Academic literature on the topic 'Vesicular Acetylcholine Transporter'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Vesicular Acetylcholine Transporter.'
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 "Vesicular Acetylcholine Transporter"
Duerr, Janet S., Jennifer Gaskin, and James B. Rand. "Identified neurons in C. elegans coexpress vesicular transporters for acetylcholine and monoamines." American Journal of Physiology-Cell Physiology 280, no. 6 (June 1, 2001): C1616—C1622. http://dx.doi.org/10.1152/ajpcell.2001.280.6.c1616.
Full textKoulen, Peter. "Vesicular acetylcholine transporter (VAChT)." NeuroReport 8, no. 13 (September 1997): 2845–47. http://dx.doi.org/10.1097/00001756-199709080-00008.
Full textBravo, Dawn T., Natalia G. Kolmakova, and Stanley M. Parsons. "Choline is transported by vesicular acetylcholine transporter." Journal of Neurochemistry 91, no. 3 (November 2004): 766–68. http://dx.doi.org/10.1111/j.1471-4159.2004.02746.x.
Full textOjeda, Ana M., Natalia G. Kolmakova, and Stanley M. Parsons. "Acetylcholine Binding Site in the Vesicular Acetylcholine Transporter†." Biochemistry 43, no. 35 (September 2004): 11163–74. http://dx.doi.org/10.1021/bi049562b.
Full textEfange, S. M. N. "In vivo imaging of the vesicular acetylcholine transporter and the vesicular monoamine transporter." FASEB Journal 14, no. 15 (December 2000): 2401–13. http://dx.doi.org/10.1096/fj.00-0204rev.
Full textEfange, S. M. N., E. M. Garland, J. K. Staley, A. B. Khare, and D. C. Mash. "Vesicular Acetylcholine Transporter Density and Alzheimer’s Disease." Neurobiology of Aging 18, no. 4 (July 1997): 407–13. http://dx.doi.org/10.1016/s0197-4580(97)00038-9.
Full textCho, Goang-Won, Myung-Hee Kim, Young-Gyu Chai, Michelle L. Gilmor, Alan I. Levey, and Louis B. Hersh. "Phosphorylation of the Rat Vesicular Acetylcholine Transporter." Journal of Biological Chemistry 275, no. 26 (March 22, 2000): 19942–48. http://dx.doi.org/10.1074/jbc.m902174199.
Full textVaroqui, Hélène, and Jeffrey D. Erickson. "Active Transport of Acetylcholine by the Human Vesicular Acetylcholine Transporter." Journal of Biological Chemistry 271, no. 44 (November 1, 1996): 27229–32. http://dx.doi.org/10.1074/jbc.271.44.27229.
Full textPrado, Vania F., Ashbeel Roy, Benjamin Kolisnyk, Robert Gros, and Marco A. M. Prado. "Regulation of cholinergic activity by the vesicular acetylcholine transporter." Biochemical Journal 450, no. 2 (February 15, 2013): 265–74. http://dx.doi.org/10.1042/bj20121662.
Full textKitzman, Patrick. "Changes in vesicular glutamate transporter 2, vesicular GABA transporter and vesicular acetylcholine transporter labeling of sacrocaudal motoneurons in the spastic rat." Experimental Neurology 197, no. 2 (February 2006): 407–19. http://dx.doi.org/10.1016/j.expneurol.2005.10.005.
Full textDissertations / Theses on the topic "Vesicular Acetylcholine Transporter"
Richards, Dannette Shanon. "CHARACTERIZATION OF EXCITATORY AMINO ACID NEUROTRANSMITTERS AT MOTONEURON SYNAPSES CONTACTING RENSHAW CELLS." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1260896604.
Full textQuinlivan, Mitchell Owen Jeffrey. "Functions of the Cholinergic System in the Morbidities Associated with Alzheimer’s Disease and the Further Evaluation of Tools for the Molecular Imaging of this System." University of Sydney, 2007. http://hdl.handle.net/2123/1933.
Full textThe aims of this project were to contribute to the elucidation of the role of the cholinergic system in attention and memory, two cognitive processes severely compromised in Alzheimer’s disease (AD), and to evaluate and develop tools for the functional molecular imaging of this system with a view to improving knowledge of AD and other neurological disorders. Towards the first aim, the specific anti-cholinergic toxin 192 IgG-saporin (SAP) was administered to female Sprague-Dawley rats via either an intracerebroventricular (icv) or an intracortical route and animals were tested with a vibrissal-stimulation reaction-time task and an object recognition task to evaluate their attentional and mnemonic function, respectively. The second aim was approached in two ways. Firstly, relative neuronal densities from animals with icv lesions were assessed with both ex vivo and in vitro autoradiography with the specific cholinergic radiopharmaceuticals [123I]iodobenzovesamicol (123IBVM) and 125I-A-85380, ligands for the vesicular acetylcholine transporter and the nicotinic acetylcholine receptor, respectively. Secondly, a number of in vivo and in vitro studies were performed on a novel and unique molecular imaging system (TOHR), with which it had been hoped initially to image eventually SAP-lesioned animals, with a view to measuring and ameliorating its performance characteristics and assessing its in-principle suitability for small-animal molecular imaging. The behavioural studies support a critical role for the cholinergic system in normal attentional function. Additionally, in accord with literature evidence, no significant impairment was observed in mnemonic function. It is postulated however that the results observed in the intracortically-lesioned animals support the published hypothesis that cholinergic projections to the perirhinal cortex are critical for object-recognition memory. In autoradiographic studies, SAP-lesioned animals demonstrated reduced uptake of 123IBVM in multiple regions. A reduction of nicotinic receptors was also seen in SAP-lesioned animals, a novel finding supportive of the excellent characteristics of radioiodinated I-A-85380. Examination of the performance characteristics of the TOHR support in principle its utility for targeted small-animal molecular imaging studies.
Miranda, Claúdia Jeane Claudino de Pontes. "Avaliação da função e da histopatologia pulmonar em modelo experimental de inflamação pulmonar alérgica crônica: efeitos da redução da função colinérgica em camundongos geneticamente modificados." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-27072012-104906/.
Full textBACKGROUND: Bronchial asthma is characterized by reversible or not airflow obstruction and pulmonary inflammation, mainly characterized by eosinophilia. The persistence of inflammation can induce lung repair process associated with progressive reduction in lung function. Recent evidence of the cholinergic anti-inflammatory system, a neural mechanism that suppresses the innate immune response and control inflammation by proinflammatory cytokines inhibition, and the detection of some of its components in airway cells suggest an important role of this system in pulmonary physiopathology. The main mediator of this system is acetylcholine (ACh), which is stored in synaptic vesicles by vesicular acetylcholine transporter (VAChT), an essential protein for ACh release. AIMS: To evaluate the effects of cholinergic deficiency by VAChT reduction on pulmonary alterations observed in an experimental model of pulmonary inflammation induced by chronic exposure to ovalbumin. METHODS: The cholinergic deficiency was induced by genetic modification on VAChT levels. Wild-type and mutant male mice were submitted to subcutaneous ovalbumin sensitization or saline protocol on days 0, 7 and 14. After, animals were submitted to inhalation challenge with ovalbumin 1% or saline for 20 minutes on days 26, 27 and 28. On day 29, we evaluated the pulmonary mechanics, inflammation in bronchoalveolar lavage and in airways, histological analysis of airway remodeling and the expression of MMP-9 and TIMP-1 by immunohistochemistry. It was also quantified by the levels of IL-4, IL-10 and TNF-a in lung homogenate. The statistical analysis were performed and a p<0.05 was considered significant. RESULTS: Sensitized animals presented bronchial hyperresponsividade, airway inflammation and edema and collagen and elastic fibers deposition of collagen and elastic fibers around the airways compared to saline group (p <0.05). Furthermore, there was an increase of IL-4 in lung homogenate and the expression of MMP-9 and TIMP-1 in inflammatory cells. The mutant animals, regardless the sensitization, showed an increase in lung content of TNF-a. The mutant and sensitized animals showed an increase in bronchial hyperresponsiveness, in eosinophils, edema and collagen deposition in airways compared to the wild type and sensitized animals. These changes can be attributed to increased IL-4 and MMP-9/TIMP-1 that were observed in mutant and sensitized animals. There was no difference in levels of IL-10 in the experimental groups. Conclusion: The cholinergic deficiency worsens bronchial hyperresponsiveness, eosinophilic inflammation, and airway remodeling mainly by interfering with the pro-inflammatory cytokine IL-4 and in MMP-9/TIMP-1 ratio. These data suggest that anti-inflammatory cholinergic pathway is involved in the asthma pathogenesis deserves further investigation
Lee, Na-Ra. "DISCOVERY OF NOVEL PHARMACOTHERAPEUTICS FOR SUBSTANCE USE DISORDERS." UKnowledge, 2019. https://uknowledge.uky.edu/pharmacy_etds/104.
Full textFranco, Rosana Banzato. "Efeitos da redução da função colinérgica na mecânica e na histopatologia pulmonar em modelo experimental de enfisema." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-27022014-145652/.
Full textBanckground: Pulmonary emphysema is a major component of chronic obstructive pulmonary disease (COPD), is characterized by enlargement, alveolar destruction and inflammation of the airways and lung tissue. The recent description of the cholinergic anti-inflammatory, a neural mechanism that controls inflammation by inhibition of proinflammatory cytokines, suggests an important role of this system in the pathophysiology of lung disease. The main mediator of this system is acetylcholine (ACh), which is stored in synaptic vesicles by vesicular acetylcholine transporter (VAChT) protein, which is essential for ACh release into the synaptic cleft. Aim: To evaluate whether the effects of cholinergic hypofunction by reduction on VAChT expression, interferes with pulmonary alterations in an experimental model of pulmonary emphysema. Methods: Male mice wild-type and mutant, the last one with reduced cholinergic function by genetic modification in the levels of VAChT, were submitted to the protocol of elastase (PPE intranasally) or saline. On day 28, pulmonary mechanics, inflammation in bronchoalveolar lavage fluid and tissue remodeling were analyzed. By immunohistochemistry, the expression of macrophage, NF-kB and isoprostane in lung was evaluated. Some proinflammatory cytokines were measured in lung homogenate by Bio Plex. Results: Wild-Type animals that received elastase presented a reduction in tissue elastance, an increase in BALF and tissue inflammation as well as in proinflammatory cytokines, IL-10, pulmonary remodeling, and expression of NF-kB and isoprostane. Cholinergic deficient in these animals submitted to the same elastase-induced emphysema protocol amplified the inflammatory response (macrophage and neutrophils) in the lungs, the levels of MCP-1 and the number of positive cells to NF-kB and isoprostane in bronchovascular axis. Conclusions: The ACh seems to have a protective role inflammation in this experimental model of emphysema, at least in part by controlling NF-kB and oxidative stress. These results further suggest that the remodeling and lung function in experimental emphysema does not depend entirely on the degree of lung inflammation
Pinheiro, Nathalia Montouro. "Efeito da redução da função colinérgica na mecânica pulmonar e na histopatologia pulmonar em modelo experimental de inflamação aguda induzida por instilação de LPS em camundongos geneticamente modificados." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-04082016-152420/.
Full textAcute lung injury (ALI) is characterized by acute lung inflammation with recruitment of polymorphonuclear and release of proinflammatory mediators. It is a severe condition since leads to death 40% of the cases. Several studies have elucidated the pathophysiology of ALI, however the treatment is still unsatisfactory. The anti-inflammatory cholinergic system was described in the lung and is related to a vagal nerve reflex that inhibits the release of inflammatory cytokines by the action o ACh on nicotinic receptors. Our hypothesis is that the VAChT reduction, which is related to the deficit in the release of ACh, modulates the pulmonary inflammatory response in a model of LPS. Aim: 1. To assess whether VAChT deficiency modulates the pulmonary response in genetically modified animals; 2. Assess whether cholinergic deficiency induced reduction VAChT is involved in pulmonary response to LPS and elucidate some mechanisms involved; 3. To evaluate the therapeutic potential of PNU, an agonist alfa7nAChR, in functional and histological changes in C57BL6 mice with LPA. Methods: Mutant genetically modified male mice (VAChT KDHOM) or wild (WT) and C57BL/6 were used. First, we evaluated lung function and lung histopathology in VAChT KDHOM animals. After, WT animals and VAChT KDHOM received intranasal instillation of LPS or saline and the inflammatory response was assessed 1.5 hours to 72 hours. Moreover, the pulmonary response was evaluated in WT and VAChT KDHOM after instillation of LPS intraperitoneally. Finally, C57BL6 instilled with intranasal LPS received prior or post-treatment with PNU, an alfa7 nicotinic receptor agonist. Results: Mutant animals had higher number of cells recovered in brochoalveolar lavage (BAL) and increased pro-inflammatory cytokines, peribronchial edema and worsening of lung function. Still, there was an increase of NF_kB expression and reduction of JAK2. The VAChT deficiency induced increase in inflammatory cells in animals receiving LPS only 1.5h after the LPS instilation, and the values were similar to WT in 24 and 72 hours. In WT mice, the stimulation of the nicotinic receptor improves inflammation, while the stimulation of muscarinic receptors appears to contribute to the worsening of the pulmonary inflammatory response. The effects of PNU seem to depend on the intact cholinergic pathway, since this drug had no effects on mutant animals. However, treatment with PNU in C57BL6 reduced pulmonar inflammation, cytokine production, collagen deposition in lung tissue and the levels of MMP-2, MMP-9 and TIMP-1, improving pulmonary function. These effects appear to be associated with reduced profile M1 macrophages and the inhibition of NF-kB. Conclusion: These data clearly demonstrate that the anti-inflammatory cholinergic system is involved in the control of lung inflammatory response, both to maintain the lung homeostasis or in the early stages of the development of ALI. Finally, it is clear that the stimulation of nicotinic receptors has great potential as a therapeutic target to be explored in ARDS
Kuznetsova, Elena. "β-AMYLOID, CHOLINERGIC TRANSMISSION, AND CEREBROVASCULAR SYSTEM - A DEVELOPMENTAL STUDY IN A TRANSGENIC MOUSE MODEL OF ALZHEIMER’S DISEASE." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-112763.
Full textSantana, Fernanda Paula Roncon. "Efeito da hipofunção colinérgica na mecânica e na histopatologia pulmonar em modelo experimental de inflamação pulmonar induzida por instilação de poluente em camundongos." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-26012015-090146/.
Full textDiesel automotive engines are widely used in urban centers and its exhausts is considered a major environmental and toxic pollutant to human health. Because of their chemical characteristics, diesel particulate reaches more distal airways, which can induce and worsen pulmonary inflammation diseases such as bronchial asthma and pulmonary emphysema. It has recently been demonstrated by our group that the cholinergic anti-inflammatory system is an important modulator of lung inflammation. Thus, the aim of this study was to evaluate whether the cholinergic deficiency induced by reduced expression of the vesicular acetylcholine transporter protein (VAChT) interferes in pulmonary function and histopathological changes in an experimental model of repeated diesel exhaust particles (DEP) instillation. To this end, male mice with reduction in VAChT were used, divided according to genotyping for wild-type (WT) and knock-down for VAChT (KD), and submitted to DEP exposure protocol, which consisted in intranasal instillation of 10 ?L of DEP in a concentration of 3 mg/mL for 30 days (5x per week). Control groups received saline following the same protocol. We evaluated: respiratory mechanics, inflammation in broncoalveolar lavage (BAL), immunohistochemistry and ELISA for cytokine detection, pulmonary extracellular matrix remodeling and bronchial and nasal epithelium mucus. Our results showed that WT animals submitted to DEP protocol showed increased macrophages in BAL and mononuclear cells in peripheral blood, increased expression of TNF-alfa, IL-4, IL-6 and IL-13 in lung tissue, collagen fibers remodeling in lung parenchyma and increase in neutral mucus production in the airways when compared to the saline exposed animals. These changes were associated with worse lung function. The cholinergic deficiency in the animals instilled with DEP induced an increase in BAL neutrophils and lymphocytes and granulocytes in the peripheral blood, in the expression of IL-4 and TNF-alfa and in lung elastic fibers content in alveolar septa. In addition, there was an increase in acid mucus in nasal epithelium. These data suggest that, at least in part, cholinergic system interferes with pulmonary inflammation induced by DEP exposures, since animals with cholinergic deficiency exhibit some inflammatory alterations which are not observed or observed on a smaller scale in wild-type animals
Schallreuter, Karin U., Bhavan Chavan, and Souna M. A. Elwary. "The vesicular acetylcholine transporter is present in melanocytes and keratinocytes in the human epidermis." 2006. http://hdl.handle.net/10454/4078.
Full textThe human epidermis holds the full machinery for cholinergic signal transduction. However, the presence of the vesicular transporter (vesicular acetylcholine (ACh) transporter (VAChT)) for both choline and ACh has never been shown in this compartment. The results of this study confirm the presence of VAChT in cutaneous nerves and in both epidermal melanocytes and keratinocytes as well as in their nuclei using immunofluorescence labelling in situ and in vitro, Western blot analysis of cellular and nuclear extracts and reverse transcription-PCR. These results underline that ACh/choline transport in the non-neuronal epidermis is no different from the neuronal pathway. However, the function of VAChT in the nucleus remains to be shown.
Landry, St-Pierre Evelyne. "Évaluation pré-clinique du (–)-[18F]FEOBV: Profil métabolique plasmatique." Thèse, 2008. http://hdl.handle.net/1866/2696.
Full textBackground. Several neurodegenerative diseases would benefit from better diagnostic tools, and Alzheimer’s disease is an obvious point in case. Of interest, that disease par-ticularly affects CNS cholinergic systems. Many studies have evaluated neurodegenera-tion in that system during the course of Alzheimer’s disease, some using imaging tech-niques with radioactive ligands targeting the cholinergic system. However, most of those studies have shown rather unsatisfying results. Therefore, our team has decided to evaluate a so far never used in primates positron emitting ligand of the VAChT which reversibly binds to its target, (-)-[18F]Fluoroethoxy-benzovesamicol ((-)-[18F]FEOBV). Of course, before being able to use this ligand in a clinical setting, a multi-step animal validation needs to be performed. As initial experiments with PET imaging yielded encouraging results, assessing the metabolism of (-)-[18F]FEOBV was the next logical step. First, an HPLC methodology had to be developed to analyse blood metabolites. Then, we were able to use that methodology to analyse metabolites and their kinetics in the rat. That data will allow quantitative studies in humans with PET. Study #1: After the chromatographic parameters had been optimised, the TR of (–)-FEOBV was established at 7.92 ± 0.18 minutes. Study#2 In vivo metabolism was found to be fairly rapid and somewhat temporally variable, but a lone hydrophilic metabolite was identified. The plasmatic input function was obtained and corrected for metabolism. Conclusion. Overall, (–)-[18F]FEOBV holds promise as a potential ACh system pre-synaptic marker.
Books on the topic "Vesicular Acetylcholine Transporter"
Siegal, Deborah M. Brain vesicular acetylcholine transporter levels in chronic users of cocaine, methamphetamine and heroin. Ottawa: National Library of Canada, 2002.
Find full textMason, Peggy. Synthesis, Packaging, and Termination of Neurotransmitters. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0012.
Full textBook chapters on the topic "Vesicular Acetylcholine Transporter"
Khare, Parul, Aubrey R. White, Anuprao Mulakaluri, and Stanley M. Parsons. "Equilibrium Binding and Transport by Vesicular Acetylcholine Transporter." In Methods in Molecular Biology, 181–219. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-700-6_10.
Full textWenzel, Barbara, Winnie Deuther-Conrad, Matthias Scheunemann, and Peter Brust. "Radioligand Development for PET Imaging of the Vesicular Acetylcholine Transporter (VAChT) in the Brain." In PET and SPECT of Neurobiological Systems, 1061–90. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-53176-8_32.
Full textTao-Cheng, J. H., and L. E. Eident. "The Vesicular Monoamine Transporter VMAT2 and Vesicular Acetylcholine Transporter VAChT Are Sorted to Separate Vesicle Populations in PC12 Cells." In Advances in Pharmacology, 250–53. Elsevier, 1997. http://dx.doi.org/10.1016/s1054-3589(08)60740-1.
Full textVaroqui, H., F. M. Meunier, F. A. Meunier, J. Molgo, S. Berrardxy, R. Cervini, J. Mallet, M. Israël, and M. F. Diebler. "Chapter 6 Expression of the vesicular acetylcholine transporter in mammalian cells." In Cholinergic Mechanisms: from Molecular Biology to Clinical Significance, 83–95. Elsevier, 1996. http://dx.doi.org/10.1016/s0079-6123(08)62090-7.
Full textSchütz, Burkhard, Eberhard Weihe, and Lee Eiden. "Targeting of the vesicular acetylcholine transporter to cholinergic subdivisions in transgenic mice." In Cholinergic Mechanisms, 691–93. CRC Press, 2004. http://dx.doi.org/10.3109/9780203493878-132.
Full textParsons, Stanley M., Gary A. Rogers, and Lawrence M. Gracz. "[7] Photoaffinity labeling of vesicular acetylcholine transporter from electric organ of Torpedo." In Methods in Enzymology, 99–116. Elsevier, 1998. http://dx.doi.org/10.1016/s0076-6879(98)96009-8.
Full textVaroqui, Helene, and Jeffrey D. Erickson. "[6] Functional identification of vesicular monoamine and acetylcholine transporters." In Methods in Enzymology, 84–99. Elsevier, 1998. http://dx.doi.org/10.1016/s0076-6879(98)96008-6.
Full textDiebler, M. F., Y. Morot Gaudry-Talarmain, J. C. Lancelot, M. Robba, J. L. Morgat, and M. Israel. "Comparison of the Effects of Vesamicol and of Cetiedil Analogues on Acetylcholine Release and Vesicular Acetylcholine Transport." In Presynaptic Receptors and Neuronal Transporters, 177–78. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-08-041165-1.50065-x.
Full textZhang, Lu, Mark Prendergast, and Jerry Buccafusco. "Estimation of the mRNAs Encoding the Cholinergic Muscarinic Receptor and Acetylcholine Vesicular Transport Proteins Involved in Central Cardiovascular Regulation." In Molecular Regulation of Arousal States. CRC Press, 1997. http://dx.doi.org/10.1201/9780849333613.ch2.
Full textZhang, Lu, Mark Prendergast, and Jerry Buccafusco. "Estimation of the mRNAs Encoding the Cholinergic Muscarinic Receptor and Acetylcholine Vesicular Transport Proteins Involved in Central Cardiovascular Regulation." In Molecular Regulation of Arousal States. CRC Press, 1997. http://dx.doi.org/10.1201/9781420048940.ch2.
Full textConference papers on the topic "Vesicular Acetylcholine Transporter"
Thayabaran, M., and S. G. Yasawardene. "Immunohistochemical localization of Vesicular Acetylcholine Transporters and Choline Acetyl Transferase activity in murine and human immune tissues." In Annual International Conference on Microscopic and Macroscopic Anatomy. Global Science & Technology Forum (GSTF), 2014. http://dx.doi.org/10.5176/2382-6096_cmma14.18.
Full text