Disease relevance of Methamphetamine hydrochloride

• Myocardial infarction after inhalation of methamphetamine [1].
• Role for excitatory amino acids in methamphetamine-induced nigrostriatal dopaminergic toxicity [2].
• Rhesus monkeys with a history of drinking methadone but currently drug-free and control monkeys with no drug history were injected with methamphetamine hydrochloride (2 to 5 milligrams per kilogram of body weight) [3].
• This study was conducted to determine if excitatory amino acids, which appear to be involved in various neurodegenerative disorders, might also contribute to the dopaminergic neurotoxicity produced in mice by either methamphetamine or MPTP [2].
• Acute lead poisoning in two users of illicit methamphetamine [4].

Psychiatry related information on Methamphetamine hydrochloride

• The smoking of crystal methamphetamine, or "ice," is a growing drug abuse problem in the United States. The toxic effects of methamphetamine smoking have not been well described [5].
• Neural activation patterns of methamphetamine-dependent subjects during decision making predict relapse [6].
• Methamphetamine [METH ("speed")] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans [7].
• These methods have already been used to reveal the profile of brain anomalies in studies of dementia, epilepsy, depression, childhood- and adult-onset schizophrenia, bipolar disorder, attention-deficit/hyperactivity disorder, fetal alcohol syndrome, Tourette syndrome, Williams syndrome, and in methamphetamine abusers [8].
• For more than 50 years, methamphetamine has been a widely used stimulant drug taken to maintain wakefulness and performance and, in high doses, to cause intense euphoria [9].

High impact information on Methamphetamine hydrochloride

• Although less active in open field tests, D4R-/- mice outperformed wild-type mice on the rotarod and displayed locomotor supersensitivity to ethanol, cocaine, and methamphetamine [10].
• The systemic administration of either methamphetamine or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to experimental animals produces degenerative changes in nigrostriatal dopaminergic neurons or their axon terminals [2].
• This review focuses on new insights, obtained from both in vivo and in vitro studies, into the molecular mechanisms whereby amphetamine, and the closely related compounds methamphetamine and methylenedioxymethamphetamine, cause monoamine, and particularly dopamine, release [11].
• Methamphetamine ingestion by a breast-feeding mother and her infant's death: People v Henderson [12].
• Methamphetamine caused a 54% to 63% rise in maternal blood pressure, a 20% to 37% increase in fetal blood pressure, and a drop in fetal oxyhemoglobin saturation and arterial pH [13].

Chemical compound and disease context of Methamphetamine hydrochloride

• PARTICIPANTS: A total of 415 cocaine or methamphetamine users beginning outpatient substance abuse treatment [14].
• The effect of elevated striatal dopamine levels on 3-NP toxicity was examined by using acute administration of methamphetamine [15].
• Neither methamphetamine nor methcathinone users showed clinical signs of parkinsonism [16].
• This critical review goes beyond the compilation of previously well-documented evidence demonstrating that oxidative stress mediates METH and MDMA toxicity to dopamine and/or serotonin nerve terminals [17].
• These results point to activated microglia as a potential source of the reactive oxygen/nitrogen species and cytokines that have been previously associated with methamphetamine toxicity and other neurotoxic conditions [18].

Biological context of Methamphetamine hydrochloride

• We report two cases in intravenous methamphetamine users who presented with abnormal liver function values, low hematocrit values, basophilic stippling of red blood cells, and elevated blood lead levels [4].
• Calcineurin/NFAT-induced up-regulation of the Fas ligand/Fas death pathway is involved in methamphetamine-induced neuronal apoptosis [7].
• The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes [19].
• Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains [19].
• To investigate the potential mechanism underlying these responses, we examined the acute in vitro and in vivo effects of amphetamine and methamphetamine (METH) on phosphorylation and down-regulation of rat DAT using wild type and N-terminal truncation mutants [20].

Anatomical context of Methamphetamine hydrochloride

• Although the ewes had higher peak concentrations, the fetuses' longer elimination half-life ultimately led to higher fetal than maternal methamphetamine concentrations [13].
• Compared with controls, abstinent methamphetamine and methcathinone users had significant decreases in DAT density in the caudate nucleus (-23 and -24%, respectively) and putamen (-25 and -16%, respectively) [16].
• Methamphetamine causes differential regulation of pro-death and anti-death Bcl-2 genes in the mouse neocortex [21].
• Mean dopamine levels in the methamphetamine users were reduced more in the caudate (-61%) than in the putamen (-50%), a pattern opposite to that of Parkinson's disease [9].
• The effect of methamphetamine on the mitochondrial membrane potential and electron transport chain and subsequent apoptotic cascades are also emphasized [22].

Associations of Methamphetamine hydrochloride with other chemical compounds

• We observed that administration of neurotoxic doses of methamphetamine to rats resulted in a two- to threefold increase in protein cysteinyl-dopamine in the striatum 2, 4, and 8 hr after treatment [23].
• The recreational drug (+/)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") is a methamphetamine derivative that selectively destroys central 5-HT axons and axon terminals in animals and, possibly, humans [24].
• METHOD: Fifteen methamphetamine abusers and 20 non-drug-abusing comparison subjects were studied with positron emission tomography (PET) and [11C]raclopride to assess the availability of dopamine D2 receptors and with [18F]fluorodeoxyglucose to assess regional brain glucose metabolism, a marker of brain function [25].
• (-)-Deprenyl (selegiline), a propargylamine derivative of methylamphetamine, is a potent, irreversible inhibitor of monoamine-oxidase type B (MAO-B) [26].
• These results suggest that the behavioral sensitization produced by the repeated administration of methamphetamine is accompanied by an enhancement in the release of DA induced by methamphetamine, nomifensine, and phenylethylamine in vitro and is also accompanied by increased DA uptake into striatal synaptosomes [27].

Gene context of Methamphetamine hydrochloride

• Regulations of methamphetamine reward by extracellular signal-regulated kinase 1/2/ets-like gene-1 signaling pathway via the activation of dopamine receptors [28].
• Neurokinin-1 (NK-1) receptor antagonists abrogate methamphetamine-induced striatal dopaminergic neurotoxicity in the murine brain [29].
• The CYP2D6 substrates amitriptyline, and (+) and (-) methamphetamine (MAMP) are both p-hydroxylated and N-demethylated (NDM) [30].
• In this study, we examined if Cdk5 signaling participates in the behavioral and biochemical effect of acute and chronic methamphetamine (METH) treatment [31].
• The increase in NPY expression produced by methamphetamine in AL animals may be mediated by the ability of this drug to decrease secretion of leptin and insulin and increase secretion of ghrelin [32].

Analytical, diagnostic and therapeutic context of Methamphetamine hydrochloride

• PARTICIPANTS AND DESIGN: Treatment-seeking methamphetamine-dependent males (N = 46) underwent fMRI 3 to 4 weeks after cessation of drug use [6].
• DESIGN: To assess regional specific metabolite levels using magnetic resonance spectroscopy imaging techniques in 2 groups of currently abstinent methamphetamine users: methamphetamine users who recently initiated abstinence and methamphetamine users who had initiated abstinence more than 1 year prior to study [33].
• To understand the mechanism of methamphetamine (MAP) craving from the viewpoint of nicotinic acetylcholinergic transmission, we examined the responsible site of the brain for anticraving effects produced by nicotinic agonists by using a MAP self-administration paradigm in rats [34].
• The grafting of undifferentiated and differentiated 1RB3AN27 cells or differentiated murine neuroblastoma (NBP2) cells into striata of 6-hydroxydopamine-lesioned rats (an animal model of PD) caused a time-dependent improvement in neurological deficits (reduction in the methamphetamine-induced turning rate) [35].
• Furthermore, as shown by striatal microdialysis, animals treated with methamphetamine at 5 degreesC showed DA release identical to that of animals treated at room temperature [23].

References