecular Sciences 22, № 14 (2021): 7552. http://dx.doi.org/10.3390/ijms22147552.

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(1) Background: The lung cholinergic pathway is important for controlling pulmonary inflammation in acute lung injury, a condition that is characterized by a sudden onset and intense inflammation. This study investigated changes in the expression levels of nicotinic and muscarinic acetylcholine receptors (nAChR and mAChR) in the lung during acute lung injury. (2) Methods: acute lung injury (ALI) was induced in wild-type and cholinergic-deficient (VAChT-KDHOM) mice using intratracheal lipopolysaccharide (LPS) instillation with or without concurrent treatment with nicotinic ligands. Bronchoalveo

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10

Montaño-Velázquez, B. B., D. A. Lara-Sánchez, A. Orozco-Sánchez, F. J. García-Vázquez, M. R. Mora-Campos та K. Jáuregui-Renaud. "Sex difference in counts of α4 and α7 nicotinic acetylcholine receptors in the nasal polyps of adults with or without exposure to tobacco smoke". Journal of Laryngology & Otology 132, № 7 (2018): 596–99. http://dx.doi.org/10.1017/s0022215118000373.

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AbstractObjectiveTo assess counts of α4 and α7 nicotinic acetylcholine receptors in nasal polyps of adults with or without long-term exposure to cigarette tobacco smoke.MethodsTwenty-two patients with and 22 patients without exposure to cigarette tobacco smoke participated in the study. After endoscopic polypectomy, the fragments of the nasal polyps were analysed by immunohistochemistry.ResultsCompared to patients with no exposure, patients with exposure showed higher counts of α4 and α7 nicotinic acetylcholine receptors (t-test, p < 0.05). However, in patients with no exposure, multivariat

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11

Garg, Brijesh K., та Ralph H. Loring. "Evaluating Commercially Available Antibodies for Rat α7 Nicotinic Acetylcholine Receptors". Journal of Histochemistry & Cytochemistry 65, № 9 (2017): 499–512. http://dx.doi.org/10.1369/0022155417725304.

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Alpha7 nicotinic acetylcholine receptors (α7 nAChRs) are important drug targets in neurological disorders and inflammation, making their detection and localization by validated antibodies highly desirable. However, tests in knockout animals raised questions about specificity of antibodies to mouse α7 nAChRs. To date, methods for validating antibodies for rat or human α7 nAChR have not been reported. We developed a gel-shift assay for western blots using GH4C1 cells expressing either native rat receptors or α7 nAChR-green fluorescent protein (GFP) chimeras to evaluate seven commercially availab

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12

Vallés, Ana S., та Francisco J. Barrantes. "Chaperoning α7 neuronal nicotinic acetylcholine receptors". Biochimica et Biophysica Acta (BBA) - Biomembranes 1818, № 3 (2012): 718–29. http://dx.doi.org/10.1016/j.bbamem.2011.10.012.

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13

Targowska-Duda, Katarzyna M., Barbara Budzynska, Agnieszka Michalak, Krzysztof Jozwiak, Grazyna Biala та Hugo R. Arias. "3-Furan-2-yl-N-p-tolyl-acrylamide, a highly selective positive allosteric modulator of α7 nicotinic receptors, produces anxiolytic-like activity in mice". Journal of Psychopharmacology 33, № 5 (2019): 558–67. http://dx.doi.org/10.1177/0269881118821100.

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Background: Several lines of investigations support the idea that nicotinic acetylcholine receptors modulate neuronal pathways involved in anxiety and depression. Aims: The purpose of this study was to determine whether 3-furan-2-yl-N-p-tolyl-acrylamide, a highly selective positive allosteric modulator of α7 nicotinic acetylcholine receptors, influences anxiety-like behaviour in mice, and to determine the modulatory activity of 3-furan-2-yl-N-p-tolyl-acrylamide on mice pretreated with either nicotine or selective α7-agonists (i.e. PNU-282987 or (2.4)-dimethoxybenzylidene anabaseine dihydrochlo

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14

Potasiewicz, Agnieszka, Joanna Golebiowska, Piotr Popik та Agnieszka Nikiforuk. "Procognitive effects of varenicline in the animal model of schizophrenia depend on α4β2- and α7-nicotinic acetylcholine receptors". Journal of Psychopharmacology 33, № 1 (2018): 62–73. http://dx.doi.org/10.1177/0269881118812097.

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Background: Varenicline, a partial agonist of the α4β2 nicotinic acetylcholine receptor (α4β2-nAChR), is currently used to facilitate smoking cessation. Preclinical and clinical studies have suggested that this compound may also be effective in treating cognitive impairments in schizophrenia. However, it is unclear which nicotinic acetylcholine receptor subtypes may be involved because varenicline is not only a partial agonist for α4β2-nAChRs but also a full agonist for α7 nicotinic acetylcholine receptors (α7-nAChRs). Aim: We investigated the effects of varenicline, compared to the α4β2-nAChR

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15

Strang, Christianne E., Margot E. Andison, Franklin R. Amthor та Kent T. Keyser. "Rabbit retinal ganglion cells express functional α7 nicotinic acetylcholine receptors". American Journal of Physiology-Cell Physiology 289, № 3 (2005): C644—C655. http://dx.doi.org/10.1152/ajpcell.00633.2004.

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It is well known that cholinergic agents affect ganglion cell (GC) firing rates and light responses in the retinas of many species, but the specific receptor subtypes involved in mediating these effects have been only partially characterized. We sought to determine whether functional α7 nicotinic acetylcholine receptors (nAChRs) contribute to the responses of specific retinal GC classes in rabbit retina. We used electrophysiology, pharmacology, immunohistochemistry, and reverse transcriptase-polymerase chain reaction to determine the pharmacological properties and expression of nAChR subtypes

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16

Papke, Roger L., та Nicole A. Horenstein. "Therapeutic Targeting of α7 Nicotinic Acetylcholine Receptors". Pharmacological Reviews 73, № 3 (2021): 1118–49. http://dx.doi.org/10.1124/pharmrev.120.000097.

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17

Bertrand, Daniel, Chih-Hung L. Lee, Dorothy Flood, Fabrice Marger та Diana Donnelly-Roberts. "Therapeutic Potential of α7 Nicotinic Acetylcholine Receptors". Pharmacological Reviews 67, № 4 (2015): 1025–73. http://dx.doi.org/10.1124/pr.113.008581.

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18

Ragab, Hanan M., Jin Sung Kim, Małgorzata Dukat, Hernán Navarro та Richard A. Glennon. "Aryloxyethylamines: Binding at α7 nicotinic acetylcholine receptors". Bioorganic & Medicinal Chemistry Letters 16, № 16 (2006): 4283–86. http://dx.doi.org/10.1016/j.bmcl.2006.05.080.

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19

Papke, Roger L., Marta Quadri та Alican Gulsevin. "Silent agonists for α7 nicotinic acetylcholine receptors". Pharmacological Research 190 (квітень 2023): 106736. http://dx.doi.org/10.1016/j.phrs.2023.106736.

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20

Liu, Qing-Song, та Darwin K. Berg. "Extracellular Calcium Regulates Responses of Both α3- and α7-Containing Nicotinic Receptors on Chick Ciliary Ganglion Neurons". Journal of Neurophysiology 82, № 3 (1999): 1124–32. http://dx.doi.org/10.1152/jn.1999.82.3.1124.

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Neuronal nicotinic receptors are generally both permeable to calcium and potentiated by it. We have examined acute calcium regulation of both native α7-containing and the less abundant α3-containing nicotinic receptors on chick ciliary ganglion neurons. Most of the receptors are concentrated on somatic spines tightly overlaid in situ by a large presynaptic calyx. Whole cell patch-clamp recording from dissociated neurons using perforated patch-clamp techniques indicates that the rapidly desensitizing nicotinic response of α7-containing receptors achieves maximum amplitude in 2 mM calcium; both

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21

Wang, JianGang, YaLi Wang, FangLi Guo, ZhiBo Feng, XiangFang Wang, and ChengBiao Lu. "Nicotinic modulation of Ca2+ oscillations in rat cortical neurons in vitro." American Journal of Physiology-Cell Physiology 310, no. 9 (2016): C748—C754. http://dx.doi.org/10.1152/ajpcell.00197.2015.

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The roles of nicotine on Ca2+ oscillations [intracellular Ca2+ ([Ca2+]i) oscillation] in rat primary cultured cortical neurons were studied. The spontaneous [Ca2+]i oscillations (SCO) were recorded in a portion of the neurons (65%) cultured for 7–10 days in vitro. Application of nicotine enhanced [Ca2+]i oscillation frequency and amplitude, which were reduced by the selective α4β2-nicotinic acetylcholine receptors (nAChRs) antagonist dihydro-β-erythroidine (DHβE) hydrobromide, and the selective α7-nAChRs antagonist methyllycaconitine citrate (MLA, 20 nM). DHβE reduced SCO frequency and prevent

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22

Fu, Wen, та Jack H. Jhamandas. "β-Amyloid Peptide Activates Non-α7 Nicotinic Acetylcholine Receptors in Rat Basal Forebrain Neurons". Journal of Neurophysiology 90, № 5 (2003): 3130–36. http://dx.doi.org/10.1152/jn.00616.2003.

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Alzheimer's disease (AD) is a progressive neurodegenerative condition characterized by profound deficits in memory and cognitive function. Neuropathological hallmarks of the disease include a loss of basal forebrain cholinergic neurons and the deposition of β-amyloid peptide (Aβ) in neuritic plaques. At a cellular level, considerable attention has focused on a study of Aβ interactions with the neuronal nicotinic acetylcholine receptor (nAChR) subtypes. In this study, using cell-attached and outside-out single channel recordings from acutely dissociated rat basal forebrain neurons, we report th

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23

Becker, Benjamin, Eva M. Klein, Nadine Striepens, et al. "Nicotinic Acetylcholine Receptors Contribute to Learning-induced Metaplasticity in the Hippocampus." Journal of Cognitive Neuroscience 25, no. 7 (2013): 986–97. http://dx.doi.org/10.1162/jocn_a_00383.

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Hippocampal learning is thought to induce metaplasticity, which can facilitate subsequent learning. Administered at single low doses, the N-methyl-d-aspartate-type glutamate receptor antagonist memantine predominantly blocks α7 nicotinic acetylcholine receptors (α7 nAChRs). Placebo-controlled administration of a single low dose of memantine in a pharmaco-fMRI experiment may thus help characterize the role of α7 nAChRs in hippocampal metaplasticity. We hypothesized that if α7 nAChRs contribute to learning-induced metaplasticity in the hippocampus, blockade of these receptors with low-dose meman

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24

Lang, P. M., R. Burgstahler, W. Sippel, D. Irnich, B. Schlotter-Weigel, and P. Grafe. "Characterization of Neuronal Nicotinic Acetylcholine Receptors in the Membrane of Unmyelinated Human C-Fiber Axons by In Vitro Studies." Journal of Neurophysiology 90, no. 5 (2003): 3295–303. http://dx.doi.org/10.1152/jn.00512.2003.

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Application of acetylcholine to peripheral nerve terminals in the skin is a widely used test in studies of human small-fiber functions. However, a detailed pharmacological profile and the subunit composition of nicotinic acetylcholine receptors in human C-fiber axons are not known. In the present study, we recorded acetylcholine-induced changes of the excitability and of the intracellular Ca2+ concentration in C-fiber axons of isolated human nerve segments. In addition, using immunohistochemistry, an antibody of a subtype of nicotinic acetylcholine receptor was tested. Acetylcholine and agonis

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25

Baxter, James C., Renuka Ramachandra, Dustin R. Mayne та Keith S. Elmslie. "Functional expression of α7-nicotinic acetylcholine receptors by muscle afferent neurons". Journal of Neurophysiology 112, № 6 (2014): 1549–58. http://dx.doi.org/10.1152/jn.00035.2014.

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The exercise pressor reflex (EPR) is generated by group III and IV muscle afferents during exercise to increase cardiovascular function. Muscle contraction is triggered by ACh, which is metabolized into choline that could serve as a signal of exercise-induced activity. We demonstrate that ACh can induce current in muscle afferents neurons isolated from male Sprague-Dawley rats. The nicotinic ACh receptors (nAChRs) appear to be expressed by some group III-IV neurons since capsaicin (TRPV1) and/or ATP (P2X) induced current in 56% of ACh-responsive neurons. α7- And α4β2-nAChRs have been shown to

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26

Lykhmus, O., M. Izmailov, and M. Skok. "Choline derivatives as natural ligands of mitochondrial nicotinic acetylcholine receptors." Ukrainian Biochemical Journal 95, no. 2 (2023): 24–32. http://dx.doi.org/10.15407/ubj95.02.024.

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Nicotinic acetylcholine receptors (nAChRs) regulate mitochondria-driven apoptosis; however, their intracellular ligands are unknown. In the present paper, we show that choline and its derivatives (phosphocholine (PC), L-α-glycerophosphocholine (G-PC) and 1-palmitoyl-sn-glycero-3-phosphocholine (P-GPC)) dose-dependently influence cytochrome c release from isolated mouse liver mitochondria. Choline inhibited Ca2+-stimulated cytochrome c release, while PC attenuated wortmannin-induced cytochrome c release. Small doses of G-PC and P-GPC (up to 0.1 µM) were protective against either Ca2+ or wortman

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27

Utkin, Yuri N. "Aging Affects Nicotinic Acetylcholine Receptors in Brain." Central Nervous System Agents in Medicinal Chemistry 19, no. 2 (2019): 119–24. http://dx.doi.org/10.2174/1871524919666190320102834.

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Background: Aging is a common and inevitable stage in the life cycle of higher organisms. Different organs, including the central nervous system, are affected by aging in different ways. Many processes are involved in aging, and neurodegeneration is one of the aging processes in which the central nervous system is engaged. Brain degeneration during normal aging underlies cognitive disorders experienced by older people. Not all molecular mechanisms associated with age-related neurodegeneration are fully understood; however, there is a whole range of data on the participation of nicotinic acetyl

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28

Schedel, Angelika, Sophia Thornton, Patrick Schloss, Harald Klüter та Peter Bugert. "Human Platelets Express Functional α7-Nicotinic Acetylcholine Receptors". Arteriosclerosis, Thrombosis, and Vascular Biology 31, № 4 (2011): 928–34. http://dx.doi.org/10.1161/atvbaha.110.218297.

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29

Svensson, T. H. "S.12.04 α7 Nicotinic acetylcholine receptors: Neuropsychopharmacological significance". European Neuropsychopharmacology 13 (жовтень 2003): S128—S129. http://dx.doi.org/10.1016/s0924-977x(03)91648-8.

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30

Zhang, Chuan-Li, Yakov Verbny, Sameh A. Malek, Peter K. Stys, and Shing Yan Chiu. "Nicotinic Acetylcholine Receptors in Mouse and Rat Optic Nerves." Journal of Neurophysiology 91, no. 2 (2004): 1025–35. http://dx.doi.org/10.1152/jn.00769.2003.

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Receptor-mediated calcium signaling in axons of mouse and rat optic nerves was examined by selectively staining the axonal population with a calcium indicator. Nicotine (1-50 μM) induced an axonal calcium elevation that was eliminated when calcium was removed from the bath, suggesting that nicotine induces calcium influx into axons. The nicotine response was blocked by d-tubocurarine and mecamylamine but not α-bungarotoxin, indicating the presence of calcium permeable, non-α7 nicotinic acetylcholine receptor (nAChR) subtype. Agonist efficacy order for eliciting the axonal nAChR calcium respons

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31

Utkin, Yuri N., Ilia Yu Cherepakhin, Elena V. Kryukova та ін. "Conjugates of α-Cobratoxin with CdSe Quantum Dots: Preparation and Biological Activity". Nano Hybrids and Composites 13 (січень 2017): 3–8. http://dx.doi.org/10.4028/www.scientific.net/nhc.13.3.

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α-Cobratoxin is the main neurotoxin in the cobra Naja kaouthia venom; it binds efficiently and selectively with neuronal α7 and muscle type nicotinic acetylcholine receptor and can be used for specific labeling and visualization of these receptors in organs and tissues. For these applications we have prepared conjugates of α-cobratoxin with CdSe quantum dots which have many benefits as compared to organic fluorescent labels. To prepare the conjugate, CdSe quantum dots with ZnS shell were functionalized using a tripeptide glutathione and coupled to toxin using water soluble carbodiimide. The co

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32

Fu, Xiao Wen, Stephen S. Rekow, and Eliot R. Spindel. "The ly-6 protein, lynx1, is an endogenous inhibitor of nicotinic signaling in airway epithelium." American Journal of Physiology-Lung Cellular and Molecular Physiology 303, no. 8 (2012): L661—L668. http://dx.doi.org/10.1152/ajplung.00075.2012.

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Our laboratory has previously reported that bronchial epithelial cells (BEC) express a regulatory cascade of classic neurotransmitters and receptors that communicate in an almost neuronal-like manner to achieve physiological regulation. In this paper we show that the similarity between neurotransmitter signaling in neurons and BEC extends to the level of transmitter receptor allosteric modulators. Lynx1 is a member of the ly-6/three-finger superfamily of proteins, many of which modulate receptor signaling activity. Lynx1 specifically has been shown to modulate nicotinic acetylcholine receptor

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Bueno, Renata V., Samuel Davis, Alice Dawson, Pauline W. Ondachi, F. Ivy Carroll, and William N. Hunter. "Interactions between 2′-fluoro-(carbamoylpyridinyl)deschloroepibatidine analogues and acetylcholine-binding protein inform on potent antagonist activity against nicotinic receptors." Acta Crystallographica Section D Structural Biology 78, no. 3 (2022): 353–62. http://dx.doi.org/10.1107/s2059798322000754.

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Low-nanomolar binding constants were recorded for a series of six 2′-fluoro-(carbamoylpyridinyl)deschloroepibatidine analogues with acetylcholine-binding protein (AChBP). The crystal structures of three complexes with AChBP reveal details of molecular recognition in the orthosteric binding site and imply how the other three ligands bind. Comparisons exploiting AChBP as a surrogate for α4β2 and α7 nicotinic acetylcholine receptors (nAChRs) suggest that the key interactions are conserved. The ligands interact with the same residues as the archetypal nAChR agonist nicotine yet display greater aff

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34

Mizrachi, Tehila, Adi Vaknin-Dembinsky, Talma Brenner та Millet Treinin. "Neuroinflammation Modulation via α7 Nicotinic Acetylcholine Receptor and Its Chaperone, RIC-3". Molecules 26, № 20 (2021): 6139. http://dx.doi.org/10.3390/molecules26206139.

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Nicotinic acetylcholine receptors (nAChRs) are widely expressed in or on various cell types and have diverse functions. In immune cells nAChRs regulate proliferation, differentiation and cytokine release. Specifically, activation of the α7 nAChR reduces inflammation as part of the cholinergic anti-inflammatory pathway. Here we review numerous effects of α7 nAChR activation on immune cell function and differentiation. Further, we also describe evidence implicating this receptor and its chaperone RIC-3 in diseases of the central nervous system and in neuroinflammation, focusing on multiple scler

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Huang, Y., C. Zhao, and X. Su. "Neuroimmune regulation of lung infection and inflammation." QJM: An International Journal of Medicine 112, no. 7 (2018): 483–87. http://dx.doi.org/10.1093/qjmed/hcy154.

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Abstract The distal airway of the lung is innervated by vagus nerve. Upon stimulation, vagus nerve endings release acetylcholine or neuropeptides via C-fiber afferents to regulate lung infection and immunity. Vagal sensory nerve endings, brain integration center, acetylcholine and α7 nicotinic acetylcholine receptor (nAChR) expressing cells are key components of pulmonary parasympathetic inflammatory reflex. Meanwhile, this local machinery synergizes with spleen (as a functional hub of cholinergic anti-inflammatory pathway) to finely tune recruitment of the splenic α7 nAChR+CD11b+ cells into t

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36

Alexandre, M., A. K. Uduman, S. Minervini, et al. "Tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone initiates and enhances pancreatitis responses." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 6 (2012): G696—G704. http://dx.doi.org/10.1152/ajpgi.00138.2012.

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Clinical studies indicate that cigarette smoking increases the risk for developing acute pancreatitis. The nicotine metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a major cigarette smoke toxin. We hypothesized that NNK could sensitize to pancreatitis and examined its effects in isolated rat pancreatic acini and in vivo. In acini, 100 nM NNK caused three- and fivefold activation of trypsinogen and chymotrypsinogen, respectively, above control. Furthermore, NNK pretreatment in acini enhanced zymogen activation in a cerulein pancreatitis model. The long-term effects of NNK wer

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37

Talka, Reeta, Outi Salminen, Paul Whiteaker, Ronald J. Lukas та Raimo K. Tuominen. "Nicotine–morphine interactions at α4β2, α7 and α3⁎ nicotinic acetylcholine receptors". European Journal of Pharmacology 701, № 1-3 (2013): 57–64. http://dx.doi.org/10.1016/j.ejphar.2013.01.005.

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38

Uteshev, Vladimir V., Edwin M. Meyer та Roger L. Papke. "Regulation of Neuronal Function by Choline and 4OH-GTS-21 Through α7 Nicotinic Receptors". Journal of Neurophysiology 89, № 4 (2003): 1797–806. http://dx.doi.org/10.1152/jn.00943.2002.

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A unique feature of α7 nicotinic acetylcholine receptor physiology is that, under normal physiological conditions, α7 receptors are constantly perfused with their natural selective agonist, choline. Studying neurons of hypothalamic tuberomammillary (TM) nucleus, we show that choline and the selective α7 receptor agonist 4OH-GTS-21 can regulate neuronal functions directly, via activation of the native α7 receptors, and indirectly, via desensitizing those receptors or transferring them into a state “primed” for desensitization. The direct action produces depolarization and thereby increases the

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39

Botticelli, Elisabetta, Claudia Guerriero, Sergio Fucile та ін. "α7 Nicotinic Acetylcholine Receptors May Improve Schwann Cell Regenerating Potential via Metabotropic Signaling Pathways". Cells 12, № 11 (2023): 1494. http://dx.doi.org/10.3390/cells12111494.

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Background: Schwann cells (SCs) are glial cells involved in peripheral axon myelination. SCs also play a strategic role after peripheral nerve injury, regulating local inflammation and axon regeneration. Our previous studies demonstrated the presence of cholinergic receptors in SCs. In particular, the α7 nicotinic acetylcholine receptors (nAChRs) are expressed in SCs after peripheral axotomy, suggesting their involvement in the regulation of SC-regenerating properties. To clarify the role that α7 nAChRs may play after peripheral axon damage, in this study we investigated the signal transductio

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40

Ho, Kenny K., та Pamela Flood. "Single Amino Acid Residue in the Extracellular Portion of Transmembrane Segment 2 in the Nicotinic α7 Acetylcholine Receptor Modulates Sensitivity to Ketamine". Anesthesiology 100, № 3 (2004): 657–62. http://dx.doi.org/10.1097/00000542-200403000-00028.

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Background Ketamine inhibits the activation of both heteromeric and homomeric nicotinic acetylcholine receptors. The site of molecular interaction is unknown. Methods The inhibition of alpha7 nicotinic acetylcholine receptors by ketamine was compared to that of 5-hydroxytryptamine-3A (5HT3A) receptors that are resistant to ketamine inhibition in Xenopus laevis oocytes. To determine whether the region of transmembrane segments 2 and 3 is relevant for ketamine inhibition of nicotinic receptors, the authors identified single amino acid residues that differ in the sequence alignment of the two pro

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41

Singh, Sushma, Neetu Agrawal, and Ahsas Goyal. "Role of Alpha-7-Nicotinic Acetylcholine Receptor in Alzheimer's Disease." CNS & Neurological Disorders - Drug Targets 23, no. 3 (2024): 384–94. http://dx.doi.org/10.2174/1871527322666230627123426.

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Abstract: Alzheimer's disease (AD) is a neurodegenerative disorder affecting millions worldwide. One of the leading hypotheses for the underlying cause of AD is a reduction in nicotinic receptor levels in the brain. Among the nicotinic receptors, the alpha-7-nicotinic acetylcholine receptor (α7nAChR) has received particular attention due to its involvement in cognitive function.α7nAChR is a ligand-gated ion channel that is primarily found in the hippocampus and prefrontal cortex, areas of the brain responsible for learning, memory, and attention. Studies have shown that α7nAChR dysfunction is

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RENNA, J. M., C. E. STRANG, F. R. AMTHOR, and K. T. KEYSER. "Strychnine, but not PMBA, inhibits neuronal nicotinic acetylcholine receptors expressed by rabbit retinal ganglion cells." Visual Neuroscience 24, no. 4 (2007): 503–11. http://dx.doi.org/10.1017/s0952523807070241.

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Strychnine is considered a selective competitive antagonist of glycine gated Cl− channels (Saitoh et al., 1994) and studies have used strychnine at low micromolar concentrations to study the role of glycine in rabbit retina (Linn, 1998; Protti et al., 2005). However, other studies have shown that strychnine, in the concentrations commonly used, is also a potent competitive antagonist of α7 nicotinic acetylcholine receptors (nAChRs; Matsubayashi et al., 1998). We tested the effects of low micromolar concentrations of strychnine and 3-[2′-phosphonomethyl[1,1′-biphenyl]-3-yl] alanine (PMBA), a sp

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43

ElNebrisi, Eslam, Yosra Lozon та Murat Oz. "The Role of α7-Nicotinic Acetylcholine Receptors in the Pathophysiology and Treatment of Parkinson’s Disease". International Journal of Molecular Sciences 26, № 7 (2025): 3210. https://doi.org/10.3390/ijms26073210.

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The α7 nicotinic acetylcholine receptor (α7-nAChR) is a pivotal regulator of neurotransmission, neuroprotection, and immune modulation in the central nervous system. This review explores its structural and functional attributes, highlighting its therapeutic potential in neurodegenerative disorders, particularly Parkinson’s disease (PD). α7-nAChRs mediate synaptic plasticity, modulate inflammatory responses, and influence dopamine release, positioning them as a promising pharmacological target. Positive allosteric modulators (PAMs) enhance α7-nAChR activity mainly by reducing desensitization, o

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Nurulain, S., T. Prytkova, A. M. Sultan та ін. "Inhibitory actions of bisabolol on α7-nicotinic acetylcholine receptors". Neuroscience 306 (жовтень 2015): 91–99. http://dx.doi.org/10.1016/j.neuroscience.2015.08.019.

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45

Lendvai, Balázs, Ferenc Kassai, Ágota Szájli та Zsolt Némethy. "α7 Nicotinic acetylcholine receptors and their role in cognition". Brain Research Bulletin 93 (квітень 2013): 86–96. http://dx.doi.org/10.1016/j.brainresbull.2012.11.003.

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46

Ashoor, Abrar, Jacob C. Nordman, Daniel Veltri та ін. "Menthol Binding and Inhibition of α7-Nicotinic Acetylcholine Receptors". PLoS ONE 8, № 7 (2013): e67674. http://dx.doi.org/10.1371/journal.pone.0067674.

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47

Tan, Yao, Zhaoli Chu, Hongyu Shan, Dongting Zhangsun, Xiaopeng Zhu та Sulan Luo. "Inflammation Regulation via an Agonist and Antagonists of α7 Nicotinic Acetylcholine Receptors in RAW264.7 Macrophages". Marine Drugs 20, № 3 (2022): 200. http://dx.doi.org/10.3390/md20030200.

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The α7 nicotinic acetylcholine receptor (nAChR) is widely distributed in the central and peripheral nervous systems and is closely related to a variety of nervous system diseases and inflammatory responses. The α7 nAChR subtype plays a vital role in the cholinergic anti-inflammatory pathway. In vivo, ACh released from nerve endings stimulates α7 nAChR on macrophages to regulate the NF-κB and JAK2/STAT3 signaling pathways, thereby inhibiting the production and release of downstream proinflammatory cytokines and chemokines. Despite a considerable level of recent research on α7 nAChR-mediated imm

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48

Alkondon, Manickavasagom, Edna F. R. Pereira, and Edson X. Albuquerque. "NMDA and AMPA Receptors Contribute to the Nicotinic Cholinergic Excitation of CA1 Interneurons in the Rat Hippocampus." Journal of Neurophysiology 90, no. 3 (2003): 1613–25. http://dx.doi.org/10.1152/jn.00214.2003.

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In the hippocampus, glutamatergic inputs to pyramidal neurons and interneurons are modulated by α7* and α3β4* nicotinic acetylcholine receptors (nAChRs), respectively, present in glutamatergic neurons. This study examines how nicotinic AMPA, and NMDA receptor nAChR activities are integrated to regulate the excitability of CA1 stratum radiatum (SR) interneurons in rat hippocampal slices. At resting membrane potentials and in the presence of extracellular Mg2+ (1 mM), nicotinic agonists triggered in SR interneurons excitatory postsynaptic currents (EPSCs) that had two components: one mediated by

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Hancock, Melissa L., Sarah E. Canetta, Lorna W. Role та David A. Talmage. "Presynaptic Type III Neuregulin1-ErbB signaling targets α7 nicotinic acetylcholine receptors to axons". Journal of Cell Biology 181, № 3 (2008): 511–21. http://dx.doi.org/10.1083/jcb.200710037.

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Type III Neuregulin1 (Nrg1) isoforms are membrane-tethered proteins capable of participating in bidirectional juxtacrine signaling. Neuronal nicotinic acetylcholine receptors (nAChRs), which can modulate the release of a rich array of neurotransmitters, are differentially targeted to presynaptic sites. We demonstrate that Type III Nrg1 back signaling regulates the surface expression of α7 nAChRs along axons of sensory neurons. Stimulation of Type III Nrg1 back signaling induces an increase in axonal surface α7 nAChRs, which results from a redistribution of preexisting intracellular pools of α7

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Buchholz, Bruno, Jazmín Kelly, Marina Muñoz, et al. "Vagal stimulation mimics preconditioning and postconditioning of ischemic myocardium in mice by activating different protection mechanisms." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 6 (2018): H1289—H1297. http://dx.doi.org/10.1152/ajpheart.00286.2017.

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Vagal stimulation (VS) during myocardial ischemia and reperfusion has beneficial effects. However, it is not known whether short-term VS applied before ischemia or at the onset of reperfusion protects the ischemic myocardium. This study was designed to determine whether short-term VS applied before ischemia or at the onset of reperfusion reduces myocardial infarct size (IS), mimicking classic preconditioning and postconditioning. A second objective was to study the participation of muscarinic and nicotinic receptors in the protection of both preischemic and reperfusion stimulation. FVB mice we

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