Guidelines on nicotine dose selection for in vivo research

Matta, Shannon G.; Balfour, David J.K.; Benowitz, Neal L.; Boyd, Ryan L.; Buccafusco, Jerry J.; Caggiula, Anthony R.; Craig, Caroline; Collins, Allan C.; Damaj, M. Imad; Donny, Eric C.; Gardiner, Phillip S.; Grady, Sharon R.; Heberlein, Ulrike; Leonard, Sherry; Levin, Edward D.; Lukas, Ronald J.; Markou, Athina; Marks, Michael J.; McCallum, Sarah E.; Parameswaran, Neeraja; Perkins, Kenneth A.; Picciotto, Marina R.; Quik, Maryka; Rose, Jed E.; Rothenfluh, Adrian; Schafer, William R.; Stolerman, I. P.; Tyndale, Rachel F.; Wehner, Jeanne M.; Zirger, Jeffrey M.

doi:10.1007/s00213-006-0441-0

Cited by 732 publications

(772 citation statements)

References 395 publications

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“…This is in agreement with data showing that the HPA axis of chronic smokers was not stimulated (Gilbert et al, 1992;Mendelson et al, 2005) by cigarettes containing the usual amount of nicotine (eg approximately 1-1.5 mg per cigarette) (Matta et al, 2007). Taken together, the present report and human studies indicate that daily intake of nicotine by established tobacco smokers is unlikely to activate the HPA axis.…”

Section: Discussionsupporting

confidence: 93%

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Chen

Sharp

2007

Neuropsychopharmacol

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We investigated the effect of chronic nicotine self-administration (SA) on hypothalamic-pituitary-adrenal (HPA) hormonal responses to acute stressors. Adult male Sprague-Dawley rats were given access to nicotine (0.03 mg/kg) for 23 h per day for 20 days. On day 1 of acquisition of nicotine SA, plasma levels of both adrenocorticotropin and corticosterone were significantly increased 15-30 min after the first dose of nicotine. These hormonal changes were no longer significant on day 3, when adrenocorticotropin levels were o60 pg/ml and corticosterone levels were o110 ng/ml during the hour after the first dose of nicotine. Chronic nicotine SA (20 days) significantly augmented (2-3-fold) both hormonal responses to mild foot shock stress (0.6 mA, 0.5 s per shock, 5 shocks per 5 min), but did not affect hormonal responses to moderate shock (1.2 mA, 0.5 s per shock, 5 shocks per 5 min), lipopolysaccharide or immobilization. Similar data were obtained in Lewis rats. These results provide further support for the concept that chronic nicotine SA is a stressor. In alignment with the effects of other stressors, nicotine activated the HPA axis on the first day of SA, but desensitization occurred with repeated exposure. Furthermore, chronic nicotine SA selectively cross-sensitized the HPA response to a novel stressor. These observations suggest that nicotine may selectively increase the HPA response to stressors in human smokers.

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Section: Discussionsupporting

confidence: 93%

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Chen

Sharp

2007

Neuropsychopharmacol

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“…Several differences exist between humans and other animals, such as the physiologically relevant range of nicotine doses used and the rate of nicotine metabolism [111], and some aspects of nicotine addiction in humans cannot be easily assessed by animal research (e.g. relapse).…”

Section: Nicotinic Acetylcholine Receptors: Animal Researchmentioning

confidence: 99%

Genetic variability in nicotinic acetylcholine receptors and nicotine addiction: Converging evidence from human and animal research

Portugal

Gould

2008

Behavioural Brain Research

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Tobacco smoking is a leading preventable cause of death in the United States and produces a major health and economic burden. Although the majority of smokers want to quit, few are successful. These data highlight the need for additional research into the neurobiology of tobacco dependence. Addiction to nicotine, the main psychoactive component of tobacco, is influenced by multiple factors that include individual differences in genetic makeup. Twin studies have demonstrated that genetic factors can influence vulnerability to nicotine addiction, and subsequent research has identified genes that may alter sensitivity to nicotine. In humans, genome-wide and candidate gene association studies have demonstrated that genes encoding nicotinic acetylcholine receptor (nAChR) proteins are associated with multiple smoking phenotypes. Similarly, research in mice has provided evidence that naturally occurring variability in nAChR genes is associated with changes in nicotine sensitivity. Furthermore, the use of genetic knockout mice has allowed researchers to determine the nAChR genes that mediate the effects of nicotine, whereas research with knockin mice has demonstrated that changes to nAChR genes can dramatically alter nicotine sensitivity. This review will examine the genetic factors that alter susceptibility to nicotine addiction, with an emphasis on the genes that encode nAChR proteins.

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“…It was reported that the sensitivity of acute effects of nicotine in mice is less than that in rats. Median effective dose (ED50) dose for seizures in mice is 2-6 mg/kg depending on strain (Matta et al, 2007). Regarding our study, the markedly depressant effects induced by acute s.c. injection were observed at 1.5 mg/kg, while the stimulant effects were at 0.5 mg/kg.…”

Section: Assessment Of Bioactivity Of Nano-nicotine Via Locomotor Tesmentioning

confidence: 72%

“…To explore the effects of nicotine dose on naïve mice locomotor activity, the travel distance against dose of nicotine before and after drug administration was plotted in The doses of nicotine (0.5 mg/kg, 1.0mg/kg, 1.5 mg/kg) chosen in this study were based on the recommended nicotine dose in mice by Matta et.al (Matta et al, 2007). It was reported that the sensitivity of acute effects of nicotine in mice is less than that in rats.…”

Section: Assessment Of Bioactivity Of Nano-nicotine Via Locomotor Tesmentioning

confidence: 99%

“…According to in vitro aerosolization study result, FPF of this nano-nicotine formulation was 24.4%, so 97.6 µg of nicotine is expected to be deposited on mouse lung. The average mouse body weight is 25g, so the dose is approximately 4 mg/kg, which is twice as much as the guided dose for mice (Matta et al, 2007). Therefore, 25 mg, 50mg and 75 mg nicotine were chosen to ensure a safe dose was delivered to the mice.…”

Section: Assessment Of Viabilitiy Of Inhalation Of Nano-nicotine Via mentioning

confidence: 99%

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Development of Nicotine Loaded Chitosan Nanoparticles for Lung Delivery

Wang¹

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Cigarette smoking has become one of the leading causes of preventable deaths all over the world, causing a serious threat to human wellbeing and a tremendous economic burden to governments. The currently available treatment options for smoking cessation are not efficient. The pulmonary delivery of drugs by methods such as dry powder inhaler (DPI) has been recognized as one of the most efficient routes of drug delivery to the targeted area. The lung delivery of nicotine in this way would be expected to mimic the effects of tobacco smoking and could significantly reduce the negative health effects of smoking that result from nicotine addiction.The aim of this study is to develop nanoparticles with controlled physicochemical properties using biodegradable polymer of chitosan (CS) loaded with nicotine salt for pulmonary delivery as DPI formulations. The outcomes of this project are expected to be a safe and effective CS-based nicotine formulation for pulmonary delivery to treat nicotine dependence. This thesis specially addresses the research questions: (1) how to develop a feasible process to manufacture the nanoparticles suitable for pulmonary drug delivery using biodegradable polymer of CS containing nicotine salt; (2) how to develop an animal model for pulmonary drug delivery from DPI formulation using a nose-only inhalation device.The current therapeutic options for treatment of smoking addiction have been reviewed, and current advancements of technology in pulmonary drug delivery are summarised. Buccal administration of drugs exhibits a low oral bioavailability, and sublingual tablets and chewing gums can be swallowed before being absorbed.Although nasal spray of nicotine is a fast way to deliver nicotine into the bloodstream, Development of Nicotine Loaded Chitosan Nanoparticles for Lung Delivery iii the rate of absorption is still not as rapid as cigarette smoking. Therefore, it is proposed that delivery of nicotine with sustained drug release profile direct into the deep lung is likely to more effectively mimic the rapid effects of cigarette smoking on a physiological level, which could eliminate patient craving and allow the tapering of nicotine level over time to improve patients' compliance.Water in oil (w/o) emulsion crosslinking method has been used to fabricate nicotine hydrogen tartrate (NHT)-loaded CS nanoparticles which separate as solid microaggregates. The physicochemical properties of particles are characterized by a series of techniques. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) shows that the prepared particles are spherical in morphology with rough surface after loading CS particles with NHT. Dynamic Light Scattering (DLS)by Zetasizer determined nanoparticle size ranging from 167.6 nm to 411 nm, while DLS by Mastersizer demonstrated that the microaggregates of these nanoparticles are in the respirable range (<5µm). The surface positive charge as measured by zeta potential tends to decrease with increase of mass ratios of NHT to CS, which is in contr...

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Guidelines on nicotine dose selection for in vivo research

Cited by 732 publications

References 395 publications

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Genetic variability in nicotinic acetylcholine receptors and nicotine addiction: Converging evidence from human and animal research

Development of Nicotine Loaded Chitosan Nanoparticles for Lung Delivery

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