Relevant bibliographies by topics / Nicotinic Acetylcholine Receptor

Academic literature on the topic 'Nicotinic Acetylcholine Receptor'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Nicotinic Acetylcholine Receptor.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Nicotinic Acetylcholine Receptor"

1

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 (July 2005): H212—H219. http://dx.doi.org/10.1152/ajpheart.01210.2004.

Full text
Abstract:
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 0.3 ± 0.1 to 1.1 ± 0.2 μl·g−1·min−1, as previously described. This nicotine-induced increase in blood-brain barrier permeability was significantly attenuated by both the blood-brain barrier-permeant nicotinic antagonist mecamylamine and the blood-brain barrier-impermeant nicotinic antagonist hexamethonium to 0.5 ± 0.2 and 0.3 ± 0.2 μl·g−1·min−1, respectively. These data suggest that nicotinic acetylcholine receptors expressed on the cerebral microvascular endothelium mediate nicotine-induced changes in blood-brain barrier permeability.
APA, Harvard, Vancouver, ISO, and other styles
2

Lavezzi, Anna. "Toxic Effect of Cigarette Smoke on Brainstem Nicotinic Receptor Expression: Primary Cause of Sudden Unexplained Perinatal Death." Toxics 6, no. 4 (October 18, 2018): 63. http://dx.doi.org/10.3390/toxics6040063.

Full text
Abstract:
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 α7-nicotinic acetylcholine receptor expression levels were only observed in the victims with smoking mothers. Frequently, these findings were associated with the hypoplasia of the brainstem structures controlling vital functions. The results of this study indicate that the exposition to nicotine in pregnancy exerts a strong direct effect on α7-nicotinic acetylcholine receptor activity especially in perinatal life and may be one of the primary risk factors leading to the sudden unexplained death of fetuses and newborns.
APA, Harvard, Vancouver, ISO, and other styles
3

White, Sean H., Christopher J. Carter, and Neil S. Magoski. "A potentially novel nicotinic receptor in Aplysia neuroendocrine cells." Journal of Neurophysiology 112, no. 2 (July 15, 2014): 446–62. http://dx.doi.org/10.1152/jn.00796.2013.

Full text
Abstract:
Nicotinic receptors form a diverse group of ligand-gated ionotropic receptors with roles in both synaptic transmission and the control of excitability. In the bag cell neurons of Aplysia, acetylcholine activates an ionotropic receptor, which passes inward current to produce a long-lasting afterdischarge and hormone release, leading to reproduction. While testing the agonist profile of the cholinergic response, we observed a second current that appeared to be gated only by nicotine and not acetylcholine. The peak nicotine-evoked current was markedly smaller in magnitude than the acetylcholine-induced current, cooperative (Hill value of 2.7), had an EC50 near 500 μM, readily recovered from desensitization, showed Ca2+ permeability, and was blocked by mecamylamine, dihydro-β-erythroidine, or strychnine, but not by α-conotoxin ImI, methyllycaconitine, or hexamethonium. Aplysia transcriptome analysis followed by PCR yielded 20 full-length potential nicotinic receptor subunits. Sixteen of these were predicted to be cation selective, and real-time PCR suggested that 15 of the 16 subunits were expressed to varying degrees in the bag cell neurons. The acetylcholine-induced current, but not the nicotine current, was reduced by double-strand RNA treatment targeted to both subunits ApAChR-C and -E. Conversely, the nicotine-evoked current, but not the acetylcholine current, was lessened by targeting both subunits ApAChR-H and -P. To the best of our knowledge, this is the first report suggesting that a nicotinic receptor is not gated by acetylcholine. Separate receptors may serve as a means to differentially trigger plasticity or safeguard propagation by assuring that only acetylcholine, the endogenous agonist, initiates large enough responses to trigger reproduction.
APA, Harvard, Vancouver, ISO, and other styles
4

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

Full text
Abstract:
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 pseudoglandular stage lungs compared with lungs at later stages. We then studied the effects of nicotine in the explant model and found that nicotine stimulated lung branching in a dose-dependent fashion. α-Bungarotoxin, an antagonist of α7 nicotinic acetylcholine receptors, blocked the stimulatory effect of nicotine, whereas GTS-21, a specific agonist, stimulated branching, thereby mimicking the effects of nicotine. Explants deficient in α7 nicotinic acetylcholine receptors did not respond to nicotine. Nicotine also stimulated the growth of the explant. Altogether, these studies suggest that nicotine stimulates lung branching morphogenesis through α7 nicotinic acetylcholine receptors and may contribute to dysanaptic lung growth, which in turn may predispose the host to airway disease in the postnatal period.
APA, Harvard, Vancouver, ISO, and other styles
5

Kim, Jinah, Daniel S. Poole, Laura E. Waggoner, Anthony Kempf, David S. Ramirez, P. Alexandra Treschow, and William R. Schafer. "Genes Affecting the Activity of Nicotinic Receptors Involved in Caenorhabditis elegans Egg-Laying Behavior." Genetics 157, no. 4 (April 1, 2001): 1599–610. http://dx.doi.org/10.1093/genetics/157.4.1599.

Full text
Abstract:
Abstract Egg-laying behavior in Caenorhabditis elegans is regulated by multiple neurotransmitters, including acetylcholine and serotonin. Agonists of nicotinic acetylcholine receptors such as nicotine and levamisole stimulate egg laying; however, the genetic and molecular basis for cholinergic neurotransmission in the egg-laying circuitry is not well understood. Here we describe the egg-laying phenotypes of eight levamisole resistance genes, which affect the activity of levamisole-sensitive nicotinic receptors in nematodes. Seven of these genes, including the nicotinic receptor subunit genes unc-29, unc-38, and lev-1, were essential for the stimulation of egg laying by levamisole, though they had only subtle effects on egg-laying behavior in the absence of drug. Thus, these genes appear to encode components of a nicotinic receptor that can promote egg laying but is not necessary for egg-laying muscle contraction. Since the levamisole-receptor mutants responded to other cholinergic drugs, other acetylcholine receptors are likely to function in parallel with the levamisole-sensitive receptors to mediate cholinergic neurotransmission in the egg-laying circuitry. In addition, since expression of functional unc-29 in muscle cells restored levamisole sensitivity under some but not all conditions, both neuronal and muscle cell UNC-29 receptors are likely to contribute to the regulation of egg-laying behavior. Mutations in one levamisole receptor gene, unc-38, also conferred both hypersensitivity and reduced peak response to serotonin; thus nicotinic receptors may play a role in regulating serotonin response pathways in the egg-laying neuromusculature.
APA, Harvard, Vancouver, ISO, and other styles
6

Entwistle, A., R. J. Zalin, A. E. Warner, and S. Bevan. "A role for acetylcholine receptors in the fusion of chick myoblasts." Journal of Cell Biology 106, no. 5 (May 1, 1988): 1703–12. http://dx.doi.org/10.1083/jcb.106.5.1703.

Full text
Abstract:
The role of acetylcholine receptors in the control of chick myoblast fusion in culture has been explored. Spontaneous fusion of myoblasts was inhibited by the nicotinic acetylcholine receptor antagonists alpha-bungarotoxin, Naja naja toxin and monoclonal antibody mcAb 5.5. The muscarinic antagonists QNB and n-methyl scopolamine were without effect. Atropine had no effect below 1 microM, where it blocks muscarinic receptors; at higher concentrations, when it blocks nicotinic receptors also, atropine inhibited myoblast fusion. The inhibitions imposed by acetylcholine receptor antagonists lasted for approximately 12 h; fusion stimulated by other endogenous substances then took over. The inhibition was limited to myoblast fusion. The increases in cell number, DNA content, the level of creatine phosphokinase activity (both total and muscle-specific isozyme) and the appearance of heavy chain myosin, which accompany muscle differentiation, followed a normal time course. Pre-fusion myoblasts, fusing myoblasts, and young myotubes specifically bound labeled alpha-bungarotoxin, indicating the presence of acetylcholine receptors. The nicotinic acetylcholine receptor agonist, carbachol, induced uptake of [14C]Guanidinium through the acetylcholine receptor. Myoblasts, aligned myoblasts and young myotubes expressed the synthetic enzyme Choline acetyltransferase and stained positively with antibodies against acetylcholine. The appearance of ChAT activity in myogenic cultures was prevented by treatment with BUDR; nonmyogenic cells in the cultures expressed ChAT at a level which was too low to account for the activity in myogenic cultures. We conclude that activation of the nicotinic acetylcholine receptor is part of the mechanism controlling spontaneous myoblast fusion and that myoblasts synthesize an endogenous, fusion-inducing agent that activates the nicotinic ACh receptor.
APA, Harvard, Vancouver, ISO, and other styles
7

Singh, Sandeep, Smitha Pillai, and Srikumar Chellappan. "Nicotinic Acetylcholine Receptor Signaling in Tumor Growth and Metastasis." Journal of Oncology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/456743.

Full text
Abstract:
Cigarette smoking is highly correlated with the onset of a variety of human cancers, and continued smoking is known to abrogate the beneficial effects of cancer therapy. While tobacco smoke contains hundreds of molecules that are known carcinogens, nicotine, the main addictive component of tobacco smoke, is not carcinogenic. At the same time, nicotine has been shown to promote cell proliferation, angiogenesis, and epithelial-mesenchymal transition, leading to enhanced tumor growth and metastasis. These effects of nicotine are mediated through the nicotinic acetylcholine receptors that are expressed on a variety of neuronal and nonneuronal cells. Specific signal transduction cascades that emanate from different nAChR subunits or subunit combinations facilitate the proliferative and prosurvival functions of nicotine. Nicotinic acetylcholine receptors appear to stimulate many downstream signaling cascades induced by growth factors and mitogens. It has been suggested that antagonists of nAChR signaling might have antitumor effects and might open new avenues for combating tobacco-related cancer. This paper examines the historical data connecting nicotine tumor progression and the recent efforts to target the nicotinic acetylcholine receptors to combat cancer.
APA, Harvard, Vancouver, ISO, and other styles
8

Javadi, Parastoo, Ameneh Rezayof, Maryam Sardari, and Zahra Ghasemzadeh. "Brain nicotinic acetylcholine receptors are involved in stress-induced potentiation of nicotine reward in rats." Journal of Psychopharmacology 31, no. 7 (May 25, 2017): 945–55. http://dx.doi.org/10.1177/0269881117707745.

Full text
Abstract:
The aim of the present study was to examine the possible role of nicotinic acetylcholine receptors of the dorsal hippocampus (CA1 regions), the medial prefrontal cortex or the basolateral amygdala in the effect of acute or sub-chronic stress on nicotine-induced conditioned place preference. Our results indicated that subcutaneous administration of nicotine (0.2 mg/kg) induced significant conditioned place preference. Exposure to acute or sub-chronic elevated platform stress potentiated the response of an ineffective dose of nicotine. Pre-conditioning intra-CA1 (0.5–4 µg/rat) or intra-medial prefrontal cortex (0.2–0.3 µg/rat) microinjection of mecamylamine (a non-selective nicotinic acetylcholine receptor antagonist) reversed acute stress-induced potentiation of nicotine reward as measured in the conditioned place preference paradigm. By contrast, pre-conditioning intra-basolateral amygdala microinjection of mecamylamine (4 µg/rat) potentiated the effects of acute stress on nicotine reward. Our findings also showed that intra-CA1 or intra-medial prefrontal cortex, but not intra-basolateral amygdala, microinjection of mecamylamine (4 µg/rat) prevented the effect of sub-chronic stress on nicotine reward. These findings suggest that exposure to elevated platform stress potentiates the rewarding effect of nicotine which may be associated with the involvement of nicotinic acetylcholine receptors. It seems that there is a different contribution of the basolateral amygdala, the medial prefrontal cortex or the CA1 nicotinic acetylcholine receptors in stress-induced potentiation of nicotine-induced conditioned place preference.
APA, Harvard, Vancouver, ISO, and other styles
9

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 (January 2006): F103—F110. http://dx.doi.org/10.1152/ajprenal.00098.2005.

Full text
Abstract:
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 reflex. mRNA for the α3, α5, α7, β3, and β4 nicotinic subunits was identified in rat urothelial cells using RT-PCR. Western blotting also confirmed urothelial expression of the α3- and α7-subunits. Application of nicotine (50 nM) to cultured rat urothelial cells elicited an increase in intracellular Ca2+ concentration, indicating that at least some of the subunits form functional channels. These effects were blocked by the application of the nicotinic antagonist hexamethonium. During in vivo bladder cystometrograms in urethane-anesthetized rats, intravesical administration of nicotine, choline, or the antagonists methyllycaconitine citrate and hexamethonium elicited changes in voiding parameters. Intravesical nicotine (50 nM, 1 μM) increased the intercontraction interval. Intravesical choline (1–100 μM) also affected bladder reflexes similarly, suggesting that α7 nicotinic receptors mediate this effect. Intravesical administration of hexamethonium (1–100 μM) potentiated the nicotine-induced changes in bladder reflexes. Methyllycaconitine citrate, a specific α7-receptor antagonist, prevented nicotine-, choline-, and hexamethonium-induced bladder inhibition. These results are the first indication that stimulation of nonneuronal nicotinic receptors in the bladder can affect micturition.
APA, Harvard, Vancouver, ISO, and other styles
10

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 (October 8, 2010): 139–47. http://dx.doi.org/10.1017/s0952523810000246.

Full text
Abstract:
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 was also analyzed in cryostat sections of albino rat retina. Changes in protein expression were tested under hypoxic conditions. Functional nAChRs were studied by examining the Ca2+transients elicited by nicotine and acetylcholine stimulation in fura-2–loaded cells. Expression of endogenous modulators of nAChRs was analyzed by RT-PCR and Western blot in retina and RPE. Cultured bovine RPE cells expressed nicotinic receptors containing α7 subunit. RT-PCR amplified the expected specific α7 fragment. Western blotting showed expression at the protein level, with a specific band being found at 57 kDa in both cultured and freshly isolated RPE cells. Expression of nAChRs was confirmed for cultured cells by immunofluorescence. Immunohistochemistry confirmed α7 receptor expression in rat RPE retina. α7 receptor expression was down-regulated by long-term hypoxia. A small subpopulation of RPE cultured cells showed functional nAChRs, as evidenced by the selective response elicited by nicotine and acetylcholine stimulation. Expression of the endogenous nicotinic receptors’ modulator lynx1 was confirmed in bovine retina and RPE, and expression of lynx1 and other endogenous nicotinic receptor modulators (SLURP1 and RGD1308195) were also confirmed in rat retina. These results suggest that nAChRs could have a significant role in RPE, which may not be related to the traditional role in nerve transmission but could more likely be related to the nonneuronal cholinergic system in the eye.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Nicotinic Acetylcholine Receptor"

1

BAVO, FRANCESCO. "SUBTYPE-SELECTIVE NEURONAL NICOTINIC ACETYLCHOLINE RECEPTOR AGONISTS AND ANTAGONISTS." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/607332.

Full text
Abstract:
This PhD thesis focuses on two specific targets, belonging to the same receptor class of Nicotinic Acetylcholine Receptors (nAChRs): the α4β2 subtype and the α7 subtype. This elaborate is divided in two parts. The aim of the first part is the design and synthesis of α4β2 selective partial agonists as potential smoking-cessation agents. The aim of the second part is the design and synthesis of α7 antagonists with mitocan properties as antitumoral agents. Part 1. In the first project, a series of 3-nitrophenyl ethers and 3-hydroxyphenyl ethers of (S)-N-methylprolinol bearing bulky and lipophilic substituents at the C5 were designed, synthesized and assayed as putative selective α4β2 ligands. Two of them, 5-substituted with a 6-hydroxy-1-hexynyl, had high α4β2 affinity and increased α4β2/α3β4 selectivity when compared with the correspondent unsubstituted parent compounds. In the second project, each -CH= of the unselective antagonist (S,R)-N-methyl-2-pyrrolidinyl-1,4-benzodioxane and of its epimer at the benzodioxane stereocenter, was replaced by a nitrogen. The resulting four diastereomeric pairs of pyrrolidinyl-pyridodioxanes, also designed as the product of rigidification of the flexible scaffolds of pyridyl ethers of N-methyl prolinol, were studied for their nicotinic affinity at the α4β2 and α3β4. The isosteric -CH= to N substitution was detrimental for all the compounds, with the only exception of N-Methyl-pyrrolidinyl 5-pyridodioxane, with the nitrogen at position 5. Indeed, this ligand had similar affinity to its benzodioxane parent compound, but it had high α4β2/α3β4 selectivity and it was shown to be a selective partial agonist. In the third project, the unselective antagonist (S,R)-N-methyl-2-pyrrolidinyl-1,4-benzodioxane and of its epimer at the benzodioxane stereocenter were substituted at position 5 of the benzodioxane moiety, to explore the possibility of introducing selectivity and/or partial agonist as previously done with -CH= to N replacement. Among the synthesized compounds, (S,S)-N-Methyl-pyrrolidinyl-5-amino-benzodioxane had slightly improved affinity at the α4β2 affinity and highly enhanced α4β2/α3β4 selectivity than the unsubstituted parent compound, and it was shown to be a very potent partial agonist. In the fourth project, we applied computational techniques to support the interpretation of the biological results regarding N-Methyl-pyrrolidinyl 5-substituted benzodioxanes and pyridodioxanes. From these findings, we suggested that partial agonism and α4β2/α3β4 selectivity could be achieved when the benzodioxane scaffold is appropriately substituted with an HBA/HBD system, that can displace a water molecule from a small and hydrophilic subpocket of the binding site. Part 2. Adenocarcinoma and glioblastoma cell lines express α7 and α9-α10 nAChRs, whose activation promotes tumor cells growth. On these cells, the triethylammoniumethyl ether of 4-stilbenol MG624, a known selective antagonist of α7 and α9-α10 nAChRs, has antiproliferative activity. The structural analogy of MG624 with the mitocan RDM- 4’BTPI, triphenylphosphoniumbutyl ether of pterostilbene, suggested us that molecular hybridization among their three substructures might result in novel antitumour agents with higher potency and selectivity. We found that replacement of ethylene with butylene in the triethylammonium derivatives results in more potent and selective toxicity towards adenocarcinoma and glioblastoma cells, which was paralleled by increased α7 and α9-α10 nAChR antagonism and improved ability of reducing mitochondrial ATP production. Further elongation to octylene (26) provided a compound with 40-fold and 10-fold increased antiglioblastoma and antiadenocarcinoma activity respectively, when compared to MG624. Elongation of the alkylene linker was greatly advantageous also for the triphenylphosphonium derivatives. RDM- 4’BTPI did not acquire, as expectable, antinicotinic activity by hybridization with MG624 stilbene scaffold, but it was surpassed in glioblastoma cell viability reduction by its stilbene analogues with > 4C alkylene linker. In particular, the analogue with decylene between stilbenoxyl and triphenylphosphonium head (24) was ten- fold and two-fold more potent than RDM-4’BTPI in reducing glioblastoma cell viability and in increasing ROS production respectively. Overall, the ammonium compound 26 reached antiproliferative activities at glioblastoma and adenocarcinoma cells in the same range of the phosphonium 24, but showed good selectivity against neuroblastoma and healthy mouse astrocytes.
APA, Harvard, Vancouver, ISO, and other styles
2

Rankin, Saffron Emily. "Lipid-protein interactions and nicotinic acetylcholine receptor function." Thesis, University of Oxford, 1996. https://ora.ox.ac.uk/objects/uuid:3deca85b-9f09-4f72-9db3-e34851e10542.

Full text
Abstract:
The effect of bilayer composition, specifically the presence of cholesterol, upon the function of the reconstituted nicotinic acetylcholine receptor (nAcChoR) was investigated using stopped-flow fluorescence. The nAcChoR was purified and reconstituted from the electroplaques of Torpedo nobiliana, using affinity column chromatography, into bilayers of defined composition and the function of each sample assessed and compared with those of the native receptor. Investigation of the effect of bilayer composition upon the kinetics of agonist binding to the nAcChoR, using the fluorescent acetylcholine analogue, Dns-C6-Cho, established that the receptor pre-existed in equilibrium between the resting and two desensitised states. However, Dns-C6-Cho inhibited channel gating at high concentrations and another fluorescent probe was sought. The kinetics of carbachol induced nAcChoR conformational changes, reported by ethidium bromide (a non-competitive inhibitor) fluorescence, in native membranes were characterised and an assay developed to investigate whether cholesterol mediated rapid conformational changes in reconstituted samples. It was found that ethidium bromide reported on the carbachol-induced development of the fast desensitised state from the open channel state, and that this conformational change was sensitive to changes in bilayer composition. The onset of fast desensitisation from the open channel state was not observed when the receptor was reconstituted into DOPC or DOPC-DOPA bilayers. However, increasing the cholesterol content in these bilayers increased the amplitude of the component reporting this conformational change, while the observed rate at which it occurred was independent of bilayer cholesterol content. This result agrees with the suggestion that cholesterol facilitates channel opening and the onset of fast desensitisation by binding to specific sites on the nAcChoR and that these must be occupied for a functionally viable receptor (Jones and McNamee, 1988).
APA, Harvard, Vancouver, ISO, and other styles
3

Nichols, Philip Paul. "Transcriptional regulation of the human nicotinic acetylcholine receptor." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326016.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Patel, Anup B. "Nicotinic acetylcholine receptor ligands from 2,4-methanoproline derivatives." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29973.

Full text
Abstract:
Since the discovery of the powerful analgesic epibatidine in 1974 from the Ecuadorian poison frog Epipedobates tricolor, there has been global interest in the synthesis of analogue molecules. Epibatidine has the unique 7-azabicyclo[2.2.1]heptane structure with a chloropyridyl ring at the 2-positon. Epibatidine acts at the nicotinic acetylcholine receptor (nAChR) and the aim of this work is to produce target compounds retaining therapeutic potential but with higher nAChR sub-type selectivity and lower toxicity. The only naturally occurring compound to have the 2-azabicyclo[2.1.1]hexane system is the nonproteinogenic amino acid 2,4-methanoproline. This alternative bicyclic framework opens the route to the construction of pioneering epibatidine analogues. The intramolecular [2+2] photocycloaddition method was employed to construct the rigid 2-azabicyclo[2.1.1]hexane skeleton. Successful nucleophilic substitution at a methylene attached to the bridgehead position of the 2-azabicyclo[2.1.1]hexane ring system opened the way to construction of innovative derivatives. These have a wider range of functional groups attached at the 1-positon via a methylene 'spacer' and provide access to epibatidine analogues containing heterocyclic substituents and to further homologation. Mechanistic studies indicate that displacements with loss of a nucleofuge require thermal activation but proceed without the rearrangement initially anticipated in such a strained bicyclic structure. A unique tricyclic carbamate has been isolated; nucleophilic attack on this carbamate leads directly to the isolation of N-deprotected substitution products with concomitant decarboxylation. The analogues produced in this study are currently being pharmacologically tested and the results will determine the course of future synthetic approaches towards original targets.
APA, Harvard, Vancouver, ISO, and other styles
5

Larsen, James D. "Nicotinic Acetylcholine Receptor Dependent Effects of Nicotine on HEK293T and HBO Cells." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5701.

Full text
Abstract:
T2R receptors are the classical bitter taste receptors which detect and transduce bitter taste in a subset of taste receptor cells (TRCs). The TRPM5-dependent T2Rs are G-protein coupled receptors (GPCRs) and are linked to G protein, gustducin to initiate an intracellular signaling cascade for the transduction of bitter tastants. Nicotine is bitter. However, at present the transduction mechanisms for the detection of nicotine in are poorly understood. Previous studies from our laboratory using TRPM5 knockout (KO) mice demonstrated that the T2R pathway is insufficient in explaining the taste perception of nicotine. TRPM5 KO mice elicited chorda tympani (CT) taste nerve responses to nicotine, albeit significantly smaller than the wild type (WT) mice and still responded to nicotine as an aversive stimulus. Following addition of mecamylamine (Mec), a non-specific blocker of neuronal nicotinic acetylcholine receptors (nAChRs), CT responses to nicotine were partially inhibited in both WT and TRPM5 KO mice. Mec also decreases the aversive response to nicotine in both WT and TRPM5 KO mice. These studies led to the hypothesis that both a TRPM5-independent and TRPM5-dependent pathways are responsible for the detection and transduction of the bitter taste of nicotine in TRCs. The TRPM5-independent pathway most likely utilizes the nAChRs expressed in TRCs and function as bitter taste receptors for nicotine. We have subsequently demonstrated the expression of nAChRs in a subset of TRPM5-positive TRCs. However, this mechanism is not well understood in other cell types, particularly undifferentiated epithelial cells, such as HEK293T cells. The specific aims of this project were: (i) To identify which components of T2R-dependent taste reception as well as components of nAChRs are expressed in HEK293T cells; (ii) To determine if HEK293T cells co-express these components; (iii) To identify if exposure to nicotine modulates the expression of T2R and nAChR dependent components in HEK293T cells; (iv) To determine if TRCs express functional nAChR ion channels; and (v) To determine if nAChRs are involved in the release of neuropeptides, such as brain-derived neurotrophic factor (BDNF) in HEK293T cells. The data obtained in HEK293T cells was compared with parallel studies on adult cultured human fungiform taste cells (HBO) done independently by Dr. Jie Qian, a postdoctoral fellow in Dr. Vijay Lyall’s lab. The results of combined studies on HBO and HEK293T cells indicates that TRPM5-positive cells also co-express ionotropic nAChRs, comprising a and β subunits. The nAChRs are capable of forming ion pores and when stimulated by nicotine and create a parallel TRPM5-independent pathway for the detection of nicotine. Using molecular and immunocytochemical techniques, our results demonstrate that mRNAs and proteins for bitter taste receptors and downstream intracellular signaling components as well as subunits necessary for the formation of nAChRs are expressed in HBO and HEK293T cells. Results demonstrated that TRPM5-positive HEK293T cells co-expressed nAChR subunits throughout the entire population. Nicotine increased the influx of Ca2+ in a dose dependent manner, which was somewhat reduced by the addition of TRPM5 blocker, triphenylphosphine oxide (TPPO). Both mRNA and protein expression were altered in a biphasic pattern with a maximum increased observed at 0.5 µM nicotine with a decrease in expression at higher concentrations. The synthesis of neurotrophic factor BDNF, required for maturation of taste bud cells and their innervating nerves, increased in HEK293T cells exposed to nicotine, however, nicotine did not trigger the release of BDNF. These results were then compared and contrasted with HBO cells to better understand the comparative effects of nicotine on both undifferentiated and differentiated cells. The data on HBO cells is presented in the Appendix.
APA, Harvard, Vancouver, ISO, and other styles
6

Brown, Jack. "α7 Nicotinic acetylcholine receptor-mediated calcium signalling in neuronal cells." Thesis, University of Bath, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.636524.

Full text
Abstract:
α7 nicotinic acetylcholine receptors (nAChR) are highly permeable to Ca2+ and are clinical targets for Alzheimer’s disease and schizophrenia. The aim of this work was to examine α7 nAChR-mediated Ca2+ signalling in neuronal cells using three different methods, and to evaluate the effects of the desensitizing agonist and prototypical smoking-cessation drug sazetidine-A on α7 nAChRs. Initial studies used 96-well plate assays with SH-SY5Y cells to characterize responses evoked by the α7 nAChR-selective agonist PNU-282987 and positive allosteric modulator PNU-120596. This was complemented by live-imaging of cortical cultures, where the compounds evoked robust Ca2+ responses from 12 % of cells. Co- application with Cd2+, ryanodine and xestospongin-C significantly inhibited these responses, suggesting the involvement of voltage-gated Ca2+ channels and Ca2+- induced Ca2+-release. CNQX and MK801 also significantly inhibited α7 nAChR mediated Ca2+ elevations, indicating a role for glutamate release. A high-content screening assay was developed to further examine these phenomena. Exploratory experiments using KCl, AMPA and NMDA validated a protocol that could be used to image Ca2+ elevations in large cell populations. Inconsistent responses to PNU-120596 and PNU2-282987 were also observed, reflecting the scarcity of α7 nAChRs in cortical cultures and the need for assay optimization. Combination with immunofluorescent labelling revealed α7 nAChR mediated Ca2+ elevations in a subpopulation of astrocytes and neurons, some of which were GABAergic. PNU-120596 potentiated the effects of sazetidine-A in SH-SY5Y cells (EC50 0.4 μM) eliciting responses in 14 % of cells in cortical cultures in a methyllycaconitine- sensitive manner, consistent with α7 nAChR activation. Pre-incubation with sazetidine-A concentration-dependently attenuated subsequent α7 nAChR-mediated responses in SH-SY5Y cells (IC50 476 nM) and cortical cultures, suggesting that α7 nAChRs could play a role in the behavioural effects of sazetidine-A. These comparative experiments enhance our understanding of α7 nAChR signalling and provide a new method to study them further.
APA, Harvard, Vancouver, ISO, and other styles
7

Covernton, Patrick John O'Neill. "Functional aspects of neuronal nicotinic receptor diversity." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321967.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Zirger, Jeffrey M. "Cloning, Expression and Functional Analysis of the Zebrafish Neuronal Nicotinic Acetylcholine Receptor." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1052847984.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Kracun, Sebastian. "Molecular and functional characterisation of nicotinic acetylcholine receptor chimaeras." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444289/.

Full text
Abstract:
Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels which exhibit considerable subunit diversity. They have been implicated in processes including synaptic transmission and modulation of neurotransmitter release. They also have a significant role in several pathological disorders as well as nicotine addiction, which makes nAChRs important targets for therapeutic drug discovery. One of the aims of this study was to investigate the influence of the intracellular domain of nAChR subunits upon receptor assembly, targeting and functional properties. A series of subunit chimaeras was constructed, each containing the intracellular loop region, located between transmembrane (TM) domains M3 and M4, from nAChR subunits al-alO or pl-p4 and from the 5-hydroxytryptamine type 3 receptor (5-HT3R) subunits 3 A and 3B. Evidence has been obtained which demonstrates that the large intracellular loop exerts a significant influence upon the levels of both cell-surface and intracellular assembled receptors. Comparisons of functional ion-channel properties revealed a significant influence upon both single-channel conductance and receptor desensitisation. Experiments conducted in polarised epithelial cells demonstrate that the nAChR loop can also influence receptor targeting. In a further study, the influence of the recently identified nAChR molecular chaperone, RIC-3 (resistance to mhibitors of cholinesterase), on receptor maturation was investigated. The influence of subunit domains upon the RIC-3's chaperone activity was investigated by co-expression with subunit chimaeras. Finally, a9/5-HT3A and alO/5-HT3A subunit chimeras were used to investigate the pharmacological properties of a9al0 nAChRs, a receptor subtype expressed in hair cells of the auditory system. Physiologically relevant concentrations of the anti-malarial compounds, quinine, quinidine and chloroquine were shown to act as competitive inhibitors, whereas the NMDA receptor antagonist, neramexane, blocked a9al0 nAChR mediated responses via a non-competitive mechanism.
APA, Harvard, Vancouver, ISO, and other styles
10

Charriez, Christina Margaret. "ALPHA7 NICOTINIC ACETYLCHOLINE RECEPTOR REGULATION IN EXPERIMENTAL NEURODEGENERATIVE DISEASE." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/19.

Full text
Abstract:
The α7 nicotinic acetylcholine receptor (nAChR) is involved in learning and memory, synaptic plasticity, neuroprotection, inflammation, and presynaptic regulation of neurotransmitter release. Alzheimer’s disease (AD), a neurodegenerative disease characterized by diminished cognitive abilities, memory loss, and neuropsychiatric disturbances, is associated with a loss of nAChRs. Similarly, traumatic brain injury (TBI) may result in long term neurobehavioral changes exemplified by cognitive dysfunction. Deficits in α7 nAChR expression have previously been shown in experimental TBI and may be related to cognitive impairment experienced in patients following TBI. The purpose of this dissertation was to investigate changes in α7 nAChR expression in models of neurodegeneration and determine if allosteric modulation of the nAChR facilitates functional recovery following experimental TBI through changes in nAChRs. Experimental models employed include a transgenic mouse model of AD that overexpresses the amyloid precursor protein (APPswe mice) and the controlled cortical impact injury model of TBI in rats. Quantitative receptor autoradiography using α-[125I]-bungarotoxin and [125I]-epibatidine and in situ hybridization were used to investigate changes in nAChR density and mRNA expression, respectively. In the first study, the effects of aging and β-amyloid on α7 nAChR expression were evaluated in APPswe mice. Hippocampal α7 nAChR density was significantly upregulated in APPswe mice compared to wild-type mice. It is postulated that elevated Aβ levels bind to the α7 nAChR resulting in upregulation. In a second study, galantamine, a medication used in the treatment of AD, was administered subchronically following experimental TBI to determine if treatment could facilitate cognitive recovery and affect nAChR expression. Interestingly, the results indicate TBI interferes with agonist mediated upregulation of nAChRs, and galantamine did not improve function in a behavioral task of learning a memory. In a third study, the regulation of TBI related deficits in α7 nAChRs was examined 48 hours following injury. α7 nAChR deficits occurred with a reduction in α7 mRNA in several hippocampal regions and non-α7 nAChR deficits occurred with a reduction in α4 mRNA in the metathalamus. The results of these studies suggest AD and TBI may involve complex but parallel processes contributing to the regulation of α7 nAChRs.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Nicotinic Acetylcholine Receptor"

1

Maelicke, Alfred, ed. Nicotinic Acetylcholine Receptor. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Barrantes, Francisco J., ed. The Nicotinic Acetylcholine Receptor. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-40279-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Li, Ming D., ed. Nicotinic Acetylcholine Receptor Technologies. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3768-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Yamamoto, Izuru, and John E. Casida, eds. Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-67933-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

1928-, Yamamoto Izuru, and Casida John E. 1929-, eds. Nicotinoid insecticides and the nicotinic acetylcholine receptor. Tokyo: Springer, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Alfred, Maelicke, ed. Nicotinic acetylcholine receptor: Structure and function. Berlin: Springer-Verlag, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Akaike, Akinori, Shun Shimohama, and Yoshimi Misu, eds. Nicotinic Acetylcholine Receptor Signaling in Neuroprotection. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8488-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Insect nicotinic acetylcholine receptors. New York: Springer Science+Business Media, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Thany, Steeve Hervé, ed. Insect Nicotinic Acetylcholine Receptors. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6445-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

A, Selyanko A., and Derkach V. A, eds. Neuronal acetylcholine receptors. New York: Consultants Bureau, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Nicotinic Acetylcholine Receptor"

1

Brisson, A. "Three-Dimensional Structure of the Acetylcholine Receptor." In Nicotinic Acetylcholine Receptor, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Giraudat, J., M. Dennis, T. Heidmann, J. P. Changeux, R. Bisson, C. Montecucco, F. Kotzyba-Hibert, M. Goeldner, C. Hirth, and J. Y. Chang. "Tertiary Structure of the Nicotinic Acetylcholine Receptor Probed by Photolabeling and Protein Chemistry." In Nicotinic Acetylcholine Receptor, 103–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hucho, F., W. Oberthür, F. Lottspeich, and B. Wittmann-Liebold. "A Structural Model of the Ion Channel of the Nicotinic Acetylcholine Receptor." In Nicotinic Acetylcholine Receptor, 115–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Prinz, Heino. "A General Treatment of Ligand Binding to the Acetylcholine Receptor." In Nicotinic Acetylcholine Receptor, 129–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

McNamee, M. G., T. M. Fong, O. T. Jones, and J. P. Earnest. "Lipid-Protein Interactions and Acetylcholine Receptor Function in Reconstituted Membranes." In Nicotinic Acetylcholine Receptor, 147–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Hess, George P. "Regulation of Intercellular Signal Transmission. New Approaches to Chemical Kinetic Measurements." In Nicotinic Acetylcholine Receptor, 159–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Neumann, Eberhard. "Hysteresis and Channel Properties of the Acetylcholine Receptor of Torpedo Californica." In Nicotinic Acetylcholine Receptor, 177–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Colquhoun, D., and D. C. Ogden. "States of the Nicotinic Acetylcholine Receptor: Enumeration, Characteristics and Structure." In Nicotinic Acetylcholine Receptor, 197–218. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Steinbach, Joe Henry, Manuel Covarrubias, Steven M. Sine, and Joy Steele. "Function of Mammalian Nicotinic Acetylcholine Receptors." In Nicotinic Acetylcholine Receptor, 219–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Siemen, D., S. Hellmann, and A. Maelicke. "Single Channel Studies of Acetylcholine Receptors Covalently Alkylated with Acetylcholine." In Nicotinic Acetylcholine Receptor, 233–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71649-2_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Nicotinic Acetylcholine Receptor"

1

Akhabir, L., X. Zhang, JE Connett, NR Anthonisen, M. Lathrop, WO Cookson, PD Pare, and AJ Sandford. "Nicotinic Acetylcholine Receptor Polymorphism, Smoking History and Lung Function Decline." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2998.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Wongtrakool, C., HN Rivera, S. Roser-Page, and J. Roman. "Nicotine Induced Nerve Growth Factor Expression Is through α7 Nicotinic Acetylcholine Receptor Mediated Signals." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2429.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Israël-Assayag, Evelyne, Luc Vachon, Sophie Aubin, and Yvon Cormier. "Targeting Nicotinic Acetylcholine Receptors To Treat Asthma: Pharmacokinetics And Metabolism Of ASM-024, A New Nicotinic Receptor Agonist." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5398.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Hong, Huixiao, Carmine Leggett, and Suguna Sakkiah. "Development of Nicotinic Acetylcholine Receptor nAChR α7 Binding Activity Prediction Model." In BCB '17: 8th ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3107411.3108191.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Palmer, Cynthia A., Thomas L. Fare, David C. Turner, Susan L. Brandow, Bruce P. Gaber, Cecile G. Silvestre, and David H. Cribbs. "Monolayer and atomic force microscopy studies of nicotinic acetylcholine receptor films." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5760885.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Palmer, Fare, Turner, Brandow, and Gaber. "Monolayer And Atomic Force Microscopy Studies Of Nicotinic Acetylcholine Receptor Films." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.589562.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Asomaning, Kofi, Rebecca Heist, Rihong Zhai, Chau-Chyun Sheu, Feng Chen, Geoffrey Liu, Li Su, Xihong Lin, Immaculata De Vivo, and David C. Christiani. "Abstract 2760: Nicotinic acetylcholine receptor SNPs are associated with smoking cessation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2760.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Salzer, Reiner, Wolfgang B. Fischer, Ines Unverricht, Dirk Schwenke, Gerald Steiner, Andre Schrattenholz, and Alfred Maelicke. "Spectroscopic investigation of the nicotinic acetylcholine receptor for application in medical diagnosis." In BiOS '98 International Biomedical Optics Symposium, edited by Henry H. Mantsch and Michael Jackson. SPIE, 1998. http://dx.doi.org/10.1117/12.306096.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Zhang, Jing, Hanssa Summah, Ying-gang Zhu, and Jie-ming Qu. "Nicotinic Acetylcholine Receptor Variants And The Susceptibility Of COPD: A Meta-Analysis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1932.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Asomaning, Kofi, Rihong Zhai, Chau-Chyun Sheu, Rebecca Heist, Feng Chen, Geoffrey Liu, Li Su, Xihong Lin, and David Christiani. "Abstract 937: Nicotinic acetylcholine receptor polymorphisms, secondhand smoke and lung cancer risk." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-937.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Nicotinic Acetylcholine Receptor"

1

Lindstrom, Jon M. Use of Monoclonal Antibodies to Study the Structure and Function of Nicotinic Acetylcholine Receptors on Electric Organ and Muscle and to Determine the Structure of Nicotinic Acetylcholine Receptors on Neurons. Fort Belvoir, VA: Defense Technical Information Center, March 1988. http://dx.doi.org/10.21236/ada198425.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Roman, Jesse. Prenatal Exposure to Nicotine and Childhood Asthma: Role of Nicotine Acetylcholine Receptors, Neuropeptides, and Fibronectin Expression in Lung. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada452269.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Roman, Jesse. Prenatal Exposure to Nicotine and Childhood Asthma: Role of Nicotine Acetylcholine Receptors, Neuropeptides and Fibronectin Expression in Lung. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada508588.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Nicotinic Acetylcholine Receptor' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography