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Journal articles on the topic 'Nicotinic partial agonist'

Author: Grafiati

Published: 9 March 2023

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1

Gonzalez-Gutierrez, Juan Pablo, Martin Hodar, Franco Viscarra, Pablo Paillali, Nicolás Guerra-Díaz, Hernán Pessoa-Mahana, Juan José Hernández-Morantes, et al. "Minimal Structural Changes Determine Full and Partial Nicotinic Receptor Agonist Activity for Nicotine Analogues." Molecules 24, no. 15 (July 24, 2019): 2684. http://dx.doi.org/10.3390/molecules24152684.

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Neuronal α4β2 nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels (LGIC) that have been implicated in nicotine addiction, reward, cognition, pain disorders, anxiety, and depression. Nicotine has been widely used as a template for the synthesis of ligands that prefer α4β2 nAChRs subtypes. The most important therapeutic use for α4β2 nAChRs is as replacement therapy for smoking cessation and withdrawal and the most successful therapeutic ligands are partial agonists. In this case, we use the N-methylpyrrolidine moiety of nicotine to design and synthesize new α4β2 nicotinic derivatives, coupling the pyrrolidine moiety to an aromatic group by introducing an ether-bonded functionality. Meta-substituted phenolic derivatives were used for these goals. Radioligand binding assays were performed on clonal cell lines of hα4β2 nAChR and two electrode voltage-clamp experiments were used for functional assays. Molecular docking was performed in the open state of the nAChR in order to rationalize the agonist activity shown by our compounds.

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2

Hussy, N., M. Ballivet, and D. Bertrand. "Agonist and antagonist effects of nicotine on chick neuronal nicotinic receptors are defined by alpha and beta subunits." Journal of Neurophysiology 72, no. 3 (September 1, 1994): 1317–26. http://dx.doi.org/10.1152/jn.1994.72.3.1317.

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1. Functional neuronal nicotinic receptors were reconstituted in Xenopus oocytes by the nuclear injection of different combinations of chick and rat cDNAs encoding alpha and beta subunits. The pharmacology of these nicotinic receptors was investigated using two-electrode voltage clamp. 2. The sensitivity of the chick alpha 3/beta 2, alpha 3/beta 4, and alpha 4/beta 2 receptors to acetylcholine (ACh) and neuronal bungarotoxin differed markedly, indicating that both subunits contribute to the pharmacological properties of the receptors. 3. Nicotine acted as an agonist on the chick alpha 3/beta 4 and alpha 4/beta 2 receptors and rat alpha 3/beta 2 receptor. In contrast, nicotine (at concentrations > 3 microM) was only a weak partial agonist of the chick alpha 3/beta 2 receptor. Moreover, nicotine coapplied with 3 microM ACh on the chick alpha 3/beta 2 receptor acted as a potent competitive antagonist, with an IC50 of 0.43 microM. No antagonist effect of nicotine could be revealed on the other nicotinic receptors. 4. The effect of nicotine was tested on hybrid receptors obtained by coinjection of chick and rat cDNAs encoding the alpha 3 and beta 2 subunits (yielding the rat alpha 3/chick beta 2 and chick alpha 3/rat beta 2 receptors). Nicotine (10 microM) strongly inhibited both hybrid receptors. 5. Chimeric subunits were constructed by exchanging a segment located in the extracellular N-termini of chick alpha 3 and alpha 4 subunits and chick alpha 3 and rat alpha 3 subunits. These subunits were coexpressed in oocytes with chick or rat beta 2 subunits. The effect of nicotine on these receptors pointed to the importance of a 15 amino acid stretch located 3' of the first transmembrane segment in the determination of the agonist and antagonist action of nicotine. 6. Within this 15 amino acid segment, a single residue differs in chick and rat alpha 3 subunits, at position 198, within the ligand binding site of alpha subunits. Gln198 of the rat alpha 3 subunit was replaced by Thr as found in the chick alpha 3 subunit, using site-directed mutagenesis. The mutant subunit was coexpressed with the rat beta 2 subunit, yielding receptors which were inhibited by nicotine. 7. It is concluded that both alpha and beta subunits not only alter considerably the sensitivity of the nicotinic receptor to agonists and antagonists, but also can turn an agonist into a potent antagonist of one receptor subtype.(ABSTRACT TRUNCATED AT 400 WORDS)

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3

Jamali, Qutub. "Galantamine as a Treatment Option for Nicotine Addiction." Journal of Smoking Cessation 2021 (July 17, 2021): 1–3. http://dx.doi.org/10.1155/2021/9975811.

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The pharmacological therapy for smoking cessation recommended by National Institute for Health and care Excellence (NICE) guidelines is nicotine replacement therapy such as gum, inhalator, lozenge, nasal spray, oral spray, sublingual tablet, and transdermal patch. Medications such as bupropion and varenicline are also used. Varenicline is the only established drug used to alleviate symptoms of craving as it acts as a partial nicotine agonist. Galantamine has a similar mechanism of action where it is an acetylcholinesterase inhibitor and nicotinic receptor agonist. However, varenicline is the only recommended drug. There are not many studies to illustrate the effectiveness of galantamine for smoking cessation. This article explores the possibility of potential use of galantamine in alleviating the symptoms of nicotine withdrawal.

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Jancin, Bruce. "Selective Nicotinic Receptor Partial Agonist May Be Cessation Advance." Family Practice News 35, no. 13 (July 2005): 34. http://dx.doi.org/10.1016/s0300-7073(05)70953-1.

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5

Potasiewicz, Agnieszka, Joanna Golebiowska, Piotr Popik, and Agnieszka Nikiforuk. "Procognitive effects of varenicline in the animal model of schizophrenia depend on α4β2- and α7-nicotinic acetylcholine receptors." Journal of Psychopharmacology 33, no. 1 (December 3, 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 partial agonist TC-2403 and the α7-nAChR full agonist PNU-282987, in a ketamine-based model of schizophrenia-like cognitive deficits on the attentional set-shifting task in rats. The second goal was to elucidate whether the procognitive efficacy of varenicline was due to the compound’s action on α4β2-nAChRs or α7-nAChRs. Methods: Ketamine was administered to rats for 10 consecutive days and the test was performed 14 days following the last injection. The tested compounds were administered 30 min prior to the attentional set-shifting task. Results: Varenicline, TC-2403 and PNU-282987 ameliorated ketamine-evoked set-shifting deficits. While the α4β2-nAChR antagonist dihydro-β-erythroidine and the α7-nAChR antagonist methyllycaconitine completely prevented the procognitive actions of TC-2403 and PNU-282987, respectively, varenicline’s effect was only partially blocked by any given antagonist. Moreover, the combined treatment with TC-2403 and PNU-282987 more effectively facilitated rats’ set-shifting ability than activation of either type of nicotinic acetylcholine receptor alone. Conclusion: The present findings demonstrated that varenicline’s actions on both α7-nAChRs and α4β2-nAChRs may be necessary to produce its full procognitive effect in the present experimental setting.

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6

McCaul, Mary E., Gary S. Wand, Hiroto Kuwabara, Robert F. Dannals, Dean Wong, and Xiaoqiang Xu. "The Relationship of Varenicline Agonism of α4β2 Nicotinic Acetylcholine Receptors and Nicotine-Induced Dopamine Release in Nicotine-Dependent Humans." Nicotine & Tobacco Research 22, no. 6 (May 16, 2019): 892–99. http://dx.doi.org/10.1093/ntr/ntz080.

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Abstract Introduction Cigarette smoking continues to be one of the most important behavioral causes of morbidity and mortality in the world. Varenicline, an α4β2 nicotinic acetylcholine receptor (nAChR) partial agonist, has been shown to increase smoking quit rates compared with nicotine-based products. This human laboratory, double-blind, placebo-controlled study examined varenicline and placebo effects on α4β2-nAChRs occupancy, nicotine-induced change in [11C]raclopride non-displaceable binding potential (BPND), and behavioral measures of cigarette smoking, nicotine craving, and withdrawal. Methods Current nicotine dependent daily smokers (N = 17) were randomized to varenicline 1 mg twice daily or placebo for 13 days. Using positron emission tomography), we characterized α4β2-nAChRs occupancy using [18F]AZAN and dopamine receptor binding using [11C]raclopride as well as behavioral measures of cigarettes smoked, craving, and nicotine withdrawal. Results Varenicline compared with placebo resulted in significant reductions in [18F]AZAN BPND in multiple brain regions including thalamus, midbrain, putamen, and ventral striatum. Following administration of a controlled-dose nicotine cigarette, dopamine release was significantly suppressed in the ventral striatum in the varenicline-treated compared with the placebo group. There was a significant relationship between α4β2-nAChRs BPND measured in thalamus during the [18F]AZAN scan and nicotine-induced change in raclopride BPND in the ventral striatum. Conclusion This is the first human study to demonstrate a direct relationship between the extent of varenicline occupancy of α4β2-nAChRs and the magnitude of dopamine release following nicotine use. Implications It has remained unclear how nicotinic receptor blockade through partial agonist medications such as varenicline promotes smoking cessation. One hypothesized mechanism is downstream dampening of the mesolimbic reward dopamine system. For the first time in human smokers, we observed a direct relationship between the extent of varenicline blockade of α4β2-nACh nicotinic receptors and the magnitude of dopamine release following smoking. This has mechanistic and therapeutic implications for improving smoking cessation interventions.

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7

Akinola, Lois S., Deniz Bagdas, Yasmin Alkhlaif, Asti Jackson, Cenk O. Gurdap, Elnaz Rahimpour, F. Ivy Carroll, Roger L. Papke, and M. Imad Damaj. "Pharmacological characterization of 5-iodo-A-85380, a β2-selective nicotinic receptor agonist, in mice." Journal of Psychopharmacology 36, no. 11 (November 2022): 1280–93. http://dx.doi.org/10.1177/02698811221132214.

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Background: Because of their implications in several pathological conditions, α4β2* nicotinic acetylcholine receptors (nAChRs) are potential targets for the treatment of nicotine dependence, pain, and many psychiatric and neurodegenerative diseases. However, they exist in various subtypes, and finding selective tools to investigate them has proved challenging. The nicotinic receptor agonist, 5-iodo-A-85380 (5IA), has helped in delineating the function of β2-containing subtypes in vitro; however, much is still unknown about its behavioral effects. Furthermore, its effectiveness on α6-containing subtypes is limited. Aims: To investigate the effects of 5IA on nociception (formalin, hot-plate, and tail-flick tests), locomotion, hypothermia, and conditioned reward after acute and repeated administration, and to examine the potential role of β2 and α6 nAChR subunits in these effects. Lastly, its selectivity for expressed low sensitivity (LS) and high sensitivity (HS) α4β2 receptors is investigated. Results: 5IA dose-dependently induced hypothermia, locomotion suppression, conditioned place preference, and antinociception (only in the formalin test but not in the hot-plate or tail-flick tests). Furthermore, these effects were mediated by β2 but not α6 nicotinic subunits. Finally, we show that 5-iodo-A-85380 potently activates both stoichiometries of α4β2 nAChRs with differential efficacies, being a full agonist on HS α4(2)β2(3) nAChRs, and a partial agonist on LS α4(3)β2(2) nAChRs and α6-containing subtypes as well.

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8

Kerr, Jessica L., Erin M. Timpe, and Julie P. Karpinski. "Varenicline: A Novel Nicotinic Receptor Partial Agonist for Smoking Cessation." Journal of Pharmacy Technology 23, no. 1 (January 2007): 23–29. http://dx.doi.org/10.1177/875512250702300105.

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9

Dunbar, Geoffrey C., and Ramana Kuchibhatla. "Cognitive Enhancement in Man With Ispronicline, A Nicotinic Partial Agonist." Journal of Molecular Neuroscience 30, no. 1-2 (2006): 169–72. http://dx.doi.org/10.1385/jmn:30:1:169.

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10

Coe, Jotham W., Paige R. Brooks, Michael G. Vetelino, Michael C. Wirtz, Eric P. Arnold, Jianhua Huang, Steven B. Sands, et al. "Varenicline: An α4β2 Nicotinic Receptor Partial Agonist for Smoking Cessation." Journal of Medicinal Chemistry 48, no. 10 (April 23, 2005): 3474–77. http://dx.doi.org/10.1021/jm050069n.

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11

Koelsch, Gerald, Michael J. Detke, Karen E. Stevens, Leonard T. Meltzer, Alvin V. Terry, Patrick M. Callahan, Ryan F. Yoshimura, et al. "APN1125: A clinical stage α7 nicotinic acetylcholine receptor partial agonist." Biochemical Pharmacology 97, no. 4 (October 2015): 636. http://dx.doi.org/10.1016/j.bcp.2015.08.042.

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12

Liu, Yi, and James P. Dilger. "Decamethonium is a partial agonist at the nicotinic acetylcholine receptor." Synapse 13, no. 1 (January 1993): 57–62. http://dx.doi.org/10.1002/syn.890130108.

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13

Grosshans, M., J. Mutschler, D. Hermann, F. Kiefer, and A. Diehl. "Is Varenicline Able to Prevent Smoking Cessation Induced Affective Symptoms?" European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70656-x.

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The selective alpha4-beta2 nicotinic acetylcholine receptor (nAChR) partial agonist varenicline has been shown to be effective in the treatment of tobacco dependence by counteracting withdrawal symptoms and reducing smoking reward. However, the need to test safety, especially in smokers with varying co-morbidities and risk patterns is highlighted. There are some publications reporting exacerbation of psychiatric symptoms in subjects with pre-existing psychiatric disorders associated with varenicline treatment.This case-report describes a patient whose several smoking cessation attempts led to enduring nicotine-related symptoms such as depression and suicidal tendencies. All further cessation attempts under medical control with nicotine patches, bupropion and psychotherapy failed. At lest reducing her daily dose by one cigarette already led to suicidal thoughts. We took her into inpatient treatment and started an uptitration with varenicline. Unlike earlier attempts there were no complications during the detoxication and depressive symptoms improved clearly.Affective symptoms like depression are known to develop during nicotine cessation. The improving of affective symptoms in this case might be a result of the partial agonistic effects of varenicline.

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14

Raines, Douglas E., and Vinu T. Zachariah. "Isoflurane Increases the Apparent Agonist Affinity of the Nicotinic Acetylcholine Receptor by Reducing the Microscopic Agonist Dissociation Constant." Anesthesiology 92, no. 3 (March 1, 2000): 775–85. http://dx.doi.org/10.1097/00000542-200003000-00021.

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Background Isoflurane increases the apparent agonist affinity of ligand-gated ion channels. This action reflects a reduction in the receptor's agonist dissociation constant and/or the preopen/open channel state equilibrium. To evaluate the effect of isoflurane on each of these kinetic constants in the nicotinic acetylcholine receptor, the authors analyzed isoflurane's actions on (1) the binding of the fluorescent agonist Dns-C6-Cho to the nicotinic acetylcholine receptor's agonist self-inhibition site and (2) the desensitization kinetics induced by the binding of the weak partial agonist suberyldicholine. Methods The dissociation constant for Dns-C6-Cho binding to the self-inhibitory site was determined using stopped-flow fluorescence spectroscopy. The values of the kinetic constants for agonist binding, channel gating, and desensitization were determined by modeling the suberyldicholine concentration-dependence of the apparent rate of desensitization. Results Isoflurane did not significantly alter the dissociation constant for Dns-C6-Cho binding to the self-inhibitory site even at a concentration as high as 1.5 mM, the highest concentration studied. At this concentration, isoflurane substantially reduced the dissociation constant for suberyldicholine binding to its channel opening site by 97% from 17 +/- 5 microM to 0.5 +/- 0.2 microM, whereas the preopen/open channel state equilibrium was reduced only from 19.1 to 5 +/- 1. Conclusions Isoflurane increases the apparent agonist affinity of the nicotinic acetylcholine receptor primarily by reducing the agonist dissociation constant of the site responsible for channel opening rather than altering channel gating kinetics.

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Ianosi, Edith Simona, Paraschiva Postolache, Luana Andreea Macovei, Mioara Szathmary, Simona Szasz, Roxana Maria Nemes, and Gabriela Jimborean. "Smoking Cessation in COPD Patients by a Selective Partial Nicotinic Agonist." Revista de Chimie 69, no. 7 (August 15, 2018): 1766–69. http://dx.doi.org/10.37358/rc.18.7.6413.

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The fight against smoking through various smoking cessation methods could be very effective by early education especially in young people for preventing the occurrence or the severity of obstructive lung diseases. The aim of the study was to present the impact of varenicline, a selective partial nicotine agonist, in adults of 40-49 year-old, active smokers, recently diagnosed with COPD, from 2009 to 2011, in a Smoking Cessation Center of the Pulmonary Rehabilitation Clinic Iasi, Romania. There were included all male employees, without occupational exposure, active smokers, with a personal history of smoking �10 packs-year cigarettes, recently diagnosed with COPD, who inform consented to be enrolled for counseling and smoking cessation treatment provided by varenicline. All patients received COPD therapy, according to the current GOLD recommendations. The method of evalution the impact of smoking cessation methods consisted in the COPD Assessment Test (CAT) completed by cases before and after 12 weeks program of smoking cessation counseling and therapy and respiratory rehabilitation. The CAT is a short questionnaire, simple and validated tool of COPD symptoms assessment, measuring the severity of COPD on a patient�s quality of life. Results reveals an important decreasing of CAT score with important amelioration of symptoms especially in severe COPD patients. Counseling, smoking cessation and respiratory rehabilitation interventions have shown positive effects of smoking cessation with varenicline among young COPD patients 40-49 year-old.

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Häggblad, J., H. Eriksson, and E. Heilbronn. "Oxotremorine Acts as a Partial Nicotinic Agonist on Cultured Chick Myotubes." Acta Pharmacologica et Toxicologica 57, no. 5 (March 13, 2009): 317–21. http://dx.doi.org/10.1111/j.1600-0773.1985.tb00051.x.

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Koelsch, Gerald, Leonard T. Meltzer, Ryan F. Yoshimura, Alvin V. Terry, Patrick M. Callahan, Geoffrey Bilcer, John Ng, Raymond Ng, Kelvin W. Gee, and Terence A. Kelly. "P4-373: APN1125: A NOVEL A7 NICOTINIC ACETYLCHOLINE RECEPTOR PARTIAL AGONIST." Alzheimer's & Dementia 10 (July 2014): P925. http://dx.doi.org/10.1016/j.jalz.2014.07.142.

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Nides, Mitchell. "Smoking Cessation With Varenicline, a Selective α4β2 Nicotinic Receptor Partial Agonist." Archives of Internal Medicine 166, no. 15 (August 14, 2006): 1561. http://dx.doi.org/10.1001/archinte.166.15.1561.

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Mihalak, Karla B., F. Ivy Carroll, and Charles W. Luetje. "Varenicline Is a Partial Agonist at α4β2 and a Full Agonist at α7 Neuronal Nicotinic Receptors." Molecular Pharmacology 70, no. 3 (June 9, 2006): 801–5. http://dx.doi.org/10.1124/mol.106.025130.

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Papke, Roger L., Hillary C. Schiff, Brian A. Jack, and Nicole A. Horenstein. "Molecular dissection of tropisetron, an α7 nicotinic acetylcholine receptor-selective partial agonist." Neuroscience Letters 378, no. 3 (April 2005): 140–44. http://dx.doi.org/10.1016/j.neulet.2004.12.025.

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21

Wilson, Robert D., Ed Cleator, Michael S. Ashwood, Matthew M. Bio, Karel M. J. Brands, Antony J. Davies, Ulf-H. Dolling, et al. "Development of a Scaleable Synthesis of a Partial Nicotinic Acid Receptor Agonist." Organic Process Research & Development 13, no. 3 (May 15, 2009): 543–47. http://dx.doi.org/10.1021/op800290t.

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22

Toffey, Brittany A., Marcie Rabin, and Roger Kurlan. "Withdrawal-Emergent Dyskinesias following Varenicline Therapy." Open Neurology Journal 9, no. 1 (June 8, 2015): 7–8. http://dx.doi.org/10.2174/1874205x01509010007.

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Varenicline (Chantix[R]) is a nicotinic acetylcholine receptor partial agonist used to aid smoking cessation. Adverse psychiatric and behavioral effects of the drug are recognized and national drug monitoring has included reports of tardive dyskinesia, but no cases have been described in the literature. We now report the first two cases of varenicline-related withdrawal emergent dyskinesias.

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Nirogi, Ramakrishna, Venkatesh Goura, Renny Abraham, and Pradeep Jayarajan. "α4β2* neuronal nicotinic receptor ligands (agonist, partial agonist and positive allosteric modulators) as therapeutic prospects for pain." European Journal of Pharmacology 712, no. 1-3 (July 2013): 22–29. http://dx.doi.org/10.1016/j.ejphar.2013.04.021.

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Kozak, Karolina, Sarah S. Dermody, Maryam Sharif-Razi, Alexandria S. Coles, Marya Morozova, Victoria C. Wing, Sherry A. McKee, and Tony P. George. "Effects of the Nicotinic Partial Agonist Varenicline on Smoking Lapse Behaviour in Schizophrenia." Canadian Journal of Addiction 10, no. 2 (June 2019): 27–35. http://dx.doi.org/10.1097/cxa.0000000000000052.

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25

Tonstad, Serena. "Smoking Cessation Efficacy and Safety of Varenicline, an α4β2 Nicotinic Receptor Partial Agonist." Journal of Cardiovascular Nursing 21, no. 6 (November 2006): 433–36. http://dx.doi.org/10.1097/00005082-200611000-00004.

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Cucchiaro, Giovanni, Yingxian Xiao, Alfredo Gonzalez-Sulser, and Kenneth J. Kellar. "Analgesic Effects of Sazetidine-A, a New Nicotinic Cholinergic Drug." Anesthesiology 109, no. 3 (September 1, 2008): 512–19. http://dx.doi.org/10.1097/aln.0b013e3181834490.

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Background The use of nicotinic agonists for analgesia is limited by their unacceptable side effects. Sazetidine-A is a new partial agonist nicotinic ligand that has very high selectivity for beta2-containing nicotinic acetylcholine receptors. It potently and selectively desensitizes alpha4beta2 nicotinic acetylcholine receptors without measurable effects on alpha3beta4 receptors. The authors investigated the analgesic effects of Sazetidine-A using the formalin model of chronic inflammatory pain. Methods The formalin test was conducted after rats received intraperitoneal saline, Sazetidine-A (0.125, 0.25, 0.5, 1, 2 mg/kg), or subcutaneous epibatidine (2.5-5-10 mug/kg). In other experiments, Sazetidine-A was preceded by naloxone (0.5 mg/kg) or mecamylamine (10 mg). Effects of Sazetidine-A and epibatidine on locomotor were tested in an open field, and seizure activity was measured using the Racine scale. Locus coeruleus neuron extracellular single-unit spontaneous discharge was recorded in anesthetized animals after Sazetidine-A and epibatidine. Results Higher doses of Sazetidine-A (0.5, 1, or 2 mg/kg) induced analgesia, with pain scores significantly lower than those seen after saline, lower doses of Sazetidine-A, and epibatidine (P < 0.001). Naloxone did not antagonize the effects of Sazetidine-A, and mecamylamine had partial, dose-dependent antagonistic effects. Epibatidine excited locus coeruleus neurons, whereas Sazetidine-A had no effect on these neurons. Epibatidine and Sazetidine-A affected animals' locomotor activity for the initial 20 min. While analgesic doses of epibatidine caused seizures, no seizure activity or other neurologic complications were seen in animals that received as much as four times the minimum analgesic dose of Sazetidine-A. Conclusions Sazetidine-A seems to be a potent analgesic without causing neurologic side effects.

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Dunbar, Geoffrey C., Fraser Inglis, Ramana Kuchibhatla, Tonmoy Sharma, Mark Tomlinson, and James Wamsley. "Effect of ispronicline, a neuronal nicotinic acetylcholine receptor partial agonist, in subjects with age associated memory impairment (AAMI)." Journal of Psychopharmacology 21, no. 2 (March 2007): 171–78. http://dx.doi.org/10.1177/0269881107066855.

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Cognitive decline seen in the normal elderly is associated with selective loss of neuronal nicotinic acetylcholine receptors (nAChRs). Nicotine given either by inhalation or transdermally helps cognition, but unacceptable side effects limit its utility. The present study assessed the safety, tolerability and effect on cognition of ispronicline, a highly selective partial agonist at the 4β2 nAChR, in elderly subjects ( n =76) with age associated memory impairment (AAMI). This double-blind, placebo-controlled cross-over study explored ascending oral doses of ispronicline in the range 50–150mg given as a single morning dose for a period of 3 weeks. Pharmacokinetics (PK) were assessed, as well as cognitive function measured by means of the Cognitive Drug Research (CDR) computerized test battery. Ispronicline had a favourable safety profile and was well tolerated at doses below 150mg. No effect of clinical importance was seen on biochemistry, haematology, urine analysis, vital signs, electrocardiogram (ECG) or Holter monitoring. The most frequent drug induced adverse event was light-headedness (dizziness). A beneficial effect was seen on cognition across the dose range. This was most marked at 50mg on factors measuring attention and episodic memory. PK analysis indicated a plasma Cmax range of 5–25/35ng/ml ispronicline was associated with the most beneficial effect. These early results demonstrate ispronicline was well tolerated and did not display the side effects typical of nicotine. Ispronicline also had a beneficial effect on cognition in subjects with AAMI. This was seen most strongly in a Cmax range that had been predicted from pre-clinical animal studies.

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Eddins, Donnie, Lisa K. Lyford, Jung Weon Lee, Sanjay A. Desai, and Robert L. Rosenberg. "Permeant but not impermeant divalent cations enhance activation of nondesensitizing α7 nicotinic receptors." American Journal of Physiology-Cell Physiology 282, no. 4 (April 1, 2002): C796—C804. http://dx.doi.org/10.1152/ajpcell.00453.2001.

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Neuronal α7 nicotinic acetylcholine receptors (nAChRs) are permeable to Ca2+ and other divalent cations. We characterized the modulation of the pharmacological properties of nondesensitizing mutant (L247T and S240T/L247T) α7 nAChRs by permeant (Ca2+, Ba2+, and Sr2+) and impermeant (Cd2+ and Zn2+) divalent cations. α7 receptors were expressed in Xenopus oocytes and studied with two-electrode voltage clamp. Extracellular permeant divalent cations increased the potency and maximal efficacy of ACh, whereas impermeant divalent cations decreased potency and maximal efficacy. The antagonist dihydro-β-erythroidine (DHβE) was a strong partial agonist of L247T and S240T/L247T α7 receptors in the presence of divalent cations but was a weak partial agonist in the presence of impermeant divalent cations. Mutation of the “intermediate ring” glutamates (E237A) in L247T α7 nAChRs eliminated Ca2+conductance but did not alter the Ca2+-dependent increase in ACh potency, suggesting that site(s) required for modulation are on the extracellular side of the intermediate ring. The difference between permeant and impermeant divalent cations suggests that sites within the pore are important for modulation by divalent cations.

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Cartereau, Alison, Emiliane Taillebois, Jean-Yves Le Questel, and Steeve H. Thany. "Mode of Action of Neonicotinoid Insecticides Imidacloprid and Thiacloprid to the Cockroach Pameα7 Nicotinic Acetylcholine Receptor." International Journal of Molecular Sciences 22, no. 18 (September 13, 2021): 9880. http://dx.doi.org/10.3390/ijms22189880.

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The functional expression of the cockroach Pameα7 nicotinic acetylcholine receptor subunit has been previously studied, and was found to be able to form a homomeric receptor when expressed in Xenopus laevis oocytes. In this study, we found that the neonicotinoid insecticide imidacloprid is unable to activate the cockroach Pameα7 receptor, although thiacloprid induces low inward currents, suggesting that it is a partial agonist. In addition, the co-application or 5 min pretreatment with 10 µM imidacloprid increased nicotine current amplitudes, while the co-application or 5 min pretreatment with 10 µM thiacloprid decreased nicotine-evoked current amplitudes by 54% and 28%, respectively. This suggesting that these two representatives of neonicotinoid insecticides bind differently to the cockroach Pameα7 receptor. Interestingly, the docking models demonstrate that the orientation and interactions of the two insecticides in the cockroach Pameα7 nAChR binding pocket are very similar. Electrophysiological results have provided evidence to suggest that imidacloprid and thiacloprid could act as modulators of the cockroach Pameα7 receptors.

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30

Rowland, Martin, Carrie Foust Koenigsfeld, and Geoffrey C. Wall. "Possible Exacerbation of Crohn's Disease Caused By Varenicline." Journal of Smoking Cessation 3, no. 1 (April 1, 2008): 63–65. http://dx.doi.org/10.1375/jsc.3.1.63.

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AbstractPurpose: To report a case of an increase in Crohn's disease (CD) activity possibly caused by varenicline. Background: Smoking cigarettes has been shown to be an independent risk factor for the development of CD and is associated with a more aggressive disease course. Smoking cessation is therefore considered a primary adjunctive goal for such patients. Varenicline is a partial nicotinic agonist, which selectively binds to the α-4, β-2 receptor. This receptor is thought to play a large role in the additive properties of nicotine and the drug is approved in the United States for this purpose. Case results: A 62-year-old female with a 12-year history of stable, quiescent CD, presented to her physician with symptoms of severe nausea, frequent episodes of vomiting, abdominal cramping, and significant diarrhoea, all of which was thought to be her first exacerbation of CD in years. The patient had started varenicline 2 days prior to the initiation of symptoms and had continued worsening symptoms for the next 2 weeks during which she continued the drug. One week after discontinuing varenicline the symptoms abated completely. Due to its pharmacology as a nicotine partial agonist, varenicline was thought to have possibly caused an exacerbation of this patient's CD. Conclusion: A patient had a possible exacerbation of her CD triggered by varenicline used for smoking cessation. Because smoking cessation is imperative in CD patients, care should be used when starting varenicline for this purpose.

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Levin, Edward D., Amir H. Rezvani, Yingxian Xiao, Susan Slade, Marty Cauley, Corinne Wells, Dawn Hampton, et al. "Sazetidine-A, a Selective α4β2 Nicotinic Receptor Desensitizing Agent and Partial Agonist, Reduces Nicotine Self-Administration in Rats." Journal of Pharmacology and Experimental Therapeutics 332, no. 3 (December 10, 2009): 933–39. http://dx.doi.org/10.1124/jpet.109.162073.

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32

Lam, Sum, and Priti N. Patel. "Varenicline: A Selective ??4??2 Nicotinic Acetylcholine Receptor Partial Agonist Approved for Smoking Cessation." Cardiology in Review 15, no. 3 (May 2007): 154–61. http://dx.doi.org/10.1097/01.crd.0000260270.12829.45.

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33

Biton, Bruno, Olivier E. Bergis, Frédéric Galli, Alain Nedelec, Alistair W. Lochead, Samir Jegham, Danielle Godet, et al. "SSR180711, a Novel Selective α7 Nicotinic Receptor Partial Agonist: (1) Binding and Functional Profile." Neuropsychopharmacology 32, no. 1 (October 4, 2006): 1–16. http://dx.doi.org/10.1038/sj.npp.1301189.

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34

Tasso, Bruno, Federica Novelli, Fabio Sparatore, Francesca Fasoli, and Cecilia Gotti. "(+)-Laburnamine, a Natural Selective Ligand and Partial Agonist for the α4β2 Nicotinic Receptor Subtype." Journal of Natural Products 76, no. 4 (March 5, 2013): 727–31. http://dx.doi.org/10.1021/np3007028.

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35

Brown, Laurence A., Makoto Ihara, Steven D. Buckingham, Kazuhiko Matsuda, and David B. Sattelle. "Neonicotinoid insecticides display partial and super agonist actions on native insect nicotinic acetylcholine receptors." Journal of Neurochemistry 99, no. 2 (October 2006): 608–15. http://dx.doi.org/10.1111/j.1471-4159.2006.04084.x.

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36

Faessel, Hélène M., Megan A. Gibbs, David J. Clark, Kevin Rohrbacher, Marilyn Stolar, and Aaron H. Burstein. "Multiple-Dose Pharmacokinetics of the Selective Nicotinic Receptor Partial Agonist, Varenicline, in Healthy Smokers." Journal of Clinical Pharmacology 46, no. 12 (December 2006): 1439–48. http://dx.doi.org/10.1177/0091270006292624.

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37

Steensland, P., J. A. Simms, J. Holgate, J. K. Richards, and S. E. Bartlett. "Varenicline, an 4beta2 nicotinic acetylcholine receptor partial agonist, selectively decreases ethanol consumption and seeking." Proceedings of the National Academy of Sciences 104, no. 30 (July 11, 2007): 12518–23. http://dx.doi.org/10.1073/pnas.0705368104.

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38

Theng, Yoong Mei, Suzaily Wahab, Noor Alaudin A. Wahab, Hatta Sidi, and Srijit Das. "Schizophrenia and Nicotine Dependence: What Psychopharmacological Treatment Options are Available for the Duo Perturbationes?" Current Drug Targets 20, no. 2 (December 19, 2018): 173–81. http://dx.doi.org/10.2174/1389450118666171017163741.

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Nicotine dependence has progressively become a foremost community health interest in both the developed and developing nations due to the economic burden and health-related problems. Smoking was significantly higher among patients with schizophrenia in comparison to the general population. Nicotine dependence is not only associated with public stress, but among patients with schizophrenia, smoking brings major challenges to the management. Nicotine may diminish the therapeutic efficacy of the bioavailability of the psychopharmacological agents in-vivo. These duo perturbations, i.e. two clinical conditions co-existed may prevent psychotic symptoms remission among patients suffering from schizophrenia who smoke at the same time. The aim of this review was to highlight the role of pharmacological treatment options and strategies for patients with nicotine dependence in schizophrenia with emphasis on the underlying neurobiological process. The role of nicotine replacement therapy, i.e. norepinephrine-dopamine reuptake inhibition (NDRI) e.g. bupropion and selective partial agonist of α4β2 and full &#945;7-nicotinic acetylcholine receptor e.g. varenicline was deliberated. An ideal choice of drug targets for patients with schizophrenia with nicotine dependence is pivotal to foster a better therapeutic alliance.

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39

Radchenko, E., O. Dravolina, and A. Bespalov. "P.6.011 Pharmacological profile of the nicotinic receptor partial agonist cytisine: effects on maintenance and relapse to nicotine seeking." European Neuropsychopharmacology 21 (April 2011): S165—S166. http://dx.doi.org/10.1016/s0924-977x(11)70212-7.

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40

Hu, Yiping, Ruoxi Liu, Jinchao Li, Ye Yue, Wenxiang Cheng, and Peng Zhang. "Attenuation of Collagen-Induced Arthritis in Rat by Nicotinic Alpha7 Receptor Partial Agonist GTS-21." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/325875.

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This research was performed to observe the effect of GTS-21 on Collagen Induced Arthritis (CIA). CIA model was used and after the onset of arthritis, the rats were divided into three groups based on their clinical symptoms score. Two groups were intraperitoneally (IP) injected daily with GTS-21 (1 mg/kg, 2.5 mg/kg) for a week, whereas phosphate buffered saline (PBS) was used for the control group. Cytokine titers, radiological, and histological examinations were performed at different time points after treatment with GTS-21. Compared with those of the control, the levels of TNF-α, IL-1, and IL-6 in the serum were significantly reduced after GTS-21 management. In addition, radiological results show that bone degradation was inhibited as well. Moreover, the hematoxylin and eosin (H&E) staining indicated that the histological score was significantly alleviated in the therapeutic group. Tartrate-resistant acid phosphatase (TRAP) stain-positive cells were also detected in the destruction of the articular cartilage, which was significantly reduced compared with the control group. This study provides the first evidence on the effect of GTS-21 as a potential treatment for RA.

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Wallace, Tanya L., Patrick M. Callahan, Ashok Tehim, Daniel Bertrand, Geoffrey Tombaugh, Shaojie Wang, Walter Xie, et al. "RG3487, a Novel Nicotinic α7 Receptor Partial Agonist, Improves Cognition and Sensorimotor Gating in Rodents." Journal of Pharmacology and Experimental Therapeutics 336, no. 1 (October 19, 2010): 242–53. http://dx.doi.org/10.1124/jpet.110.171892.

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Déglise, Patrice, Bernd Grünewald, and Monique Gauthier. "The insecticide imidacloprid is a partial agonist of the nicotinic receptor of honeybee Kenyon cells." Neuroscience Letters 321, no. 1-2 (March 2002): 13–16. http://dx.doi.org/10.1016/s0304-3940(01)02400-4.

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43

Farook, Justin M., Ben Lewis, Justin G. Gaddis, John M. Littleton, and Susan Barron. "Lobeline, a nicotinic partial agonist attenuates alcohol consumption and preference in male C57BL/6J mice." Physiology & Behavior 97, no. 3-4 (June 2009): 503–6. http://dx.doi.org/10.1016/j.physbeh.2009.02.031.

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Crunelle, Cleo L., Michelle L. Miller, Jan Booij, and Wim van den Brink. "The nicotinic acetylcholine receptor partial agonist varenicline and the treatment of drug dependence: A review." European Neuropsychopharmacology 20, no. 2 (February 2010): 69–79. http://dx.doi.org/10.1016/j.euroneuro.2009.11.001.

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45

Breining, Scott R., John F. Genus, J. Pike Mitchener, Timothy J. Cuthbertson, Ronald Heemstra, Matt S. Melvin, Gary M. Dull, and Daniel Yohannes. "Development of a Scalable Synthesis of a Pyridinyl-3-azabicyclononene, a Novel Nicotinic Partial Agonist." Organic Process Research & Development 17, no. 3 (February 21, 2013): 413–21. http://dx.doi.org/10.1021/op400002r.

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46

Kuang, Shanming, Pingsheng Zhang, Eric Z. Dong, Geremia Jennings, Baoshu Zhao, and Michael Pierce. "Crystal form control and particle size control of RG3487, a nicotinic α7 receptor partial agonist." International Journal of Pharmaceutics 508, no. 1-2 (July 2016): 109–22. http://dx.doi.org/10.1016/j.ijpharm.2016.04.066.

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47

Tonstad, Serena, and Charl Els. "Varenicline: Smoking Cessation in Patients with Medical and Psychiatric Comorbidity." Clinical Medicine Insights: Therapeutics 2 (January 2010): CMT.S4012. http://dx.doi.org/10.4137/cmt.s4012.

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Smoking remains a major public health challenge. Nicotine is the main psychoactive drug responsible for the addictive nature of tobacco, explaining why many smokers fail to quit without assistance. Pharmacotherapy for smoking cessation is deemed effective for a broad range of populations and should be routinely offered to smokers interested in making a quit attempt. Varenicline, a partial agonist at the α4β2 nicotinic receptor increases chances of quitting three-fold compared to placebo in smokers without comorbidities, and in smokers with cardiovascular disease or chronic obstructive pulmonary disease. Persons with mental illness have high rates of smoking, and the potential impact of varenicline on mental status and the underlying pathophysiology of mental illness, has become a salient concern. Varenicline is an appropriate aid for smoking cessation in patients with medical and/or psychiatric comorbidity. This conclusion is supported by current evidence on the safety and tolerability of the drug.

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Szczupak, L., J. Edgar, ML Peralta, and WB Kristan. "Long-lasting depolarization of leech neurons mediated by receptors with a nicotinic binding site." Journal of Experimental Biology 201, no. 12 (June 15, 1998): 1895–906. http://dx.doi.org/10.1242/jeb.201.12.1895.

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The serotonergic Retzius neurons of the leech midbody ganglia respond in a complex manner to pressure pulses of acetylcholine (ACh) applied onto their soma with a fast depolarization followed by a slower hyperpolarization and an additional delayed long-lasting depolarization. The delayed depolarization is the subject of the present study. The delayed depolarization could be elicited by long (>1 s) ACh pressure pulses or by short pulses (10 ms) of carbachol, nicotine and DMPP, but not by muscarinic agonists. It was inhibited by bath application of nicotine (10-100 micromol l-1), strychnine (100 micromol l-1) and atropine (10-100 micromol l-1). Nicotinic antagonists that blocked the fast depolarization and the slow hyperpolarization (100 micromol l-1 mecamylamine and d-tubocurarine) did not affect the delayed depolarization induced by carbachol. Partial replacement of the extracellular Na+ by glucamine caused a decrease in the amplitude of the response and a shift of its reversal potential to more negative values. Carbachol pulses applied to Retzius neurons of the ganglia innervating the reproductive segments elicited delayed depolarizations of much smaller amplitude than the ones recorded in Retzius neurons from standard segments. The delayed depolarization could be elicited by the application of short agonist pulses onto different loci over the surface of the ganglion, at a distance from the soma. Isolated cultured Retzius neurons did not exhibit the delayed depolarization although they readily expressed the earlier phases of the complex cholinergic response. Carbachol pulses applied to the soma of other neurons in the leech ganglion produced a variety of specific responses.The results suggest that the delayed depolarization was produced by the activation of a cationic conductance mediated by receptors with a pharmacological profile similar to that of the <IMG src="/images/symbols/&agr ;.gif" WIDTH="9" HEIGHT= "12" ALIGN="BOTTOM" NATURALSIZEFLAG="3">9 nicotinic receptors and was not a byproduct of the early phases of the cholinergic response. The response seemed to be initiated in the extensive neuropilar processes of the Retzius cell, enabling a persistent excitatory signal.

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Bobak, Alex. "Varenicline: Implications for the Field." Journal of Smoking Cessation 2, S1 (December 1, 2007): 8–11. http://dx.doi.org/10.1375/jsc.2.supp.8.

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AbstractVarenicline tartrate (Champix) is the first in a new class of therapy for smoking cessation and has been available on NHS prescription since December 2006. It has received approval from The National Institute for Health and Clinical Excellence (NICE) and the Scottish Medicines Consortium and NICE final guidance was issued in July 2007. Varenicline is a partial agonist of the nicotinic receptor (·4, 2 subtype) and also prevents nicotine from binding to it. Studies comparing safety and efficacy with bupropion (Zyban) have been favourable and efficacy with varenicline has been shown to be greater than that with bupropion. A study comparing the nicotine patch is due for publication this year. Varenicline has a good safety profile with nausea being the most common side effect in about a third of those who take it. Despite the treatment's advantages there have been numerous issues which have affected its use. These include funding and administrative issues and this paper looks at ways of overcoming those barriers to prescribing what is a valuable addition to the range of treatments on offer to smokes who want to stop.

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STRANG, CHRISTIANNE E., JORDAN M. RENNA, FRANKLIN R. AMTHOR, and KENT T. KEYSER. "Nicotinic acetylcholine receptor expression by directionally selective ganglion cells." Visual Neuroscience 24, no. 4 (July 2007): 523–33. http://dx.doi.org/10.1017/s0952523807070435.

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Acetylcholine (ACh) enhances the preferred direction responses of directionally selective ganglion cells (DS GCs; Ariel & Daw, 1982; Ariel & Adolph, 1985) through the activation of nicotinic acetylcholine receptors (nAChRs; Ariel & Daw, 1982; Massey et al., 1997; Kittila & Massey, 1997). DS GCs appear to express at least two types of nAChRs, those that are sensitive to the partially subtype-specific antagonist methyllycaconitine (MLA), and those that are MLA-insensitive (Reed et al., 2002). Our purpose was to confirm the expression of α7 nAChRs by DS GCs and to assess the contributions of other nAChR subtypes to DS GC responses. Using choline as a nAChR partially subtype-specific agonist, we found that the majority of DS GCs demonstrated responses to choline while under synaptic blockade. The blockade or reduction of choline-induced responses by bath application of nanomolar (nM) concentrations of MLA provided direct evidence that the choline responses were mediated by α7 nAChRs. Because choline is a partial agonist for α3β4 nAChRs (Alkondon et al., 1997), the residual choline responses are consistent with mediation by α3β4 nAChRs. Additionally, a subset of DS GCs responded to nicotine but not to choline, indicating the expression of a third nAChR subtype. The pharmacological results were supported by single cell reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry experiments. The expression of α7 and specific non-α7 nAChR subtypes was correlated with the preferred direction. This indicates the possibility of differential responses to ACh depending on the direction of movement. This is the first description of differential expression of multiple nAChR subtypes by DS GCs.

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