Stimulant drugs pharmacology

Schuster CR The behavioral pharmacology of psychomotor stimulant drugs, in Psychotropic Agents, Part II. Edited by Hoffineister F, Stille G. New York, Springer-Verlag, 1981, pp 587-605... 

Rush, C., Sullivan, J. and Griffiths, R., Intravenous caffeine in stimulant drug abusers Subjective reports and physiological effects. Journal of Pharmacology and Experimental Therapeutics 273(1), 351-358, 1995. 

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... 

Robbins TW, Sahakian BJ (1979) Paradoxical effects of psychomotor stimulant drugs in hyperactive children from the standpoint of behavioural pharmacology. Neuropharmacology 75 931-950. 

Cocaine and other stimulant drugs are often taken in combination with other drugs, particularly alcohol and opiates. Laboratory studies in humans have shown that alcohol can enhance and prolong the subjective pleasure associated with cocaine, and this is likely the basis for their frequent association. Recent studies have revealed that when cocaine is taken with alcohol, a new compound called cocaethylene is formed in the body. Cocaethylene has pharmacological properties similar to cocaine, but it may be more toxic. Many cases of cocaine overdose may in fact involve cocaethylene toxicity caused by combining cocaine and alcohol (Raven, Necessary, Danluck, Ettenberg,... 

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. 

Amphetamine and methamphetamine (Figure 34-19) are CNS stimulant drugs that have limited legitimate pharmacological use. ° They are used to treat narcolepsy, obesity, and attention-deficit hyperactivity disorders. However, they produce an initial euphoria and have a high abuse potential. Other sympathomimetic amines that also have high potential for abuse include the designer amphetamines, ephedrine, pseudoephedrine, phenylpropanolamine, and methylphenidate (Ritalin). 

Caffeine s pharmacologic actions are similar to those of other stimulant drugs. As such, abstinence from caffeine induces a distinct withdrawal syndrome that includes headache, drowsiness, and fatigue. 

Calpain inhibition may represent an important mechanism for future drug development. Control of calpain activity may limit the invasive properties of cells and thereby provides a possible mechanism to limit the invasiveness of tumors or inhibits the development of chronic inflammation. For the moment, pharmacological inhibitors of calpains are still not capable of differentiating among different calpain isoforms in cellular systems or in vivo. The importance of calpains in diseases will continue to stimulate the development of new and better inhibitors. 

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