Stimulant drugs nicotine

In this cliaptcr and in C hapter 8 we review two more stimulant drugs nicotine and caffeine. We cover these two drugs apart from other stimulant drugs because nicotine and caffeine arc used so prominently in societies around the world. Use of other stimulant drugs lias a small fraction of the prevalence that use of nicotine or caffeine docs. 

True. Tobacco contains nicotine, a highly addictive stimulant drug. 

Stewart J (1983) Conditioned and unconditioned drug effects in relapse to opiate and stimulant drug-administration. Prog Neuropsychopharmacol Biol Psychiatry 7 591-597 Stolerman IP (1988) Characterization of central nicotinic receptors by studies on the nicotine cue and conditioned taste aversion in rats. Pharmacol Biochem Behav 30 235-242 Stolerman IP (1989) Discriminative stimulus effects of nicotine in rats trained under different schedules of reinforcement. Psychopharmacology 97 131-138 Stolerman IP (1999) Inter-species consistency in the behavioural pharmacology of nicotine dependence. Behav Pharmacol 10 559-580... 

Newhouse PA, Potter A, Corwin J, et al Acute nicotinic blockade produces cognitive impairment in normal humans. Psychopharmacology 108 480-484, 1992a Newhouse PA, Penetar D, Fertig J Stimulant drug effects after prolonged total sleep deprivation a comparison of amphetamine, nicotine, and deprenyl. Mil Psychol 4 207-234, 1992b... 

A suitable treatment to reduce many of the effects of the anticholinesterase would be atropine, a muscarinic antagonist. This would not reverse the twitching of skeletal muscle, which is due to stimulation of nicotinic receptors. Cholinesterase activity in the body can be reactivated by the drug pralidoxime, which must be given soon after exposure to the anticholinesterase. 

Nicotine is classified as a stimulant drug, but people who use it often report decreased arousal. That is, the perception is that nicotine has a calming effect, and nicotine users find this effeet reinforcing (Todd, 2004). The reasons for this perception of lowered arousal are complex. One factor may be nicotine s acute effect of relaxing the skeletal muscles (see Table 7.5 also see Jones, 1987b). Another pharmacological reason is nicotine s biphasic action at higher doses its effects are more depressant. 

The three most popular psychoactive drugs—nicotine, caffeine, and alcohol—deliver their effects according to processes that are consistent with those discussed above. Nicotine, for example, binds to nicotinic receptors in the brain,. stimulating an increase in the release of dopamine. Caffeine binds to adenosine receptors. 

The various stimulants have no obvious chemical relationships and do not share primary neurochemical effects, despite their similar behavioral effects. Cocaines chemical strucmre does not resemble that of caffeine, nicotine, or amphetamine. Cocaine binds to the dopamine reuptake transporter in the central nervous system, effectively inhibiting dopamine reuptake. It has similar effects on the transporters that mediate norepinephrine and serotonin reuptake. As discussed later in this chapter in the section on neurochemical actions mediating stimulant reward, dopamine is very important in the reward system of the brain the increase of dopamine associated with use of cocaine probably accounts for the high dependence potential of the drug. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

In contrast to the nicotinic antagonists and indeed both nicotinic and muscarinic agonists, there are a number of muscarinic antagonists, like atropine, hyoscine (scopolamine) and benztropine, that readily cross the blood-brain barrier to produce central effects. Somewhat surprisingly, atropine is a central stimulant while hyoscine is sedative, as least in reasonable doses. This would be the expected effect of a drug that is blocking the excitatory effects of ACh on neurons but since the stimulant action of atropine can be reversed by an anticholinesterase it is still presumed to involve ACh in some way. Generally these compounds are effective in the control of motion but not other forms of sickness (especially hyoscine), tend to impair memory (Chapter 18) and reduce some of the symptoms of Parkinsonism (Chapter 15). 

The dopaminergic system plays a role in the abuse liability for some, if not most, drugs. The stimulants — opiates, marijuana, nicotine, and ethanol — all interact directly or indirectly with... 

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