Methamphetamine neurotoxicity

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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. 

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Battaglia G, Fornai F, Busceti C L et al (2002) Selective blockade of mGlu5 metabotropic glutamate receptors is protective against methamphetamine neurotoxicity. J Neurosci 22 2135 41... 

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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. 

COMMENT You have presented some evidence that dopamine may be involved in the neurotoxic action of methamphetamine in terms of dopaminergic neurons, and you presented evidence suggesting that it may be involved in not only the dopamine system but also the serotonin system. 

Seiden, L.S., and Ricaurte, G.A. Neurotoxicity of methamphetamine and related drugs. In Meltzer, H.Y., ed. Psychopharmacology The Third Generation of Progress. New York Raven Press, 1987. pp. 359-366. 

During the 1970s, evidence accumulated that amphetamine and methamphet-amine could also be neurotoxic (Ellison et al. 1978 Hotchkiss and Gibb 1980 Wagner et al. 1980). The effects of amphetamine seem mostly limited to dopamine neurons, whereas methamphetamine affects dopamine and serotonin neurons (Warren et al. 1984). Most recently, MDMA and MDA have been shown to produce neurotoxicity toward brain serotonin neurons much like that of the halogenated amphetamines (Ricaurte et al. 1985 Stone et al. 1986). 

Rats that have lost dopamine and/or serotonin terminals following treatment with amphetamine, methamphetamine, MDMA, MDA, / -chloroamphetamine, or fenfluramine show little in the way of overt ehanges in appearanee or behavior. Dr. Rieaurte (this volume) emphasized the need for more studies in primates, since MPTP-treated miee also show little in the way of observable functional changes, whereas MPTP-treated monkeys show marked neurologie deficits. It may be neeessary to do more detailed analysis of speeifie behaviors and other funetional outputs that are influeneed by dopamine and/or serotonin neurons, to detect functional deficits induced by some neurotoxic drugs. For instance, specific behaviors sueh as appetite-eontrolled behavior (Leibowitz and Shor-Posner 1986), murieidal behavior (Katz 1980), and sexual behavior (Tucker and File 1983) elieited by drugs... 

Role of dopamine in the neurotoxic effects of methamphetamine. J Pharmacol Exp Ther 233 539-544, 1985. 

LaVoie, M.J., Hastings, T.G. Dopamine quinone formation and protein modification associated with the striatal neurotoxicity of methamphetamine evidence against a role for extracellular dopamine. J. Neurosci. 19 1484, 1999. 

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Kita, T., Wagner, G.C., Nakashima, T. Current research on methamphetamine-induced neurotoxicity animal models of monoamine disruption. J. Pharmacol. Sci. 92 178, 2003. 

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Villemagne, V., Yuan, J., Wong, D.F. et al. Brain dopamine neurotoxicity in baboons treated with doses of methamphetamine comparable to those recreationally abused by humans evidence from [llC]WIN-35,428 positron emission tomography studies and direct in vitro determinations. J. Neu-rosci. 18 419, 1998. 

Frey, K., Kilboum, M., Robinson, T. Reduced striatal vesicular monoamine transporters after neurotoxic but not after behaviorally-sensitizing doses of methamphetamine. Eur. J. Pharmacol. 334 273, 1997. 

Melega, W.R, Lacan, G., Harvey, D.C., Huang, S.C., Phelps, M.E. Dizocilpine and reduced body temperature do not prevent methamphetamine-induced neurotoxicity in the vervet monkey [1 lC]WfN 35,428-positron emission tomography studies. Neurosci. Eett. 258 17, 1998. 

Melega, W.P., Raleigh, M.J., Stout, D.B. et al. Recovery of striatal dopamine function after acute amphetamine- and methamphetamine-induced neurotoxicity in the vervet monkey. Brain Res. 766 113, 1997. 

Cass, W.A., Manning, M.W. Recovery of presynaptic dopaminergic functioning in rats treated with neurotoxic doses of methamphetamine. J. Neurosci. 19 7653, 1999. 

Friedman, S.D., Castaneda, E., Hodge, G.K. Long-term monoamine depletion, differential recovery, and subtle behavioral impairment following methamphetamine-induced neurotoxicity. Pharmacol. Biochem. Behav. 61 35, 1998. 

Cadet, J.L., Sheng, P., Ah, S. et al. Attenuation of methamphetamine-induced neurotoxicity in cop-per/zinc superoxide dismutase transgenic mice. J. Neurochem. 62 380, 1994. 

Itzhak, Y., Gandia, C., Huang, P.L., Ali, S.F. Resistance of neuronal nitric oxide synthase-deficient mice to methamphetamine-induced dopaminergic neurotoxicity. J. Pharmacol. Exp. Ther. 284 1040, 1998. 

Ali, S.F., Martin, J.L., Black, M.D., Itzhak, Y. Neuroprotective role of melatonin in methamphetamine-and l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine-induced dopaminergic neurotoxicity. Ann. N.Y. Acad. Sci. 890 119, 1999. 

Pubill, D., Canudas, A.M., Pallas, M., Camins, A., Camarasa, J., and Escubedo, E., Different glial response to methamphetamine- and methylenedioxymethamphetamine-induced neurotoxicity, Naunyn Schmiedeberg s Arch. Pharmacol. 367(5), 490 199, 2003. 

Yu X, Imam SZ, Newport GD, Slikker W Jr, Ali SF. (1999). Ibogaine blocked methamphetamine-induced hyperthermia and induction of heat shock protein in mice. Brain Res. 823(1-2) 213-16. Zaczek R, Coyle JT. (1982). Excitatory amino acid analogues neurotoxicity and seizures. Neuropharmacology. 21(1) 15-26. 

Dopaminergic activity. Smoke was administered intranasally to mice for 20 minutes twice daily for 3 days before methamphet-amine treatment. The treatment significantly attenuated the neurotoxicity as judged by a lesser depletion of dopamine, dihydrophenylacetic acid, and homovanillic acid. The lesser effect of methamphetamine on the content of serotonin level was unaltered by prior inhalation of smoke h Tobacco glycoside, administered to mice, increased behavior via dopamine 2 neuronal activity but not dopamine 1 activity in a dose-dependent manner. The results indicated that smoking can affect the human brain function via not only the nicotinic cholinergic neuron but also the dopamine 2 neuron . 

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