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Behavioral effects of caffeine coadministered with nicotine, benzodiazepines, and alcohol
Published in B.S. Gupta, Uma Gupta, Caffeine and Behavior, 2020
Like caffeine, nicotine is classed as a stimulant. Its behavioral effects are due to a number of actions, including agonist activity at central nicotinic cholinergic receptors.1 At moderate doses, nicotine can increase rates of schedule-controlled responding, an effect that is blocked by the nicotinic receptor antagonist mecamylamine.2 Nicotine is administered in the form of tobacco smoke, other tobacco products, nicotine chewing gum, and transdermal patches. Studies of coffee drinking and cigarette smoking have shown a moderately strong positive relationship between the two.3 This could be explained by individual factors, such as a predisposition to use stimulants, but may possibly reflect an interaction of some kind between the two drugs.
Cholinergic Antagonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Vishal S. Gulecha, Manoj S. Mahajan, Aman Upaganlawar, Abdulla Sherikar, Chandrashekhar Upasani
Ganglionic blocking agents are used for the treatment of chronic hypertension but nowadays they are replaced by other superior agents. These drugs have utility in facilitating but newer alternatives like nitroprusside or other depressive sedatives are superior to produce controlled hypotension and to minimize hemorrhage and blood loss (Fukusaki et al., 1999). Currently, mecamylamine is used therapeutically in the United States. Trimethaphan, a short-acting drug, due to its direct vasodilating properties is used as antihypertensive agents particularly in patients with acute aortic aneurysm. It also produces prolonged neuromuscular blockade and may potentiate the neuromuscular blocking action of tubocurarine (Brunton et al., 2011).
Drugs Affecting Autonomic Ganglia (Including the Adrenal Medulla)
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
The effects of different blockers on the rate of decay are not as clear cut as the simple model predicts since there are multiple phases of decay and evidence for both fast and slow channels. The results with the methonium compounds show an initial shortening of decay of the synaptic current and frequency-dependence. This is consistent with them interacting not with the nicotinic receptor but with the ion channel itself in the open position. The reduced activity of compounds smaller than C5 may be due to them passing straight through the channel without blocking, while compounds larger than C8 may prevent channel closure and thus escape quickly. Tubocurarine behaved in a similar fashion, which contrasts with its competitive receptor blocking activity at the neuronmuscular junction. Mecamylamine and trimetaphan, however, blocked in a manner consistent with a competitive interaction with the nicotinic receptor. They did not affect the decay, but reduced the amplitude of the excitatory synaptic current (Gurney & Rang 1984).
Mirtazapine decreased induction and expression of cocaine + nicotine-induced locomotor sensitisation in rats
Published in The World Journal of Biological Psychiatry, 2020
Susana Barbosa Méndez, Alberto Salazar-Juárez
As mentioned in Experiment 3, dosing of cocaine, nicotine and cocaine + nicotine significantly increased the duration of locomotor activity (two-way repeated measures ANOVA; F(63,495) = 67.04, P < 0.0001), which peaked at 30 min (P < 0.002) after drug administration (Figure 5(B)). In contrast, treatment with mecamylamine considerably reduced cocaine-, nicotine- and cocaine + nicotine-induced locomotor activity. The MEC + COC, the MEC + NIC and the MEC + COC + NIC groups reached their highest levels of activity 30 min after cocaine, nicotine and cocaine + nicotine administration and were significantly different in the SAL + COC (P < 0.002), the SAL + NIC (P < 0.003) and the SAL + COC + NIC (P < 0.001) groups. Locomotor activity in the MEC + NIC groups decreased rapidly, at 60 min (P = 0.30). After mecamylamine administration, activity returned to baseline levels. In contrast, locomotor activity in the MEC + COC and the MEC + COC + NIC groups decreased gradually, reaching baseline values at 130 and 150 min after drug administration, respectively (Figure 5(B)).
Understanding the implications of the biobehavioral basis of nicotine addiction and its impact on the efficacy of treatment
Published in Expert Review of Respiratory Medicine, 2018
Nikki Bozinoff, Bernard Le Foll
As mentioned earlier, different subunits of nAChRs have been involved in nicotine addiction process. The focus has been initially on the role of β2 and α4 subunits, notably based on the findings that β2 subunit deletion decreases sensitivity to nicotine’s reinforcing effects [11] and the fact that α4 subunit overexpression increases sensitivity to nicotine reinforcement [51]. Varenicline and cytisine, both α4β2* receptor partial agonists, are used in the treatment of tobacco use disorder and are explored in more detail below. Lobeline, also a nicotinic receptor partial agonist, was the subject of a Cochrane review which found no evidence that it is helpful for smoking cessation [52]. Mecamylamine, a nonselective nicotine receptor antagonist, has been explored for its potential to decrease nicotine’s reinforcing effects and was the subject of two trials that used it in combination with NRT [53,54]. At this time, there is inconclusive evidence to support the use of mecamylamine in combination with NRT [4].
Green tobacco sickness: mecamylamine, varenicline, and nicotine vaccine as clinical research tools and potential therapeutics
Published in Expert Review of Clinical Pharmacology, 2019
Green tobacco sickness is a debilitating occupational hazard experienced by farm workers whose skin contacts freshly harvested green tobacco leaves.The hot humid climate of tobacco farms decreases worker compliance in the use of personal protective equipment; workers come from economically underserved, rural, and often uneducated communities.Of the 33 million tobacco farm workers worldwide, approximately 8 million are afflicted with green tobacco sickness.Mecamylamine (3-methylaminoisocamphane hydrochloride; Inversine, Vecamyl®) is a non-competitive nAChR antagonist that was originally prescribed for blood pressure control.Mecamylamine is an effective blocker of many effects of nicotine in humans and non-humans, including seizures and death in rodents and cats.Mecamylamine is approved as an oral tablet, is safe at doses well above those that block the effects of nicotine, is off-patent, and is readily available.Varenicline (Chantix), an nAChR agonist with lower efficacy than nicotine at some nAChR subtypes, is a smoking cessation aid that might prove effective against green tobacco sickness.Nicotine vaccines and passive immunizations through direct administration of anti-nicotine antibodies, which prevent nicotine from crossing the blood-brain barrier and gaining access to brain nAChRs, offer another possible approach for treating green tobacco sickness.If mecamylamine is shown to alleviate green tobacco sickness, nicotine’s critical involvement would be confirmed and millions of tobacco farm workers worldwide would be protected from a debilitating illness.