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Journal articles on the topic 'Nicotine'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Zenkner, Fernanda Fleig, Márcia Margis-Pinheiro, and Alexandro Cagliari. "Nicotine Biosynthesis in Nicotiana: A Metabolic Overview." Tobacco Science 56, no. 1 (2019): 1–9. http://dx.doi.org/10.3381/18-063.

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Alkaloids are important compounds found in Nicotiana plants, essential in plant defense against herbivores. The main alkaloid of Nicotiana tabacum, nicotine, is produced in roots and translocated to the leaves. Nicotine is formed by a pyrrolidine and a pyridine ring in a process involving several enzymes. The pyridine ring of nicotine is derived from nicotinic acid, whereas the pyrrolidine ring originates from polyamine putrescine metabolism. After synthesis in root cortical cells, a set of transporters is known to transport nicotine upward to the aerial part and store it in leaf vacuoles. Mor

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Page, Stephen J., Mingyan Zhu, and Suzanne M. Appleyard. "Effects of acute and chronic nicotine on catecholamine neurons of the nucleus of the solitary tract." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 316, no. 1 (2019): R38—R49. http://dx.doi.org/10.1152/ajpregu.00344.2017.

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Nicotine is an addictive drug that has broad effects throughout the brain. One site of action is the nucleus of the solitary tract (NTS), where nicotine initiates a stress response and modulates cardiovascular and gastric function through nicotinic acetylcholine receptors (nAChRs). Catecholamine (CA) neurons in the NTS influence stress and gastric and cardiovascular reflexes, making them potential mediators of nicotine’s effects; however nicotine’s effect on these neurons is unknown. Here, we determined nicotine’s actions on NTS-CA neurons by use of patch-clamp techniques in brain slices from

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Liu, Zhi, Yo Otsu, Cristina Vasuta, Hiroyuki Nawa, and Timothy H. Murphy. "Action-Potential-Independent GABAergic Tone Mediated by Nicotinic Stimulation of Immature Striatal Miniature Synaptic Transmission." Journal of Neurophysiology 98, no. 2 (2007): 581–93. http://dx.doi.org/10.1152/jn.00768.2006.

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Stimulation of presynaptic nicotinic acetylcholine receptors (nAChRs) increases the frequency of miniature excitatory synaptic activity (mEPSCs) to a point where they can promote cell firing in hippocampal CA3 neurons. We have evaluated whether nicotine regulation of miniature synaptic activity can be extended to inhibitory transmission onto striatal medium spiny projection neurons (MSNs) in acute brain slices. Bath application of micromolar nicotine typically induced 12-fold increases in the frequency of miniature inhibitory synaptic currents (mIPSCs). Little effect was observed on the amplit

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DeVito, Elise E., Kevin P. Jensen, Stephanie S. O’Malley, et al. "Modulation of “Protective” Nicotine Perception and Use Profile by Flavorants: Preliminary Findings in E-cigarettes." Nicotine & Tobacco Research 22, no. 5 (2019): 771–81. http://dx.doi.org/10.1093/ntr/ntz057.

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Abstract Introduction Characterizing flavors are widely available in e-cigarettes and motivate initiation and continued use. Flavors may enhance appeal and facilitate development of addiction to tobacco products through modulation of tobacco products’ reinforcing or aversive actions. Palatable flavors (eg, fruit) may increase appeal through primary reinforcing properties. Menthol’s cooling and anesthetic effects may increase appeal by counteracting nicotine’s aversive effects. Genetics provide a method for modeling individual differences in sensitivity to nicotine’s effects. A common polymorph

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Sansone, Luigi, Francesca Milani, Riccardo Fabrizi, et al. "Nicotine: From Discovery to Biological Effects." International Journal of Molecular Sciences 24, no. 19 (2023): 14570. http://dx.doi.org/10.3390/ijms241914570.

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Nicotine, the primary psychoactive agent in tobacco leaves, has led to the widespread use of tobacco, with over one billion smokers globally. This article provides a historical overview of tobacco and discusses tobacco dependence, as well as the biological effects induced by nicotine on mammalian cells. Nicotine induces various biological effects, such as neoangiogenesis, cell division, and proliferation, and it affects neural and non-neural cells through specific pathways downstream of nicotinic receptors (nAChRs). Specific effects mediated by α7 nAChRs are highlighted. Nicotine is highly add

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Grieder, Taryn E., Morgane Besson, Geith Maal-Bared, Stéphanie Pons, Uwe Maskos та Derek van der Kooy. "β2* nAChRs on VTA dopamine and GABA neurons separately mediate nicotine aversion and reward". Proceedings of the National Academy of Sciences 116, № 51 (2019): 25968–73. http://dx.doi.org/10.1073/pnas.1908724116.

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Evidence shows that the neurotransmitter dopamine mediates the rewarding effects of nicotine and other drugs of abuse, while nondopaminergic neural substrates mediate the negative motivational effects. β2* nicotinic acetylcholine receptors (nAChR) are necessary and sufficient for the experience of both nicotine reward and aversion in an intra-VTA (ventral tegmental area) self-administration paradigm. We selectively reexpressed β2* nAChRs in VTA dopamine or VTA γ-amino-butyric acid (GABA) neurons in β2−/−mice to double-dissociate the aversive and rewarding conditioned responses to nicotine in n

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Kedmi, Merav, Arthur L. Beaudet та Avi Orr-Urtreger. "Mice lacking neuronal nicotinic acetylcholine receptor β4-subunit and mice lacking both α5- and β4-subunits are highly resistant to nicotine-induced seizures". Physiological Genomics 17, № 2 (2004): 221–29. http://dx.doi.org/10.1152/physiolgenomics.00202.2003.

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Nicotine, the main addictive component of tobacco, evokes a wide range of dose-dependent behaviors in rodents, and when administrated in high doses, it can induce clonic-tonic seizures. Nicotine acts through the nicotinic acetylcholine receptors (nAChRs). Mutations in the human α4- and the β2-nAChR subunit genes cause autosomal dominant nocturnal frontal lobe epilepsy. Using transgenic mice with mutations in nAChR subunits, it was demonstrated previously that the α4-, α5-, and α7-subunits are involved in nicotine-induced seizures. To examine the possibility that the β4-subunit is also involved

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Kizawa, Yasuo, Michiko Shinkai, and Issei Takayanagi. "Effects of chronic nicotine treatment on nicotinic receptors in the rabbit urinary bladder." Canadian Journal of Physiology and Pharmacology 68, no. 1 (1990): 99–103. http://dx.doi.org/10.1139/y90-015.

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Nicotine induced a phasic contraction in the rabbit urinary bladder. The response was abolished by hexamethonium and partially reduced by atropine and capsaicin. Simultaneous atropine and capsaicin treatment did not abolish the contraction. These findings suggest that the response to nicotine is due to acetylcholine, tachykinins, and unknown mediator release. In contrast, nicotine-induced contraction diminished following the chronic nicotine treatment without a change of its pharmacological properties. These results suggest the possibility that chronic nicotine treatment causes a decrease in n

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Bhanu Prakash G, Rajagopalan Vijayaraghavan, Senthilkumar Sivanesan, and Madhankumar Swaminathan. "A study on the agents that reduces the nicotine induced nicotinic receptor density in wistar rats." International Journal of Research in Pharmaceutical Sciences 12, no. 1 (2021): 430–35. http://dx.doi.org/10.26452/ijrps.v12i1.4074.

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The most important substance causing addiction towards cigarette is nicotine. Nicotine abstinence causes withdrawal symptoms in smokers. It is not just nicotine, along with it is the upregulation of nicotinic receptor density (NRD) that leads to addiction. All together makes nicotine deaddiction the most difficult aspect. Nicotine receptor density increases as long as the person is exposed to nicotine. When once the NRD is initiated by nicotine, later though you stop smoking, the increased nicotine receptors create an urge to smoke. Hence the person feels to smoke for satisfying the nicotine r

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

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

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Intskirveli, Irakli, and Raju Metherate. "Nicotinic neuromodulation in auditory cortex requires MAPK activation in thalamocortical and intracortical circuits." Journal of Neurophysiology 107, no. 10 (2012): 2782–93. http://dx.doi.org/10.1152/jn.01129.2011.

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Activation of nicotinic acetylcholine receptors (nAChRs) by systemic nicotine enhances sensory-cognitive function and sensory-evoked cortical responses. Although nAChRs mediate fast neurotransmission at many synapses in the nervous system, nicotinic regulation of cortical processing is neuromodulatory. To explore potential mechanisms of nicotinic neuromodulation, we examined whether intracellular signal transduction involving mitogen-activated protein kinase (MAPK) contributes to regulation of tone-evoked responses in primary auditory cortex (A1) in the mouse. Systemic nicotine enhanced charac

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Dhar, S., F. Nagy, J. M. McIntosh, and H. N. Sapru. "Receptor subtypes mediating depressor responses to microinjections of nicotine into medial NTS of the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 1 (2000): R132—R140. http://dx.doi.org/10.1152/ajpregu.2000.279.1.r132.

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Microinjections (50 nl) of nicotine (0.01–10 μM) into the nucleus of the solitary tract (NTS) of adult, urethan-anesthetized, artificially ventilated, male Wistar rats, elicited decreases in blood pressure and heart rate. Prior microinjections of α-bungarotoxin (α-BT) and α-conotoxin ImI (specific toxins for nicotinic receptors containing α7 subunits) elicited a 20–38% reduction in nicotine responses. Similarly, prior microinjections of hexamethonium, mecamylamine, and α-conotoxin AuIB (specific blockers or toxin for nicotinic receptors containing α3β4 subunits) elicited a 47–79% reduction in

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Washington, Thomas E. "Nicotine's Potential to Protect Brain Cells: The Influence of Nicotine on Alzheimer's Disease Risk in the United States: A Scoping Review." Journal of Medicine, Nursing & Public Health 6, no. 1 (2023): 1–12. http://dx.doi.org/10.53819/81018102t4132.

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Nicotine consumption increases brain excitability in a dispersed system of brain areas, such as the frontal cortex, amygdala, cingulate, and frontal lobes, in a dose-dependent manner. Stimulation in these areas is compatible with nicotine's ability to arouse and reinforce behaviour in humans. However, the effects of nicotine consumption on brain cells and the way it modifies them to either inhibit AD or facilitate AD is still unknown, therefore, the current scientific article aimed to address this research gap through analysing prior but latest research studies in this domain. Since there was

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Huang, Zheng-Gui, Xin Wang, Cory Evans, Allison Gold, Evguenia Bouairi, and David Mendelowitz. "Prenatal Nicotine Exposure Alters the Types of Nicotinic Receptors That Facilitate Excitatory Inputs to Cardiac Vagal Neurons." Journal of Neurophysiology 92, no. 4 (2004): 2548–54. http://dx.doi.org/10.1152/jn.00500.2004.

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Nicotinic receptors play an important role in modulating the activity of parasympathetic cardiac vagal neurons in the medulla. Previous work has shown nicotine acts via at least three mechanisms to excite brain stem premotor cardiac vagal neurons. Nicotine evokes a direct increase in holding current and facilitates both the frequency and amplitude of glutamatergic neurotransmission to cardiac vagal neurons. This study tests whether these nicotinic receptor–mediated responses are endogenously active, whether α4β2 and α7 nicotinic receptors are involved, and whether prenatal exposure to nicotine

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Bagdas, Deniz, Laura E. Rupprecht, Eric J. Nunes, Emma Schillinger, Judah J. Immanuel, and Nii A. Addy. "Evaluation of Flavor Effects on Oral Nicotine Liking and/or Disliking Using the Taste Reactivity Test in Rats." Nicotine & Tobacco Research 24, no. 5 (2021): 753–60. http://dx.doi.org/10.1093/ntr/ntab241.

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Abstract Introduction Tobacco product flavors may change the sensory properties of nicotine, such as taste and olfactory cues, which may alter nicotine reward and aversion and nicotine taking behavior. The hedonic or aversive value of a taste stimulus can be evaluated by examining affective orofacial movements in rodents. Aims and Methods We characterized taste responses to various oral nicotine concentrations using the taste reactivity test in rats. We also evaluated the impact of menthol and benzaldehyde (cherry, almond) flavorants on both ingestive and aversive responses to oral nicotine. A

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Wu, Bin, and Hongmin Qin. "Feeding Behavior Analyses Reveal Nicotine Selectively Inhibits Sap Ingestion in Crapemyrtle Bark Scale (Acanthococcus lagerstroemiae), an Invasive Insect in the U.S.1." Journal of Environmental Horticulture 43, no. 2 (2025): 56–66. https://doi.org/10.24266/0738-2898-43.2.56.

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Abstract Crapemyrtle bark scale (CMBS; Acanthococcus lagerstroemiae Kuwana) is an invasive pest that primarily infests crapemyrtles (Lagerstroemia spp.), along with a few other economically important plants in the U.S. Current management practices predominantly rely on neonicotinoid insecticides, which are structurally similar to nicotine and act as agonists at nicotinic acetylcholine receptors (nAChRs), disrupting insect nervous systems. However, the specific impact of these insecticides on CMBS herbivory performance remains unclear. This study combines pectinolytic enzyme detection and elect

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Boye, Sandra M., and Paul BS Clarke. "Enhancement of haloperidol-induced catalepsy by nicotine: an investigation of possible mechanisms." Canadian Journal of Physiology and Pharmacology 78, no. 11 (2000): 882–91. http://dx.doi.org/10.1139/y00-070.

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Nicotine has been reported to potentiate the cataleptic effect of the dopamine receptor antagonist haloperidol in rats. This effect is paradoxical, since nicotine alone tends to increase nigrostriatal dopamine release. In the present experiments, a pro-cataleptic effect of nicotine was confirmed statistically but was small and variable. Three potential mechanisms underlying this effect were investigated. (i) Desensitization of brain nicotinic receptors appears to make little if any contribution to the pro-cataleptic effect of nicotine, insofar as the latter was not mimicked by two centrally ac

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Vigna, Steven R. "Nicotine InhibitsClostridium difficileToxin A-Induced Colitis but Not Ileitis in Rats." International Journal of Inflammation 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/4705065.

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Nicotine is protective in ulcerative colitis but not Crohn’s disease of the small intestine, but little is known about the effects of nicotine onClostridium difficiletoxin A-induced enteritis. Isolated ileal or colonic segments in anesthetized rats were pretreated with nicotine bitartrate or other pharmacological agents before intraluminal injection of toxin A. After 3 hours, the treated segments were removed and inflammation was assessed. Nicotine biphasically inhibited toxin A colitis but not ileitis. Pretreatment with the nicotinic receptor antagonist, hexamethonium, blocked the effects of

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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 (2017): 945–55. http://dx.doi.org/10.1177/0269881117707745.

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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 pr

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Abdrakhmanova, Galya R., Shakir AlSharari, Minho Kang, M. Imad Damaj та Hamid I. Akbarali. "α7-nAChR-mediated suppression of hyperexcitability of colonic dorsal root ganglia neurons in experimental colitis". American Journal of Physiology-Gastrointestinal and Liver Physiology 299, № 3 (2010): G761—G768. http://dx.doi.org/10.1152/ajpgi.00175.2010.

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Controlled clinical trials of nicotine transdermal patch for treatment of ulcerative colitis have been shown to improve histological and global clinical scores of colitis. Here we report that nicotine (1 μM) suppresses in vitro hyperexcitability of colonic dorsal root ganglia (DRG) (L1–L2) neurons in the dextran sodium sulfate (DSS)-induced mouse model of acute colonic inflammation. Nicotine gradually reduced regenerative multiple-spike action potentials in colitis mice to a single action potential. Nicotine's effect on hyperexcitability of inflamed neurons was blocked in the presence of an α7

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Smucny, Jason, and Jason R. Tregellas. "Targeting neuronal dysfunction in schizophrenia with nicotine: Evidence from neurophysiology to neuroimaging." Journal of Psychopharmacology 31, no. 7 (2017): 801–11. http://dx.doi.org/10.1177/0269881117705071.

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Patients with schizophrenia self-administer nicotine at rates higher than is self-administered for any other psychiatric illness. Although the reasons are unclear, one hypothesis suggests that nicotine is a form of ‘self-medication’ in order to restore normal levels of nicotinic signaling and target abnormalities in neuronal function associated with cognitive processes. This brief review discusses evidence from neurophysiological and neuroimaging studies in schizophrenia patients that nicotinic agonists may effectively target dysfunctional neuronal circuits in the illness. Evidence suggests th

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Pan, Yiou, Pengjun Xu, Xiaochun Zeng, Xuemei Liu, and Qingli Shang. "Characterization of UDP-Glucuronosyltransferases and the Potential Contribution to Nicotine Tolerance in Myzus persicae." International Journal of Molecular Sciences 20, no. 15 (2019): 3637. http://dx.doi.org/10.3390/ijms20153637.

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Uridine diphosphate (UDP)-glycosyltransferases (UGTs) are major phase II detoxification enzymes involved in glycosylation of lipophilic endobiotics and xenobiotics, including phytoalexins. Nicotine, one of the most abundant secondary plant metabolites in tobacco, is highly toxic to herbivorous insects. Plant-herbivore competition is the major impetus for the evolution of large superfamilies of UGTs and other detoxification enzymes. However, UGT functions in green peach aphid (Myzus persicae) adaptation are unknown. In this study, we show that UGT inhibitors (sulfinpyrazone and 5-nitrouracil) s

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Angaraj, Kapgate, Dahake Yadnyesha, Pachraiya Palash, and Channe Krutika. "THE ROLE OF NICOTINE IN CANCER PATHOGENESIS: MECHANISMS OF CARCINOGENESIS AND POTENTIAL THERAPEUTIC INTERVENTIONS." INTERNATIONAL EDUCATION AND RESEARCH JOURNAL - IERJ 11, no. 3 (2025): 162–68. https://doi.org/10.5281/zenodo.15584448.

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Nicotine, a major component of tobacco, plays a critical role in cancer development, acting primarily as a tumour promoter rather than a direct carcinogen. It exerts its effects by binding to nicotinic acetylcholine receptors (nAChRs) on cancer cells, activating various signalling pathways that promote cell proliferation, metastasis, angiogenesis, and immune suppression. Additionally, nicotine induces epigenetic modifications, such as DNA methylation and histone changes, which further drive tumorigenesis and contribute to cancer resistance. While nicotine replacement therapy (NRT) can aid in s

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Xu, Shuqing, Thomas Brockmöller, Aura Navarro-Quezada, et al. "Wild tobacco genomes reveal the evolution of nicotine biosynthesis." Proceedings of the National Academy of Sciences 114, no. 23 (2017): 6133–38. http://dx.doi.org/10.1073/pnas.1700073114.

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Nicotine, the signature alkaloid of Nicotiana species responsible for the addictive properties of human tobacco smoking, functions as a defensive neurotoxin against attacking herbivores. However, the evolution of the genetic features that contributed to the assembly of the nicotine biosynthetic pathway remains unknown. We sequenced and assembled genomes of two wild tobaccos, Nicotiana attenuata (2.5 Gb) and Nicotiana obtusifolia (1.5 Gb), two ecological models for investigating adaptive traits in nature. We show that after the Solanaceae whole-genome triplication event, a repertoire of rapidly

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Wang, Rui, and Zunzhe Wang. "Three different vasoactive responses of rat tail artery to nicotine." Canadian Journal of Physiology and Pharmacology 78, no. 1 (1999): 20–28. http://dx.doi.org/10.1139/y99-114.

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The vasoactive effects of nicotine on isolated rat tail artery tissues were studied. Nicotine transiently contracted rat tail artery tissues (EC50, 55.6 ± 2 µM) in an extracellular Ca2+ dependent and endothelium-independent fashion. The blockade of alpha1-adrenoceptors, but not alpha2-adrenoceptors or P2X purinoceptors, inhibited the nicotine-induced contraction by 38 ± 7% (p < 0.05). Nicotine (1 mM) depolarized membrane by 13 ± 3 mV, but did not affect L-type Ca2+ channel currents, of the isolated rat tail artery smooth muscle cells. The phenylephrine-precontracted tail artery tissues were

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Sharma, Geeta, and Sukumar Vijayaraghavan. "Nicotinic Receptors: Role in Addiction and Other Disorders of the Brain." Substance Abuse: Research and Treatment 1 (January 2008): 117822180800100. http://dx.doi.org/10.1177/117822180800100005.

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Nicotine, the addictive component of cigarette smoke has profound effects on the brain. Activation of its receptors by nicotine has complex consequences for network activity throughout the brain, potentially contributing to the addictive property of the drug. Nicotinic receptors have been implicated in psychiatric illnesses like schizophrenia and are also neuroprotective, potentially beneficial for neurodegenerative diseases. These effects of nicotine serve to emphasize the multifarious roles the drug, acting through multiple nicotinic acetylcholine receptor subtypes. The findings also remind

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Wollman, Lila Buls, Richard B. Levine, and Ralph F. Fregosi. "Developmental nicotine exposure alters glycinergic neurotransmission to hypoglossal motoneurons in neonatal rats." Journal of Neurophysiology 120, no. 3 (2018): 1135–42. http://dx.doi.org/10.1152/jn.00600.2017.

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We tested the hypothesis that nicotine exposure in utero and after birth [developmental nicotine exposure (DNE)] disrupts development of glycinergic synaptic transmission to hypoglossal motoneurons (XIIMNs). Glycinergic spontaneous and miniature inhibitory postsynaptic currents (sIPSC/mIPSC) were recorded from XIIMNs in brain stem slices from 1- to 5-day-old rat pups of either sex, under baseline conditions and following stimulation of nicotinic acetylcholine (ACh) receptors with nicotine (i.e., an acute nicotine challenge). Under baseline conditions, there were no significant effects of DNE o

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

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

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Jinks, Steven L., and E. Carstens. "Activation of Spinal Wide Dynamic Range Neurons by Intracutaneous Microinjection of Nicotine." Journal of Neurophysiology 82, no. 6 (1999): 3046–55. http://dx.doi.org/10.1152/jn.1999.82.6.3046.

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Nicotine evokes pain in the skin and oral mucosa and excites a subpopulation of cutaneous nociceptors, but little is known about the central transmission of chemogenic pain. We have investigated the responses of lumbar spinal wide dynamic range (WDR)-type dorsal horn neurons to intracutaneous (ic) microinjection of nicotine in pentobarbital-anesthetized rats. Nearly all (97%) units responded to nicotine microinjected ic (1 μl) into the low-threshold region of the hind-paw mechanosensitive receptive field in a concentration-related manner (0.01–10%). Responses to repeated injections of 10% nico

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Simons, Christopher T., Yves Boucher, Mirela Iodi Carstens, and E. Carstens. "Nicotine Suppression of Gustatory Responses of Neurons in the Nucleus of the Solitary Tract." Journal of Neurophysiology 96, no. 4 (2006): 1877–86. http://dx.doi.org/10.1152/jn.00345.2006.

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This study investigated effects of nicotine applied to the tongue surface on responses of gustatory neurons in the nucleus of the solitary tract (NTS) in rats. In pentobarbital-anesthetized rats, single-unit recordings were made from NTS units responsive to one or more tastants (sucrose, NaCl, citric acid, monosodium glutamate, quinine). Application of nicotine (0.87, 8.7, or 600 mM) excited gustatory NTS units and significantly attenuated NTS unit responses to their preferred tastant in a dose-dependent manner. The depressant effect of nicotine was equivalent regardless of which tastant best

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Huang, Z. G., K. J. S. Griffioen, X. Wang, et al. "Nicotinic Receptor Activation Occludes Purinergic Control of Central Cardiorespiratory Network Responses to Hypoxia/Hypercapnia." Journal of Neurophysiology 98, no. 4 (2007): 2429–38. http://dx.doi.org/10.1152/jn.00448.2007.

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Prenatal nicotine exposure alters the cardiorespiratory network responses to hypoxia/hypercapnia; however the mechanism(s) responsible for these cardiorespiratory network responses and their alteration by prenatal nicotine exposure are unknown. We used an in vitro medullary slice that allows simultaneous examination of rhythmic respiratory-related activity and excitatory synaptic neurotransmission to cardioinhibitory vagal neurons (CVNs). Respiratory related increases in glutamatergic neurotransmission only occurred on recovery from hypoxia/hypercapnia in unexposed animals. These responses wer

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Lapner, K. N., C. J. Montpetit, and S. F. Perry. "Desensitisation of chromaffin cell nicotinic receptors does not impede catecholamine secretion during acute hypoxia in rainbow trout (Oncorhynchus mykiss)." Journal of Experimental Biology 203, no. 10 (2000): 1589–97. http://dx.doi.org/10.1242/jeb.203.10.1589.

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Experiments were performed on adult rainbow trout (Oncorhynchus mykiss) in vivo using chronically cannulated fish and in situ using a perfused posterior cardinal vein preparation (i) to characterise the desensitisation of chromaffin cell nicotinic receptors and (ii) to assess the ability of fish to secrete catecholamines during acute hypoxia with or without functional nicotinic receptors. Intra-arterial injection of nicotine (6.0×10(−)(7)mol kg(−)(1)) caused a rapid increase in plasma adrenaline and noradrenaline levels; the magnitude of this response was unaffected by an injection of nicotine

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

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

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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.

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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 expr

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Taylor, George, Carl Bassi, and Juergen Weiss. "Limits of learning enhancements with nicotine in old male rats." Acta Neurobiologiae Experimentalis 65, no. 2 (2005): 125–36. http://dx.doi.org/10.55782/ane-2005-1545.

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Findings with young adult humans and animal models suggest that nicotine may serve both neuroprotective and cognition enhancing roles in old animals. A pair of experiments was conducted to examine drug-induced modification of the cholinergic nicotinic receptor subtype on rates of learning by young and aged rats. In experiment I males (4-7 months or 20-25 months old) were administered nicotine (0.0, 0.3 or 0.7 mg/kg injected s.c. daily) and tested in both a T-maze non-spatial discrimination paradigm and a hole board spatial task. Nicotine failed to improve acquisition by young animals on either

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Pal, Vikas Kumar. "Chemico-analytical parameters and findings of nicotine from pan masala." Journal of Medical Pharmaceutical and Allied Sciences 14, no. 1 (2025): 6915–21. https://doi.org/10.55522/jmpas.v14i1.6691.

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Nicotine, is an alkaloid found in different amounts ranging from 2% to 14% in the leaves of Nicotiana rustica, Nicotiana tobacum, Duboisia hopwoodii, and Asclepias syriaca. The main perspective of this work is to extract and isolate nicotine from various brands of paan masala and perform chemical test and analytical studies on it. UV and IR parameters are applied for the purpose of standardization of it, after the isolation. Then the method development through UV is done and is compared with the standard nicotine solution. The approach is suitable for use in the regular analysis of nicotine an

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CATTANEO, G. Maria, Fabio D'ATRI, and M. Lucia VICENTINI. "Mechanisms of mitogen-activated protein kinase activation by nicotine in small-cell lung carcinoma cells." Biochemical Journal 328, no. 2 (1997): 499–503. http://dx.doi.org/10.1042/bj3280499.

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We have previously reported that nicotine stimulates cell proliferation of three small-cell lung carcinoma (SCLC) cell lines by activating nicotinic receptors of the neuronal type. Here we report that, in the GLC-8 SCLC cell line, nicotine stimulates mitogen-activated protein (MAP) kinase activity in a concentration- and time-dependent manner (ED50 = 10 nM). The nicotine effect was antagonized by mecamylamine, an antagonist specific for neuronal nicotinic receptors. The absence of extracellular Ca2+, or pretreatment with pertussis toxin or the tyrosine kinase inhibitor genistein inhibited the

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Yoo, Seong Ho, Won Tae Lee, and Jung-bin Lee. "Evaluating the Forensic Inferences of Oral Nicotine Ingestion: Autopsy Case Review, Animal Experimentation, and Legal Implications." Korean Journal of Legal Medicine 48, no. 3 (2024): 102–9. http://dx.doi.org/10.7580/kjlm.2024.48.3.102.

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Nicotine, a highly lipophilic alkaloid derived from Nicotiana tabacum and Nicotiana rustica, can be lethal even in small doses when ingested in concentrated forms like e-cigarette liquids. This study examined a murder case in South Korea where a 52-year-old man was allegedly killed by oral administration of nicotine. Despite the absence of typical signs, such as chemical burns or vomiting, the case posed questions about the lethal concentration of nicotine and the presence of gastrointestinal symptoms in nicotine poisoning. Through literature review, autopsy analysis, and animal experiments, t

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Duncan, Jhodie R., Marianne Garland, Michael M. Myers, et al. "Prenatal nicotine-exposure alters fetal autonomic activity and medullary neurotransmitter receptors: implications for sudden infant death syndrome." Journal of Applied Physiology 107, no. 5 (2009): 1579–90. http://dx.doi.org/10.1152/japplphysiol.91629.2008.

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During pregnancy, exposure to nicotine and other compounds in cigarette smoke increases the risk of the sudden infant death syndrome (SIDS) two- to fivefold. Serotonergic (5-HT) abnormalities are found, in infants who die of SIDS, in regions of the medulla oblongata known to modulate cardiorespiratory function. Using a baboon model, we tested the hypothesis that prenatal exposure to nicotine alters 5-HT receptor and/or transporter binding in the fetal medullary 5-HT system in association with cardiorespiratory dysfunction. At 87 (mean) days gestation (dg), mothers were continuously infused wit

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Leventhal, Adam M., Tyler B. Mason, Sam N. Cwalina, Lauren Whitted, Marissa Anderson, and Carly Callahan. "Flavor and Nicotine Effects on E-cigarette Appeal in Young Adults: Moderation by Reason for Vaping." American Journal of Health Behavior 44, no. 5 (2020): 732–43. http://dx.doi.org/10.5993/ajhb.44.5.15.

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Objectives: Effective regulations that reduce nicotine vaping among young adult dual (combustible and e-cigarette) users may differ depending on whether e-cigarettes are used for helping with smoking cessation. This laboratory experiment examined flavor and nicotine effects on e-cigarette product appeal among young adult dual users, stratified by reported use of e-cigarettes to quit smoking. Methods: Dual users aged 18-35 years that did (N = 31) or did not (N = 22) report vaping for the purpose of quitting smoking puffed e-cigarette solutions varied by a flavor (fruit, menthol, tobacco) and ni

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Papapostolou, Irida, Daniela Ross-Kaschitza, Florian Bochen, Christine Peinelt та Maria Constanza Maldifassi. "Contribution of the α5 nAChR Subunit and α5SNP to Nicotine-Induced Proliferation and Migration of Human Cancer Cells". Cells 12, № 15 (2023): 2000. http://dx.doi.org/10.3390/cells12152000.

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Nicotine in tobacco is known to induce tumor-promoting effects and cause chemotherapy resistance through the activation of nicotinic acetylcholine receptors (nAChRs). Many studies have associated the α5 nicotinic receptor subunit (α5), and a specific polymorphism in this subunit, with (i) nicotine administration, (ii) nicotine dependence, and (iii) lung cancer. The α5 gene CHRNA5 mRNA is upregulated in several types of cancer, including lung, prostate, colorectal, and stomach cancer, and cancer severity is correlated with smoking. In this study, we investigate the contribution of α5 in the nic

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Kanniah, Guna, and Rishi Kumar. "A selective literature review exploring the role of the nicotinic system in schizophrenia." General Psychiatry 36, no. 2 (2023): e100756. http://dx.doi.org/10.1136/gpsych-2022-100756.

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Nicotine use is more prevalent in patients with psychiatric disorders, especially those diagnosed with psychotic illnesses. Previously, this higher prevalence has been partially attributed to the potential ameliorative effects of nicotine on symptom severity and cognitive impairment. Some healthcare professionals and patients perceive there is a beneficial effect of nicotine on mental health. Emerging data show that the harm associated with nicotine in the population of patients with mental health conditions outweighs any potential benefit. This paper will review the evidence surrounding the n

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Alkire, Michael T., Jayme R. McReynolds, Emily L. Hahn, and Akash N. Trivedi. "Thalamic Microinjection of Nicotine Reverses Sevoflurane-induced Loss of Righting Reflex in the Rat." Anesthesiology 107, no. 2 (2007): 264–72. http://dx.doi.org/10.1097/01.anes.0000270741.33766.24.

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Background Neuronal nicotinic acetylcholine receptors are both potently inhibited by anesthetics and densely expressed in the thalamus. Brain imaging shows that thalamic activity suppression accompanies anesthetic-induced unconsciousness. Therefore, anesthetic-induced unconsciousness may involve direct antagonism of thalamic nicotinic receptors. The authors test this by separately attempting to block or enhance anesthetic-induced loss of righting in rats using intrathalamic microinjections of nicotine or its antagonist. Methods Rats were implanted with a cannula aimed at the thalamus or contro

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Lian, Jie, De Ji Wang, and Jun Ming Xie. "Data Mining of Nicotine Demethylase Genes in Modern Tobacoo." Advanced Materials Research 787 (September 2013): 356–60. http://dx.doi.org/10.4028/www.scientific.net/amr.787.356.

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The predominant pyridine alkaloid in modern tobacco (Nicotiana tabacum) is Nicotine. However, with the existence of a class of Nicotine demethylases, a large proportion of Nicotine will be converted into Nornicotine during leaf senescence. Identification of Nicotine demethylases in modern tobacco is important, since Nornicotine will be nitrosated into N'-nitrosonornicotine (NNN), which exhibit carcinogenic properties in laboratory animals and is harmful for human heath. Although many efforts have been performed to identified, no comprehensive analysis was carried out for the subfamily of Nicot

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Liu, L., W. Zhu, Z. S. Zhang, et al. "Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors." Journal of Neurophysiology 91, no. 4 (2004): 1482–91. http://dx.doi.org/10.1152/jn.00922.2003.

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Nicotine is an alkaloid that is used by large numbers of people. When taken into the body, it produces a myriad of physiological actions that occur primarily through the activation of neuronal nicotinic acetylcholine receptors (nAChRs). We have explored its ability to modulate TRPV1 receptors and voltage-gated sodium channels. The reason for investigating nicotine's effect on sodium channels is to obtain a better understanding of its anti-nociceptive properties. The reasons for investigating its effects on capsaicin-activated TRPV1 channels are to understand how it may modulate this channel th

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Calarco, Cali A., and Marina R. Picciotto. "Nicotinic Acetylcholine Receptor Signaling in the Hypothalamus: Mechanisms Related to Nicotine’s Effects on Food Intake." Nicotine & Tobacco Research 22, no. 2 (2019): 152–63. http://dx.doi.org/10.1093/ntr/ntz010.

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Abstract Despite health risks associated with smoking, up to 20% of the US population persist in this behavior; many smoke to control body weight or appetite, and fear of post-cessation weight gain can motivate continued smoking. Nicotine and tobacco use is associated with lower body weight, and cessation yields an average weight gain of about 4 kg, which is thought to reflect a return to the body weight of a typical nonsmoker. Nicotine replacement therapies can delay this weight gain but do not prevent it altogether, and the underlying mechanism for how nicotine is able to reduce weight is no

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Perry, Robin N., Hera E. Schlagintweit, Christine Darredeau, et al. "The impacts of actual and perceived nicotine administration on insula functional connectivity with the anterior cingulate cortex and nucleus accumbens." Journal of Psychopharmacology 33, no. 12 (2019): 1600–1609. http://dx.doi.org/10.1177/0269881119872205.

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Background: Changes in resting state functional connectivity between the insula and dorsal anterior cingulate cortex as well as between the insula and nucleus accumbens have been linked to nicotine withdrawal and/or administration. However, because many of nicotine’s effects in humans appear to depend, at least in part, on the belief that nicotine has been administered, the relative contribution of nicotine’s pharmacological actions to such effects requires clarification. Aims: The purpose of this study was to examine the impacts of perceived and actual nicotine administration on neural respon

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Whitton, Alexis E., Norka E. Rabinovich, John D. Lindt, Michele L. Pergadia, Diego A. Pizzagalli, and David G. Gilbert. "Genetic and Depressive Traits Moderate the Reward-Enhancing Effects of Acute Nicotine in Young Light Smokers." Nicotine & Tobacco Research 23, no. 10 (2021): 1779–86. http://dx.doi.org/10.1093/ntr/ntab072.

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Abstract Introduction Rates of light smoking have increased in recent years and are associated with adverse health outcomes. Reducing light smoking is a challenge because it is unclear why some but not others, progress to heavier smoking. Nicotine has profound effects on brain reward systems and individual differences in nicotine’s reward-enhancing effects may drive variability in smoking trajectories. Therefore, we examined whether a genetic risk factor and personality traits known to moderate reward processing, also moderate the reward-enhancing effects of nicotine. Methods Light smokers (n

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Ene, Corina-Daniela, Mircea Penescu, Ilinca Nicolae, and Emanoil Ceauşu. "Anti-inflammatory effects of nicotine." Romanian Journal of Infectious Diseases 18, no. 1 (2015): 5–12. http://dx.doi.org/10.37897/rjid.2015.1.1.

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A number of epidemiological and experimental data have shown that nicotine stimulates anti-inflammatory response in extraneuronal tissues, response mediated by homopentameric nicotinic receptors, 7nAChR- alpha. The receptors are located mainly on immune and inflammatory cells. These pharmacological mechanisms, through which inflammatory process could be adjusted is the use of selective nicotinic agonists and antagonists, called anti-inflammatory. Treatment with nicotine initiates a series of intracellular events associated with stimulation of several signaling pathways: NFkB, JAK/STAT, MyD88/T

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Fu, Yitong, Shannon G. Matta, James D. Valentine, and Burt M. Sharp. "Adrenocorticotropin Response and Nicotine-Induced Norepinephrine Secretion in the Rat Paraventricular Nucleus Are Mediated through Brainstem Receptors*." Endocrinology 138, no. 5 (1997): 1935–43. http://dx.doi.org/10.1210/endo.138.5.5122.

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Abstract Nicotine is a potent stimulus for the secretion of ACTH, and norepinephrinergic neurons originating in the brainstem are involved. Prior reports using in vivo microdialysis in alert rats have shown that nicotine, administered ip or into the fourth ventricle, stimulated the release of norepinephrine (NE) into the hypothalamic paraventricular nucleus (PVN), the site of neurons containing CRH. In the present studies, rats received an iv infusion of nicotine into the jugular vein on alternate days during their active (dark) phase; therefore, direct correlations between the levels of NE mi

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