Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.Nicotinic Agonists: Drugs that bind to and activate nicotinic cholinergic receptors (RECEPTORS, NICOTINIC). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission.Tobacco Use Disorder: Tobacco used to the detriment of a person's health or social functioning. Tobacco dependence is included.Ganglionic Stimulants: Agents that mimic neural transmission by stimulation of the nicotinic receptors on postganglionic autonomic neurons. Drugs that indirectly augment ganglionic transmission by increasing the release or slowing the breakdown of acetylcholine or by non-nicotinic effects on postganglionic neurons are not included here nor are the nonspecific cholinergic agonists.Receptors, Nicotinic: One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.Mecamylamine: A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.Cotinine: The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to tobacco SMOKING. It has CNS stimulating properties.Nicotinic Antagonists: Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.Chewing Gum: A preparation of chicle, sometimes mixed with other plastic substances, sweetened and flavored. It is masticated usually for pleasure as a candy substitute but it sometimes acts as a vehicle for the administration of medication.Substance Withdrawal Syndrome: Physiological and psychological symptoms associated with withdrawal from the use of a drug after prolonged administration or habituation. The concept includes withdrawal from smoking or drinking, as well as withdrawal from an administered drug.Tobacco Use Cessation Products: Items used to aid in ending a TOBACCO habit.Smoking Cessation: Discontinuation of the habit of smoking, the inhaling and exhaling of tobacco smoke.Smoking: Inhaling and exhaling the smoke of burning TOBACCO.Administration, Cutaneous: The application of suitable drug dosage forms to the skin for either local or systemic effects.Dihydro-beta-Erythroidine: Dihydro analog of beta-erythroidine, which is isolated from the seeds and other plant parts of Erythrina sp. Leguminosae. It is an alkaloid with curarimimetic properties.Tars: Viscous materials composed of complex, high-molecular-weight compounds derived from the distillation of petroleum or the destructive distillation of wood or coal. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Self Administration: Administration of a drug or chemical by the individual under the direction of a physician. It includes administration clinically or experimentally, by human or animal.alpha7 Nicotinic Acetylcholine Receptor: A member of the NICOTINIC ACETYLCHOLINE RECEPTOR subfamily of the LIGAND-GATED ION CHANNEL family. It consists entirely of pentameric a7 subunits expressed in the CNS, autonomic nervous system, vascular system, lymphocytes and spleen.AzocinesDose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Aconitine: A C19 norditerpenoid alkaloid (DITERPENES) from the root of ACONITUM plants. It activates VOLTAGE-GATED SODIUM CHANNELS. It has been used to induce ARRHYTHMIAS in experimental animals and it has antiinflammatory and antineuralgic properties.Conditioning, Operant: Learning situations in which the sequence responses of the subject are instrumental in producing reinforcement. When the correct response occurs, which involves the selection from among a repertoire of responses, the subject is immediately reinforced.Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.QuinolizinesTobacco, Smokeless: Powdered or cut pieces of leaves of NICOTIANA TABACUM which are inhaled through the nose, chewed, or stored in cheek pouches. It includes any product of tobacco that is not smoked.Tobacco Products: Substances and products derived from NICOTIANA TABACUM.Reward: An object or a situation that can serve to reinforce a response, to satisfy a motive, or to afford pleasure.Tobacco: A plant genus of the family SOLANACEAE. Members contain NICOTINE and other biologically active chemicals; its dried leaves are used for SMOKING.Anabasine: A piperidine botanical insecticide.Bicyclo Compounds, Heterocyclic: A class of saturated compounds consisting of two rings only, having two or more atoms in common, containing at least one hetero atom, and that take the name of an open chain hydrocarbon containing the same total number of atoms. (From Riguady et al., Nomenclature of Organic Chemistry, 1979, p31)Reinforcement (Psychology): The strengthening of a conditioned response.Carbon Monoxide: Carbon monoxide (CO). A poisonous colorless, odorless, tasteless gas. It combines with hemoglobin to form carboxyhemoglobin, which has no oxygen carrying capacity. The resultant oxygen deprivation causes headache, dizziness, decreased pulse and respiratory rates, unconsciousness, and death. (From Merck Index, 11th ed)Behavior, Animal: The observable response an animal makes to any situation.Self Stimulation: Stimulation of the brain, which is self-administered. The stimulation may result in negative or positive reinforcement.Hexamethonium: A nicotinic cholinergic antagonist often referred to as the prototypical ganglionic blocker. It is poorly absorbed from the gastrointestinal tract and does not cross the blood-brain barrier. It has been used for a variety of therapeutic purposes including hypertension but, like the other ganglionic blockers, it has been replaced by more specific drugs for most purposes, although it is widely used a research tool.Dopamine: One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.Benzazepines: Compounds with BENZENE fused to AZEPINES.Bungarotoxins: Neurotoxic proteins from the venom of the banded or Formosan krait (Bungarus multicinctus, an elapid snake). alpha-Bungarotoxin blocks nicotinic acetylcholine receptors and has been used to isolate and study them; beta- and gamma-bungarotoxins act presynaptically causing acetylcholine release and depletion. Both alpha and beta forms have been characterized, the alpha being similar to the large, long or Type II neurotoxins from other elapid venoms.Hexamethonium Compounds: Compounds containing the hexamethylenebis(trimethylammonium) cation. Members of this group frequently act as antihypertensive agents and selective ganglionic blocking agents.Tobacco Smoke Pollution: Contamination of the air by tobacco smoke.Ventral Tegmental Area: A region in the MESENCEPHALON which is dorsomedial to the SUBSTANTIA NIGRA and ventral to the RED NUCLEUS. The mesocortical and mesolimbic dopaminergic systems originate here, including an important projection to the NUCLEUS ACCUMBENS. Overactivity of the cells in this area has been suspected to contribute to the positive symptoms of SCHIZOPHRENIA.QuinoxalinesNitrosamines: A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.SmokeAnalysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.Motor Activity: The physical activity of a human or an animal as a behavioral phenomenon.Nucleus Accumbens: Collection of pleomorphic cells in the caudal part of the anterior horn of the LATERAL VENTRICLE, in the region of the OLFACTORY TUBERCLE, lying between the head of the CAUDATE NUCLEUS and the ANTERIOR PERFORATED SUBSTANCE. It is part of the so-called VENTRAL STRIATUM, a composite structure considered part of the BASAL GANGLIA.Asclepias: A plant genus of the family ASCLEPIADACEAE. This is the true milkweed; APOCYNUM & EUPHORBIA hirta are rarely called milkweed. Asclepias asthmatica has been changed to TYLOPHORA.Duboisia: A plant genus of the family SOLANACEAE that is a source of SCOPOLAMINE HYDROBROMIDE and other TROPANES.Solanaceae: A plant family of the order Solanales, subclass Asteridae. Among the most important are POTATOES; TOMATOES; CAPSICUM (green and red peppers); TOBACCO; and BELLADONNA.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Plants, Edible: An organism of the vegetable kingdom suitable by nature for use as a food, especially by human beings. Not all parts of any given plant are edible but all parts of edible plants have been known to figure as raw or cooked food: leaves, roots, tubers, stems, seeds, buds, fruits, and flowers. The most commonly edible parts of plants are FRUIT, usually sweet, fleshy, and succulent. Most edible plants are commonly cultivated for their nutritional value and are referred to as VEGETABLES.

(S)-(-)-Cotinine, the major brain metabolite of nicotine, stimulates nicotinic receptors to evoke [3H]dopamine release from rat striatal slices in a calcium-dependent manner. (1/3904)

Cotinine, a major peripheral metabolite of nicotine, has recently been shown to be the most abundant metabolite in rat brain after peripheral nicotine administration. However, little attention has been focused on the contribution of cotinine to the pharmacological effects of nicotine exposure in either animals or humans. The present study determined the concentration-response relationship for (S)-(-)-cotinine-evoked 3H overflow from superfused rat striatal slices preloaded with [3H]dopamine ([3H]DA) and whether this response was mediated by nicotinic receptor stimulation. (S)-(-)-Cotinine (1 microM to 3 mM) evoked 3H overflow from [3H]DA-preloaded rat striatal slices in a concentration-dependent manner with an EC50 value of 30 microM, indicating a lower potency than either (S)-(-)-nicotine or the active nicotine metabolite, (S)-(-)-nornicotine. As reported for (S)-(-)-nicotine and (S)-(-)-nornicotine, desensitization to the effect of (S)-(-)-cotinine was observed. The classic nicotinic receptor antagonists mecamylamine and dihydro-beta-erythroidine inhibited the response to (S)-(-)-cotinine (1-100 microM). Additionally, 3H overflow evoked by (S)-(-)-cotinine (10-1000 microM) was inhibited by superfusion with a low calcium buffer. Interestingly, over the same concentration range, (S)-(-)-cotinine did not inhibit [3H]DA uptake into striatal synaptosomes. These results demonstrate that (S)-(-)-cotinine, a constituent of tobacco products and the major metabolite of nicotine, stimulates nicotinic receptors to evoke the release of DA in a calcium-dependent manner from superfused rat striatal slices. Thus, (S)-(-)-cotinine likely contributes to the neuropharmacological effects of nicotine and tobacco use.  (+info)

Neurogenic vasodilatation of canine isolated small labial arteries. (2/3904)

Mechanisms underlying vasodilatation to nerve stimulation by electrical pulses and nicotine were analyzed in isolated canine small labial arteries. Transmural electrical stimulation (5 and 20 Hz) produced a contraction followed by a relaxation in labial arterial strips denuded of the endothelium, partially contracted with prostaglandin F2alpha. The contraction was abolished by prazosin or combined treatment with alpha, beta-methylene ATP. In the treated strips, neurogenic relaxation was abolished by NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor, and restored by L-arginine. The D-enantiomers were without effect. Nicotine (10(-4) M) also relaxed the arteries, in which the contractile response was abolished by prazosin and alpha, beta-methylene ATP. The relaxant response was attenuated but not abolished by L-NA; the inhibition was reversed by L-arginine. The remaining relaxation by nicotine was abolished by calcitonin gene-related peptide (CGRP)-[8 to 37], a CGRP1 receptor antagonist. Relaxations elicited by a lower concentration of nicotine (2 x 10(-5) M) sufficient to produce similar magnitudes of response to those induced by 5-Hz electrical nerve stimulation were also inhibited partially by L-NA. Histochemical study with the NADPH-diaphorase method demonstrated positively stained nerve fibers and bundles in the arterial wall, suggesting the presence of neuronal NO synthase. It is concluded that the relaxation induced by electrical nerve stimulation of small labial arteries is mediated exclusively by NO synthesized from L-arginine in nerve terminals, whereas nicotine in the concentrations used evokes relaxations by a mediation of nerve-derived NO and also CGRP, possibly from sensory nerves. The reason why nicotine but not electrical pulses stimulates sensory nerves and elicits vasorelaxation remains unsolved.  (+info)

Acquisition of nicotine discrimination and discriminative stimulus effects of nicotine in rats chronically exposed to caffeine. (3/3904)

Caffeine and nicotine are the main psychoactive ingredients of coffee and tobacco, with a high frequency of concurrent use in humans. This study examined the effects of chronic caffeine exposure on 1) rates of acquisition of a nicotine discrimination (0.1 or 0.4 mg/kg, s.c., training doses) and 2) the pharmacological characteristics of the established nicotine discrimination in male Sprague-Dawley rats. Once rats learned to lever-press reliably under a fixed ratio of 10 schedule for food pellets, they were randomly divided into two groups; 12 animals were maintained continuously on caffeine added to the drinking water (3 mg/ml) and another 12 control rats continued to drink tap water. In each group of water- and caffeine-drinking rats, there were six rats trained to discriminate 0.1 mg/kg of nicotine from saline and six rats trained to discriminate 0.4 mg/kg of nicotine from saline. Regardless of the training dose of nicotine, both water- and caffeine-drinking groups required a comparable number of training sessions to attain reliable stimulus control, although there was a trend for a slower acquisition in the caffeine-drinking group trained with 0.1 mg/kg of nicotine. Tests for generalization to different doses of nicotine revealed no significant differences in potency of nicotine between water- and caffeine-drinking groups. The nicotinic-receptor antagonist mecamylamine blocked the discriminative effects of 0.1 and 0.4 mg/kg nicotine with comparable potency and efficacy in water- and caffeine-drinking groups. There was a dose-related generalization to both the 0.1 and 0.4 mg/kg nicotine cue (maximum average of 51-83%) in water-drinking rats after i.p. treatment with d-amphetamine, cocaine, the selective dopamine uptake inhibitor GBR-12909, apomorphine, and the selective dopamine D1 receptor agonist SKF-82958, but not in caffeine-drinking rats (0-22%). There was no generalization to the nicotine cues after i.p. treatment with caffeine or the selective D2 (NPA) and D3 (PD 128,907) dopamine-receptor agonists in water- and caffeine-drinking rats. The dopamine-release inhibitor CGS 10746B reduced the discriminative effects of 0.4 mg/kg nicotine in water-drinking rats, but not in caffeine-drinking rats. There was no evidence of development of tolerance or sensitization to nicotine's effects throughout the study. In conclusion, chronic caffeine exposure (average, 135 mg/kg/day) did not affect the rate of acquisition of the nicotine discrimination, but it did reduce the dopaminergic component of the nicotine-discriminative cue. The reduction of the dopaminergic component of the nicotine cue was permanent, as this effect was still evident after the caffeine solution was replaced with water in caffeine-drinking rats. That nicotine could reliably serve as a discriminative stimulus in the absence of the dopaminergic component of its discriminative cue may differentiate nicotine from "classical dopaminergic" drugs of abuse such as cocaine and amphetamine.  (+info)

A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation. (4/3904)

BACKGROUND AND METHODS: Use of nicotine-replacement therapies and the antidepressant bupropion helps people stop smoking. We conducted a double-blind, placebo-controlled comparison of sustained-release bupropion (244 subjects), a nicotine patch (244 subjects), bupropion and a nicotine patch (245 subjects), and placebo (160 subjects) for smoking cessation. Smokers with clinical depression were excluded. Treatment consisted of nine weeks of bupropion (150 mg a day for the first three days, and then 150 mg twice daily) or placebo, as well as eight weeks of nicotine-patch therapy (21 mg per day during weeks 2 through 7, 14 mg per day during week 8, and 7 mg per day during week 9) or placebo. The target day for quitting smoking was usually day 8. RESULTS: The abstinence rates at 12 months were 15.6 percent in the placebo group, as compared with 16.4 percent in the nicotine-patch group, 30.3 percent in the bupropion group (P<0.001), and 35.5 percent in the group given bupropion and the nicotine patch (P<0.001). By week 7, subjects in the placebo group had gained an average of 2.1 kg, as compared with a gain of 1.6 kg in the nicotine-patch group, a gain of 1.7 kg in the bupropion group, and a gain of 1.1 kg in the combined-treatment group (P<0.05). Weight gain at seven weeks was significantly less in the combined-treatment group than in the bupropion group and the placebo group (P<0.05 for both comparisons). A total of 311 subjects (34.8 percent) discontinued one or both medications. Seventy-nine subjects stopped treatment because of adverse events: 6 in the placebo group (3.8 percent), 16 in the nicotine-patch group (6.6 percent), 29 in the bupropion group (11.9 percent), and 28 in the combined-treatment group (11.4 percent). The most common adverse events were insomnia and headache. CONCLUSIONS: Treatment with sustained-release bupropion alone or in combination with a nicotine patch resulted in significantly higher long-term rates of smoking cessation than use of either the nicotine patch alone or placebo. Abstinence rates were higher with combination therapy than with bupropion alone, but the difference was not statistically significant.  (+info)

Higher dosage nicotine patches increase one-year smoking cessation rates: results from the European CEASE trial. Collaborative European Anti-Smoking Evaluation. European Respiratory Society. (5/3904)

The Collaborative European Anti-Smoking Evaluation (CEASE) was a European multicentre, randomized, double-blind placebo controlled smoking cessation study. The objectives were to determine whether higher dosage and longer duration of nicotine patch therapy would increase the success rate. Thirty-six chest clinics enrolled a total of 3,575 smokers. Subjects were allocated to one of five treatment arms: placebo and either standard or higher dose nicotine patches (15 mg and 25 mg daily) each given for 8 or 22 weeks with adjunctive moderately intensive support. The 12 month sustained success rates were: 25 mg patch for 22 weeks (L-25), 15.4%; 25 mg patch for 8 weeks (S-25), 15.9%; 15 mg patch for 22 weeks (L-15), 13.7%; 15 mg patch for 8 weeks (S-15), 11.7%; and placebo (P-0) 9.9% (placebo versus 15 mg, p<0.05; 25 mg versus 15 mg, p<0.03; 25 mg versus placebo, p<0.001, Chi-squared test). There was no significant difference in success rate between the two active treatment durations. Of the first week abstainers (n=1,698), 25.1% achieved success at 12 months as opposed to first week smokers, 2.7% of 1,877 subjects (p< 0.001). In summary, a higher than standard dose of nicotine patch was associated with an increase in the long-term success in smoking cessation but continuation of treatment beyond 8-12 weeks did not increase the success rates.  (+info)

Nicotine increases plasminogen activator inhibitor-1 production by human brain endothelial cells via protein kinase C-associated pathway. (6/3904)

BACKGROUND AND PURPOSE: Smoking both increases stroke risk and reduces the risk of thrombolysis-associated intracerebral hemorrhage. Plasminogen activator inhibitor-1 (PAI-1) is a major regulator of fibrinolysis; elevation of PAI-1 is associated with an increased risk of thrombotic disorders. We studied the effect of nicotine, an important constituent of cigarette smoke, on PAI-1 production by human brain endothelial cells. METHODS: Adult human central nervous system endothelial cells (CNS-EC) were used for tissue culture experiments. We analyzed culture supernatant for PAI-1 protein and measured PAI-1 mRNA (by Northern blot analysis) and protein kinase C (PK-C) activity. RESULTS: Nicotine at 100 nmol/L increased PAI-1 protein production and mRNA expression by CNS-EC. After 72 hours of exposure to nicotine, the concentration of secreted PAI-1 in the cell supernatant was increased 1.90+/-0.2 fold compared with untreated cells. PAI-1 mRNA also increased approximately twofold. Inhibition of PK-C completely abolished this effect. Nicotine had no effect on the concentration of tissue plasminogen activator. CONCLUSIONS: Nicotine increases brain endothelial cell PAI-1 mRNA expression and protein production via PK-C-dependent pathway. These findings provide new insights into why smoking may be associated with predisposition to thrombosis and inversely associated with intracerebral hemorrhage after therapeutic tissue plasminogen activator therapy.  (+info)

Nicotine-modified postinfarction left ventricular remodeling. (7/3904)

Cigarette smoking has been noted to impair wound healing in tissues such as skin, bone, and gut. This study was designed to examine whether nicotine adversely affects postinfarction cardiac wound healing and remodeling in an experimental model of myocardial infarction. For this purpose, two groups of rats were studied. The control group received a simple bandage, and the nicotine group had a section (1.75 mg/day) of a nicotine patch attached on their backs. After a 7-day treatment period, an anterior wall infarction was induced. A bandage-free 7-day healing period followed, after which hearts were isolated for mechanical tests. Nicotine-treated rats developed significantly enlarged left ventricles with thin, infarcted walls and a rightward shift in the passive pressure-volume relationship. Pressure-strain analysis also indicated possible changes in the material properties of the wound for nicotine-treated rats. In conclusion, nicotine has significant adverse effects on postinfarction healing and left ventricular remodeling. These observations have important clinical implications because of the enhanced risk for development of heart failure.  (+info)

Metabolites of a tobacco-specific carcinogen in urine from newborns. (8/3904)

BACKGROUND: Cigarette smoking during pregnancy can result in fetal exposure to carcinogens that are transferred from the mother via the placenta, but little information is available on fetal uptake of such compounds. We analyzed samples of the first urine from newborns whose mothers did or did not smoke cigarettes for the presence of metabolites of the potent tobacco-specific transplacental carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). METHODS: The urine was collected and analyzed for two metabolites of NNK, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronide (NNAL-Gluc). Gas chromatography and nitrosamine-selective detection, with confirmation by mass spectrometry, were used in the analyses, which were performed without knowledge of the origin of the urine samples. RESULTS: NNAL-Gluc was detected in 22 (71%) of 31 urine samples from newborns of mothers who smoked; NNAL was detected in four of these 31 urine samples. Neither compound was detected in the 17 urine samples from newborns of mothers who did not smoke. The arithmetic mean level of NNAL plus NNAL-Gluc in the 27 newborns of smokers for which both analytes were quantified was 0.14 (95% confidence interval [CI] = 0.083-0.200) pmol/mL. The levels of NNAL plus NNAL-Gluc in the urine from these babies were statistically significantly higher than those in the urine from newborns of nonsmoking mothers (geometric means = 0.062 [95% CI = 0.035-0.110] and 0.010 [considered as not detected; no confidence interval], respectively; two-sided P<.001). NNAL plus NNAL-Gluc levels in the 18 positive urine samples in which both analytes were quantified ranged from 0.045 to 0.400 pmol/mL, with an arithmetic mean level of 0.20 (95% CI = 0.14-0.26) pmol/mL, about 5%-10% of the levels of these compounds detected in the urine from adult smokers. CONCLUSIONS: Two metabolites of the tobacco-specific transplacental carcinogen NNK can be detected in the urine from newborns of mothers who smoked cigarettes during pregnancy.  (+info)

  • Nicotine is actually a bit like cannabis, in that the metabolites it makes, both in original nicotine, and the main metabolite cotinine, bind to fat more readily than other types of metabolite. (
  • The main problem you've actually got is that the main alkaloid in tobacco, cotinine , is discoverable for longer in blood than nicotine itself. (
  • So although you could be clean of nicotine in your blood in three days, if you are a chronic smoker, cotinine can stay in your blood for up to 10 days. (
  • We demonstrate the efficient re-expression of electrophysiologically responsive, ligand-binding nicotinic acetylcholine receptors in dopamine-containing neurons of the VTA, together with the recovery of nicotine-elicited dopamine release and nicotine self-administration. (
  • King and Picciotto have also identified a novel brain circuit - glutamate neurons, which originate in the cortex and project to the thalamus (corticothalmic neurons) - as the likely site where changes occur in the brain during early nicotine exposure. (
  • They are currently working to identify the molecular changes that developmental exposure to nicotine triggers in the corticothalamic neurons. (
  • 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. (
  • For others, who have quit smoking, it allows them to enjoy the ability to smoke, enjoy the flavors, and the sensation of having a cigarette in hand, and be free of the negatives and the actual nicotine. (
  • Thus while use of nicotine patch may be harmful, nicotine gum use has not been found to be that harmful for a baby and the mom who is trying to quit smoking. (
  • It can be a challenge to quit using products that contain nicotine but remember… you are not alone. (
  • But scientists at Selecta Biosciences in Boston have developed a new solution for those looking to quit the nasty habit: a nicotine vaccine. (
  • Higher doses of nicotine patch may produce small increases in quit rates. (
  • In this study quit rates with bupropion were higher than with nicotine patch or placebo. (
  • Apparently, nicotine binds to the receptors in the brain normally occupied by acetylcholine, which benefits people who need more, but it has no apparent effect on those who don't. (
  • Acetylcholine receptors containing the β2 subunit are involved in the reinforcing properties of nicotine. (
  • This response was identical to one the researchers had reported on previously ( Journal of Neuroscience , May 2003) in genetically altered mice that lack high affinity nicotine receptors as a result of a knockout mutation. (
  • Previous animal studies have found that nicotine interrupts endogenous acetylcholine receptors in the brain and lungs, which can cause developmental disruptions and abnormalities. (
  • Slotkin TA, Epps TA, Stenger ML, Sawyer KJ, Seidler FJ: Cholinergic receptors in heart and brainstem of rats exposed to nicotine during development: implications for hypoxia tolerance and perinatal mortality. (
  • Nicotine work via nicotinic receptors in brain.B2 subunit of this receptor is considered crucial to nicotine's effects. (
  • To check whether immunisation has the desired effect, subjects were given IV nicotine and scans were repeated to measure binding to receptors. (
  • abstract = "Nicotine reportedly improves covert orienting of spatial attention, but enhanced alertness may also play a role. (
  • Having the e-cigarette battery in hand simulates the action of smoking, and puffing with vapor recreates it almost exactly, whether you are using cartridges with nicotine or not. (
  • But the therapy is still recommended as it is slightly better than putting the baby under the direct influence of cigarette smoking which has many other chemicals present other than nicotine. (
  • To put it simply, when you take your first drag of a cigarette or nicotine product, within 10 seconds the nicotine will enter your brain and trigger happy, euphoric feelings. (
  • Whether you vape freebase nicotine or nicotine salts, you're going to be inhaling a lot less harmful chemicals than you would with a traditional cigarette. (
  • u003c\/p\u003e\n\u003cp\u003eNicotine salts aim to replicate the same nicotine hit that is provided by smoking a cigarette, as the nicotine salts are absorbed into your bloodstream much faster than the freebase nicotine found in 'traditional' eliquids on the market, meaning that a nicotine hit is felt quicker from inhaling vaporized eliquid containing nicotine salts. (
  • The nicotine vaccine does not eliminate the craving for nicotine-instead, it diminishes the effect from smoking the cigarette. (
  • Selecta's researchers have used synthetic nanoparticles to trigger an immune response to nicotine, causing the body to create antibodies that bind specifically to the toxin. (
  • It doesn't matter if you inhale nicotine from a vape, or through tobacco, it will still test exactly the same. (
  • Nicotine salts are by far the best possible way to vape. (
  • Even though freebase nicotine is generally considered easier to vape, some companies have found that by adding benzoic acid to their nicotine salts that they can get nicotine levels comparable to freebase nicotine with the added benefits of nicotine salts. (
  • You can use a less-powerful vape - Since nicotine salts are more efficient at delivering nicotine to your system, you won't need some monstrous quad-18650 box mod . (
  • It comes with packed nicotine salts, which ensures that you can vape them all day without a harsh throat hit. (
  • If this nicotine is added to the vape liquid, it has to be vape at very high temperatures for it to be effective. (
  • Moreover, the freebase nicotine has very pH that increases alkalinity that results in harsher throat-hit, causing you to vape a smaller amount than you need. (
  • It also makes it possible to vape effectively at a much lower temperature as in the cheap vape pens and those cigs-like with a high concentration of nicotine. (
  • Generally, mixing vape juices with nicotine salts makes the salts less potent while providing high experience and satisfaction. (
  • experience: according to users, the vape is free from the harsh nicotine hit, which is experienced in most conventional e-liquids. (
  • Nicotine salt based eliquids allow you to vape a higher concentration of nicotine, with a surprisingly smooth draw. (
  • Low and high doses of nicotine altered behavior in opposite directions: The low-dose group tended to learn faster and the high-dose group tended to learn slower than the control animals. (
  • Logically, nicotine replacement should be safer than smoking, but several animal studies indicate that the total dose of nicotine that the fetus is exposed to may be what really matters for brain development," the authors of a 2007 study write in their conclusion. (
  • Nicotine patches provide a measured dose of nicotine through the skin and can be purchased without a prescription. (
  • Wear each patch for 24 hours to provide a steady dose of nicotine around the clock, so you can avoid highs and lows. (
  • A fatal dose of nicotine for an adult is between 50 to 60 milligrams, and a fatal dose for children is expected to be less. (
  • DATA COLLECTION AND ANALYSIS: We extracted data in duplicate on the type of participants, the dose, duration and form of nicotine therapy, the outcome measures, method of randomization, and completeness of follow up.The main outcome measure was abstinence from smoking after at least six months of follow up. (
  • Available in 30ml bottles, this highly-affordable brand is a great way to get started with vaping nicotine salts. (
  • Abnormal avoidance learning in mice lacking functional high-affinity nicotine receptor in the brain. (
  • These alterations were blocked by co-administration of the peroxisome proliferator-activated receptor-γ agonist, rosiglitazone, implicating downregulation of this receptor in the nicotine effects. (
  • Nicotine induction of the asthma phenotype was found to result from a downregulation of mesenchymal peroxisome proliferator-activated receptor-γ (PPARγ), which plays a critical role in the development, homeostasis and repair of the lung [ 7 ]. (
  • We believe that nicotine exposure during development- the same kind of exposure that occurs in mothers who smoke during pregnancy - disrupts normal nicotine receptor activity, much like the knockout mutation, and that this leads to altered emotional learning in adulthood," says King. (
  • They were scanned (SPECT or receptor binding) before and after four monthly immunisations.Subjects abstained from tobacco for the 5 days before each SPECT scan day to allow for any nicotine or metabolites to clear the brain. (
  • The protocol for the ex-vivo experiment included three groups: control, nicotine (0.1 g/mL) and nicotine plus mecamylamine, a nicotinic receptor inhibitor (0.2 g/mL). (
  • The best nicotine salt e-liquid is Yami Vapor . (
  • Now you can enjoy the smooth vapor and rapid nicotine absorption of nicotine salts combined with the award-winning Yami Vapor flavors. (
  • The vapor is less harsh - Nicotine salts, in the formulation that some companies use, can help lower the pH balance of your e-juice. (
  • While the jury is still out on the health effects of vaping, it's important to note that you'll be inhaling much less vapor when using nicotine salts (due to the fact that you can absorb more of the nicotine ) so if you're concerned about the potential negative health effects of vaping then nicotine salts can possibly help reduce your risk. (
  • E-juice containers may have varying amounts of nicotine, from zero milligrams up to 34 milligrams or higher. (
  • King and Picciotto found that nicotine-treated mice showed a hypersensitive response and avoided the dark compartment longer than non-exposed mice. (
  • Animal research has found that nicotine exposure in adolescence causes long-lasting changes in brain development. (
  • Such studies suggest that nicotine - or drugs that mimic nicotine - may one day prove beneficial in the treatment of neurological disorders. (
  • This is because nicotine patches send a constant flow of nicotine through the skin whereas gums or lozenge have a discontinuous flow, thereby reducing the overall nicotine that reaches the baby and may harm them. (
  • The ORs for the different forms of NRT were 1.66 (95% CI: 1.52 to 1.81) for gum, 1.81 (95% CI: 1.63 to 2.02) for patches, 2.35 (95% CI: 1.63 to 3.38) for nasal spray, 2.14 (95% CI: 1.44 to 3.18) for inhaled nicotine and 2.05 (95% CI: 1.62 to 2.59) for nicotine sublingual tablet/lozenge. (
  • Nicotine is chemically similar to acetylcholine, a neurotransmitter in the brain that declines in Alzheimer's disease. (
  • Nicotine is fetotoxic, but one could argue that if nicotine replacement (patches, gum, or inhalers) is the only effective smoking cessation tool, for some pregnant women it is a better alternative than smoking because hundreds of potentially harmful substances are replaced by a single one. (
  • T]his study suggests that two milligrams of nicotine gum does not increase smoking cessation rates, but may reduce overall tobacco exposure during pregnancy. (
  • Which makes it far more uncertain about when you will be clean, especially if you have high body fat, and are a chronic nicotine smoker. (
  • Transmission electron microscopy (TEM) following chronic nicotine treatment showed loosening of the boundary and tearing of the zp. (
  • This study documented that chronic nicotine treatment adversely affects the ultrastructure of oocytes, while gamma-tocotrienol treatment at least minimizes the nicotine-induced damage to oocytes. (
  • They found that maternal nicotine exposure exerted adverse effects on lung development, not only for the immediate offspring but also for the next generation. (
  • The purpose of the present study was to measure the effect of chronic maternal nicotine consumption during gestation only, gestation continuing through lactation, lactation only, and a no-drug control group on physical development, and gross and fine motor coordination of the offspring. (
  • Delayed swimming development provided evidence for a teratogenic effect of maternal nicotine consumption. (
  • The beam walk, roto rod, swimming ontogeny, and open field provided significant evidence that maternal nicotine consumption delays fine motor coordination. (
  • Results showed that the most damaging effects of maternal nicotine consumption occur during gestation. (
  • It's also what we use in nicotine replacement therapies-like gums, patches, sprays, and lozenges. (
  • reports the results of a proof of concept study based on the above assumption.The vaccine was 3:aminomethylnicotine conjugated to recombinant Pseudomonas exoprotein A (3:-AmNic-rEPA).This has high affinity for nicotine. (
  • Nicotine salts last longer - Since nicotine salts are much more stable than freebase nicotine, you'll get a much longer shelf life out of your e-liquid. (
  • u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eNicotine salt e-juice has a longer shelf-life:\u003c\/strong\u003e Nicotine salts are more stable than freebase nicotine, which means that nicotine salt e-juice will last longer in storage without the nicotine degrading. (
  • Identifying the molecular mechanisms involved in nicotine reinforcement and cognition is a priority and requires the development of new in vivo experimental paradigms. (
  • Thus epigenetic mechanisms appear to underlie the multigenerational transmission of a nicotine-induced asthma-like phenotype. (
  • Pregnant women should also be concerned due to evidence that nicotine can harm fetal brain and lung development. (
  • The present study investigated the role of sex on nicotine-induced changes to stimulus-response behavior and associated BDNF protein levels. (
  • Further, non-significant changes to BDNF expression in brain regions highly associated with PCA indicate that BDNF is unlikely to drive nicotine-enhanced conditioned behavior. (