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Methamphetamine pharmacology

In view of this neurotoxicity, we will review some data relevant to this process. First, we will review data showing that methamphetamine (METH), a prototypic psychomotor stimulant, which has been widely used for nonmedical purposes at doses often a good deal higher than therapeutie doses, is neurotoxic to dopamine (DA) and serotonin (5-hydroxytryptamine (5-HI)) systems. Second, we will examine the evidence that other substituted phenethylamines are also neurotoxic to certain transmitter systems. Last, we will examine the behavioral and pharmacological consequences of neurotoxicity that result from exposure to some of these amphetamine-related drugs. [Pg.146]

Rothman, R.B., Partilla, J.S., Baumann, M.H. et al. Neurochemical neutralization of methamphetamine with high-affinity nonselective inhibitors of biogenic amine transporters a pharmacological strategy for treating stimulant abuse. Synapse. 35 222, 2000. [Pg.71]

Ali, S.F., Newport, G.D., Holson, R.R., Slikker, W.J., Bowyer, J.F. Low environmental temperatures or pharmacologic agents that produce hypothermia decrease methamphetamine neurotoxicity in mice. Brain Res. 58 33, 1994. [Pg.77]

Seiden, L.S., Woolverton, W.L., Lorens, S.A., Williams, J.E., Corwin, R.L., Hata, N., and Olimski, M., Behavioral consequences of partial monoamine depletion in the CNS after methamphetamine-like drugs the conflict between pharmacology and toxicology, NIDA Res. Monogr. 136, 34-46 discussion 46-52, 1993. [Pg.141]

Systemic effects of methamphetamine are similar to those of cocaine. Inhalation or IV injection results in an intense rush that lasts a few minutes. Methamphetamine has a longer duration of effect than cocaine. Pharmacologic effects include increased wakefulness, increased physical activity, decreased appetite, increased respiration, hyperthermia, euphoria, irritability, insomnia, confusion, tremors, anxiety, paranoia, aggressiveness, convulsions, increased heart rate and blood pressure, stroke, and death. [Pg.840]

A final pharmacological strategy for treatment of Parkinson s disease comes from enzyme inhibition. This was initally done with an MAO inhibitor, L-deprenyl (selegiline, Eldepryl), but more recent drugs have become available that are COMT inhibitors. L-Deprenyl is an inhibitor of MAOB, which is the form of MAO selective to dopamine. Thus, it may increase the amount of available dopamine for release. Second, it may protect dopamine neurons by reducing the oxidative stress concomitant with dopamine metabolism (Olanow 1997). Third, L-deprenyl is metabolized into amphetamine and methamphetamine, which may contribute to their antiparkinsonian effects. Unlike other treatments for Parkinson s disease, L-deprenyl seems to slow the progression of the disease. Tolcapone (Tasmar) is a COMT inhibitor, which prevents extracellular breakdown of dopamine. [Pg.155]

This book will focus on forensic pharmacology and drugs of abuse. Drugs of abuse, such as cocaine, heroin, marijuana, PCP, benzodiazepines, and methamphetamine, are often involved in criminal and civil matters concerning personal injury, motor vehicle accidents, drug overdose, and murder, and thus, are discussed to illustrate forensic pharmacology issues and investigations. [Pg.12]

Amphetamine and methamphetamine occur as structural isomers and stereoisomers. Structural isomers are compounds with the same empirical formula but a different atomic arrangement, e.g., methamphetamine and phentermine. Stereoisomers differ in the three-dimensional arrangement of the atoms attached to at least one asymmetric carbon and are nonsuperimposable mirror images. Therefore, amphetamine and methamphetamine occur as both d- and L-isomeric forms. The two isomers together form a racemic mixture. The D-amphetamine form has significant stimulant activity, and possesses approximately three to four times the central activity of the L-form. It is also important to note that the d- and L-enantiomers may have not only different pharmacological activity but also varying pharmacokinetic characteristics. [Pg.27]

Since 1971, the DEA has described Ritalin as a powerful stimulant that shares many of the pharmacological effects of amphetamine, methamphetamine, and cocaine. The American Psychiatric Association (APA) agrees. In its book Treatments of Psychiatric Disorders (1989), the association states that Ritalin is neuropharma-cologically similar to cocaine and amphetamines, and that all three drugs share the same abuse patterns. The Diagnostic and Statistic... [Pg.64]

Zaczek, R., Battaglia, G., Contrera, J., Culp, S., De Souza, E. (1989). Methylphenidate and pemoline do not cause depletion of rat brain monoamine markers similar to that observed with methamphetamine. Toxicology and Applied Pharmacology, 100, 227—233. [Pg.526]

Newton, T. F., De La Garza, R., Kalechstein, A. D., 8c Nestor, L. (2005). Cocaine and methamphetamine produce different patterns of subjective and cardiovascular effects. Pharmacology, Biochemistry and Behavior, 82, 90-97. [Pg.473]

Synthesis. The synthesis of the amphetamine and methamphetamine derivatives in the benzobicyclo[2.2.2]-octene system has been described elsewhere (141 and references cited therein). To be able to study certain of the pharmacological aspects of these compounds, 3H-derivatives were prepared of NM-X and NM-N by reducing the N-formyl derivatives of the amphetamine analogs NH-X and NH-N with lithium aluminum tritiide (142). [Pg.467]

Pharmacology. In order to assess the importance of conformational preferences in the action of amphetamine at the adrenergic nerve endings, the effect of the amphetamine and methamphetamine analogs (NH-X,-NH-N, NM-X and NM-N) on the uptake and release of JH-norepinephrine (NE) and H-dopamine (DA) in chopped tissues from various regions of rat brain was examined. NH-X and NM-X were nearly as potent as amphetamine in the inhibition of uptake of 3H-NE into chopped cortex... [Pg.467]

It is not clear when or by whom methamphetamine was first synthesized. Various accounts indicate its first preparation somewhere between 1888 and 1934 (5). In any case, Hauschild (10) published the first studies of the pharmacology of methamphetamine in 1938, characterized its stimulant effects in animals, and also carried out a self-experiment. [Pg.172]

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). [Pg.1320]

Mewaldt, S. P., Ghoneim, M. M. (1979). The effects and interactions of scopolamine, physostigmine and methamphetamine on human memory. Pharmacology Biochemistry and Behavior, 10, 205-210. [Pg.36]

Determine and compare the clinical consequences of CYP2D6 genotype to the metabolism, kinetics, pharmacologic effects, and abuse liability of methamphetamine, d-amphetamine, and dextromethorphan. [Pg.19]


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See also in sourсe #XX -- [ Pg.186 ]




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