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At least 847 records · Page 47Linked to original sources

PubMed1994

A new visual enzyme immunoassay of methamphetamine using linear water-soluble polyelectrolytes.

A new visual enzyme immunoassay (EIA) technique has been developed. Oppositely charged synthetic linear water-soluble polyelectrolytes (poly-N-ethyl-4-vinyl-pyridine as polycation and polymethacrylate as polyanion) were used as carriers for reagent immobilization. The ability of these molecules to form an insoluble complex was applied for the separation of bound and free components of the immunoassay reaction mixture. This approach was realized in methamphetamine visual EIA. In the first stage of the assay two specific reactions took place during incubation of the analytical reagents with the probe to be analyzed: (1) competition between methamphetamine and hapten conjugated with peroxidase for the interaction with specific antibodies and (2) interaction of these antibodies with the protein A-polymethacrylate conjugate. As a result of these reactions the (polyanion-protein A)-antibody-(hapten-peroxidase) complex was formed. Then the reaction mixture was filtered through an Ultrabind membrane (0.45 microns) with adsorbed poly-N-ethyl-4-vinylpyridine, and the immunological complexes were immobilized to the membrane by electrostatic interaction. The level of peroxidase binding on the membrane was measured by diaminobenzidine substrate. The system described was optimized to achieve both high rapidity (20 min) and an appropriate sensitivity (0.4 micrograms/ml) for methamphetamine assay.

Animals↗

PubMed1987

Haloperidol prevents the methamphetamine-induced apomorphine subsensitivity of dopamine metabolism in rat striatum.

Our previous experiment showed that the sensitivity of striatal dopaminergic metabolism to apomorphine was lowered after pretreating rats with methamphetamine. This study further demonstrated that haloperidol administered with methamphetamine prevented the effect of the methamphetamine pretreatment. Since gamma-butyrolactone was administered in combination with apomorphine so as to remove complications which might arise from the modification of impulse flow through the striatonigral feedback loop, it is possible that the observed effect of apomorphine upon striatal dopaminergic metabolism and its antagonism with haloperidol may be mediated by autoreceptors of dopaminergic axon terminals in rat striatum.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1991

Involvement of central beta-adrenoceptors in the induction of hypothalamic interleukin-1 beta mRNA by methamphetamine.

Methamphetamine (2-15 mg/kg, i.p.) has been shown to induce interleukin-1 beta (IL-1 beta) mRNA in the rat hypothalamus. The induction of IL-1 beta mRNA was blocked by intraperitoneal pretreatment with beta-blockers propranolol (0.1-1 mg/kg, but not 0.01 mg/kg) and pindolol (0.3 and 1 mg/kg). Prazosin (1 and 5 mg/kg) and yohimbine (1 and 5 mg/kg), alpha-blockers and haloperidol (1 mg/kg), a dopamine antagonist, produced partial and little suppression, respectively. When injected intracerebroventricularly (i.c.v.), propranolol, but neither prazosin nor yohimbine, significantly suppressed the methamphetamine-induced expression of IL-1 beta mRNA at a dose of 1 nmol/rat. An i.c.v. injection of the beta-adrenoceptor agonist isoproterenol (1 and 3 micrograms/rat) dose-dependently increased the hypothalamic level of IL-1 beta mRNA. The present results suggest that the induction of hypothalamic IL-1 beta mRNA by methamphetamine is mediated by beta-adrenoceptors in the brain.

Adrenergic alpha-Antagonists↗

PubMed1995

Methamphetamine-induced nuclear c-Fos in rat brain regions.

To explore the possible robust changes in neuronal activity in dopamine-poor brain regions after an indirect dopamine agonist, methamphetamine, we have investigated its effects on c-fos expression in rat brain using immunocytochemistry of c-Fos. Intraperitoneal injection of methamphetamine (1.6-4.8 mg/kg), but not of saline, induced a widespread nuclear c-Fos-like immunoreactivity in the pyriform cortex and olfactory tubercle with greatest density followed by the II-VI layers of the neocortex, amygdala, hypothalamus, thalamus, nucleus accumbens and striatum. These expression patterns resemble those elicited by amphetamine and suggest that not only the dopamine-rich subcortical regions but also the cerebral cortex may play a crucial role in behavioral abnormality induced by methamphetamine.

Animals↗

PubMed1991

Antagonism of EEGraphic and behavioural effects of methamphetamine by selective receptor blockers (SCH 23390 and raclopride) in the rabbit.

1. The interactions between selective D1 and D2 antagonists (SCH 23390 and raclopride) and methamphetamine on EEG arousal and behaviour was studied in rabbits. Haloperidol, a "classic neuroleptic" was used as reference drug. 2. Both 23390 and raclopride, which were used at low dosage (0.03-0.09 mg/kg i.v. for the former and 1-3 mg/kg for the latter), were able to block completely the behaviour induced but do not inhibit completely the EEG arousal pattern induced by methamphetamine. 3. The blockade of both behaviour and EEG arousal took only when the two drugs were administered concomitantly at the lower dosage. 4. The antagonistic effects obtained with the concomitantly administration of the two drugs were of higher degree in confront of those obtained with the pretreatment with haloperidol 0.3 mg/kg i.v. 5. Our data indicate that both D1 and D2 antagonists are able to block, at the dosage used, motor hyperactivity and stereotyped behaviour typically induced by methamphetamine and that SCH 23390 and raclopride are potentiated also in this experimental model.

Animals↗

PubMed1991

Survival of developing dopaminergic neurons in reaggregate tissue culture following treatment with methamphetamine.

Developing central dopamine (DA)-containing neurons in rotation-mediated reaggregate tissue culture exposed to 10(-4) M methamphetamine for 1 week (at a time corresponding to the 2nd week of postnatal development) exhibit decreased DA levels. DA neurons were visualized either by a histofluorescent method after 'loading' with exogenous DA, or by tyrosine hydroxylase (TH) immunocytochemistry. An apparent loss of histofluorescent DA cell bodies was observed due to a methamphetamine-induced reduction in exogenous DA accumulation. No decrease in the number of TH-immunoreactive neurons was observed. Thus, developing DA neurons when visualized by TH immunocytochemistry survive despite methamphetamine-induced reductions in DA levels.

Animals↗

PubMed1991

Methamphetamine-induced expression of interleukin-1 beta mRNA in the rat hypothalamus.

The effect of methamphetamine on the expression of interleukin-1 beta (IL-1 beta) mRNA in the rat brain was investigated with Northern blot analysis. Methamphetamine (2-15 mg/kg, i.p.) caused a marked induction of IL-1 beta mRNA in the hypothalamus among the 8 brain regions examined, in a dose-dependent manner. The level of IL-1 beta mRNA reached a maximum at 1 h and rapidly declined within 2 h after the injection of 15 mg/kg. These results provide the first evidence that methamphetamine induces the expression of IL-1 beta mRNA in the hypothalamus, which may be partly involved in the production of central actions of this drug.

Animals↗

PubMed1995

Methamphetamine and dopamine neurotoxicity: differential effects of agents interfering with glutamatergic transmission.

The effects of riluzole and lamotrigine, two agents which interfere with the release of glutamate (GLU), and MK-801, a blocker of N-methyl-D-aspartate (NMDA) receptors, were compared in the model of methamphetamine-induced depletion of dopamine (DA) levels in mice. Repeated injections with methamphetamine (4 x 5 mg/kg i.p.) markedly decreased levels of DA, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels. When mice were treated with riluzole (2 x 10 mg/kg p.o.), no protection was observed against the decrease in DA and the two metabolites. Lamotrigine (2 x 10 mg/kg p.o.) was also inactive. Treatment with MK-801 (2 x 2.5 mg/kg i.p.) antagonized the decrease in DA, DOPAC and HVA levels induced by the neurotoxin. Thus, unlike an NMDA blocker, drugs that interfere with GLU release did not antagonize the methamphetamine-induced DA neurotoxicity in mice. The consequences of this inactivity are discussed in terms of the reliability of this model to test new drugs with putative efficacy in the treatment of Parkinson's disease.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1985

Effects of chronic methamphetamine on the nigral-striatal dopamine system in rat brain: tyrosine hydroxylase immunochemistry and quantitative light microscopic studies.

Chronic administration of methamphetamine (20 mg/kg, IP, every 12 hours for 10 days) produced a large decrease in tyrosine hydroxylase staining axons and terminal boutons in the caudate nucleus in rats when examined 60 days following the final methamphetamine injection. This effect was quantitated using the Leitz Data Acquisition and Display System (DADS) revealing that there was a 74% decrease in tyrosine hydroxylase positive processes in the caudate nucleus. Furthermore, this treatment also produced a large decrease in the number of tyrosine hydroxylase positive staining neuronal perikarya in the pars compacta of the substantia nigra. This effect was also quantitative using the Leitz-(DADS) system, revealing a decrease of 89% in tyrosine hydroxylase positive material. These data demonstrate that chronic administration of methamphetamine produces a long-term loss of tyrosine hydroxylase enzyme in both the cell bodies of the substantia nigra and the nerve terminals in the caudate nucleus. Whether this effect is due to the degeneration of the neurons or some metabolic effect remains to be determined.

Animals↗

PubMed1979

Methamphetamine-induced changes in brain catecholamines in rats and guinea pigs.

Repeated administration of methamphetamine was found to cause long-term changes in caudate dopamine levels in the rat and guinea pig. Methamphetamine was administered twice a day for thirty days. Two weeks following the last injection, the animals were killed and brains assayed for catecholamine content. These long-term depletions of dopamine, when combined with similar observations previously reported in rhesus monkeys, indicate a species generality of the effects of methamphetamine on caudate dopamine levels.

Animals↗

PubMed1981

Folic acid in serum and cerebrospinal fluid of chronic alcoholics and methamphetamine addicts.

The folic acid (FA) levels in serum and cerebrospinal fluid (CSF) of 39 chronic alcoholics, 15 methamphetamine addicts and 18 control subjects were determined using the technique of Lactobacillus casei assay. Twelve of the 39 alcoholics developed delirium tremens (DT) after determination of the FA level. The serum FA level of the alcoholics with DT was significantly lower than that of the controls, and showed a tendency to be lower than in the alcoholics without DT. The CSF FA of the DT group was significantly lower than that of the control group and of the alcoholics without DT. In the methamphetamine addicts, although the serum FA was significantly lower than that of the controls, the CSF FA remained unchanged. All the methamphetamine addicts demonstrated psychological dependence and tolerance development as did the alcoholics, but they did not show any physical dependence. From these results, a mechanism underlying the development of symptoms of physical dependence such as DT was discussed in relation to the CSF FA.

Adult↗

PubMed1990

Platelet monoamine oxidase activity and personality traits in alcoholics and methamphetamine dependents.

Personality traits of alcoholics and methamphetamine dependents were examined by Karolinska scales of personality (KSP). The two groups differed with respect to Aggression, but, they were basically same in Impulsiveness. The biological marker platelet monoamine oxidase (MAO) activity showed a significant difference between the two groups. The low platelet MAO activity in alcoholics may suggest a certain biological basis to be involved in the etiology of dependence whereas the higher platelet MAO activity observed in methamphetamine dependents may reflect the prolonged use of methamphetamine and/or treatment with neuroleptics, or some biological basis.

Adult↗

PubMed1995

Amphetamine and methamphetamine determination in urine by reversed-phase high-performance liquid chromatography with sodium 1,2-naphthoquinone 4-sulfonate as derivatizing agent and solid-phase extraction for sample clean-up.

A rapid method is described for the identification and determination of amphetamine and methamphetamine in human urine samples by liquid chromatography with UV-Vis detection. The samples were transferred onto a C18 solid-phase extraction column and chromatographed on a Hypersil ODS RP C18, 5 microns (250 x 4 mm I.D.) with an acetonitrile-water elution gradient containing propylamine. Under these conditions, the amines are eluted with a short retention time. The procedure has been applied to the determination of amphetamine and methamphetamine in the range 0.3-4.0 micrograms/ml in spiked urine samples. The detection limits at 280 nm were 4 and 2 ng/ml for amphetamine and methamphetamine, respectively. The intra-day and inter-day precision and accuracy of the method were studied.

Amphetamine↗

PubMed1995

Investigation of the impurities found in methamphetamine synthesised from pseudoephedrine by reduction with hydriodic acid and red phosphorus.

The synthesis of methamphetamine from pseudoephedrine via the reduction with hydriodic acid and red phosphorus was studied and the impurities which were generated, along with the methamphetamine, were investigated. Some of the impurities found have been reported previously, while the diastereoisomers of N-methyl-N-(alpha- methylphenethyl)amino-1-phenyl-2-propanone and the cis-cinnamoyl derivative of methamphetamine are reported here for the first time. Further work on the sequence of reactions occurring in this reduction is also reported.

Acids↗

PubMed2026

Brain network alterations underlying cue reactivity and craving in abstinent methamphetamine users: a systematic review of functional MRI findings.

BACKGROUND: Methamphetamine use disorder (MUD) is marked by intense craving and high relapse risk, often triggered by drug-related cues. Functional magnetic resonance imaging (fMRI) provides key insight into the neural basis of this cue reactivity, implicating large-scale brain networks for reward, motivation, and control. Yet, findings remain inconsistent across studies due to differences in task design, abstinence duration, and participant characteristics. OBJECTIVE: This systematic review synthesises evidence on how abstinence influences brain network alterations underlying cue reactivity and craving in methamphetamine users, integrating task-based and resting-state fMRI findings within leading neurobiological models of addiction. METHODS: A systematic search of PubMed, Scopus, Web of Science, and Ovid was conducted up to August 10, 2025, following PRISMA 2020 guidelines. Eligible fMRI studies examined cue reactivity or craving in abstinent methamphetamine users. Data were extracted on activation, connectivity, and brain-behaviour associations, and synthesised narratively. RESULTS: Task-based studies revealed heightened activation across reward, salience, and control networks during cue exposure, which diminished as parietal and executive control systems re-engaged with longer abstinence. Resting-state findings showed disrupted intrinsic connectivity among default mode, salience, and frontoparietal networks, reflecting persistent imbalances linked to craving and use severity. CONCLUSION: fMRI evidence shows that MUD is marked by network-level disruption linking reward, salience, and control systems. Task-based findings reveal strong cue reactivity in reward circuits, while resting-state data show persistent imbalance among default mode and control networks. With abstinence, partial restoration of network integrity emerges, highlighting both vulnerability and opportunities for targeted, recovery-based interventions.

Humans↗

PubMed2004

Facial and ocular injuries associated with methamphetamine production accidents.

PURPOSE: To evaluate the relative contribution of methamphetamine production-related accidents to facial and ocular injuries admitted to a regional burn unit. DESIGN: Retrospective observational case series. METHODS: Chart review of all patients admitted to the Burn Unit at the University of Iowa Hospitals and Clinics (UIHC) over a 16-month interval. RESULTS: Methamphetamine related accidents were responsible for thirteen (9.8%) of 132 patients admitted with facial burns to UIHC during the study period. All victims were male. In addition to facial burns, eight patients (14 eyes) suffered chemical or thermal burns of the ocular surface of Hughes grade I or worse. One patient required full-thickness skins grafts for cicatricial ectropion of all four eyelids. CONCLUSION: In endemic areas such as Iowa, methamphetamine production accidents contribute to as many as 10% of admissions to burn care units for facial and ocular injuries.

Accidents, Occupational↗

PubMed2006

Methamphetamine exposure presenting as caustic ingestions in children.

With the growing prevalence of methamphetamine use and production in home laboratories, children are at risk for injuries resulting from living in a drug-endangered environment. Although the ingestion of household cleaners is usually accidental and not a result of illicit drug use or production, medical providers must be aware of the chemicals associated with methamphetamine and illicit drug production to identify patients harmed in this environment. We present the first reported cases of children harmed by ingesting caustic substances used in the production of methamphetamine in the home.

Administration, Oral↗

PubMed2003

Methamphetamine-induced gene expression profiles in the striatum of male rat pups exposed to the drug in utero.

Methamphetamine is a neurotoxic pychostimulant which affects monoaminergic and non-monoaminergic systems in the brain. Clinical studies in humans have found that exposure to methamphetamine in the developing embryo can cause significant behavioral and cognitive anomalies later in life. Exposure of animals to methamphetamine (METH) in utero can cause neurobehavioral effects that do not become apparent until young adulthood. In the present study, we sought to determine the effects of in utero METH exposure on the striata of perinatal rat pups using a recently developed 17 k cDNA microarray. We found that METH administration caused alterations in 913 genes according to strict criteria. These alterations include changes in genes that participate in signal transduction, heat shock responses and neuronal development. The majority of the changes in gene expression were more prominent at the 7-day time point. These observations suggest that in utero METH exposure might initiate molecular programs that significantly impact gene expression during the developmental period long after the last exposure to this drug. Thus, during development, METH exposure in utero might cause significant long-term changes in gene expression that might constitute, in part, some of the substrates for the behavioral and cognitive anomalies reported in the literature.

Animals↗