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At least 19 recordsLinked to original sources
PubMed1990

[Relationship between years of methamphetamine use and symptoms of methamphetamine psychosis].

The authors researched the demographic characteristics of 233 patients with methamphetamine-associated disorders, and the relation between years of methamphetamine use and symptoms of methamphetamine psychosis. The results were as follows: There were more male users than females. However there were signs that the female users were gradually increasing. Users tended to be older, but users in their 20's and 30's continued to be predominant. Their school careers were usually limited and most of them had left school at a young age. Relations with a particular social group (e.g. organized gangs) has given most of them a chance to use methamphetamine. The symptoms that were seen with high frequency at the first examination were anxiety, fretfulness, auditory hallucination, insomnia, irritability, psychomotor excitement, delusion of persecution, suspicion, delusion of reference, mistake of circumstance, loss of appetite, affective disorder, hypobulia and personality change. With these symptoms, there is a possibility that five years of methamphetamine use is the turning point in terms of the frequency of symptoms occurrence. It was suggested that affective and perceptual disorders depend on the dose of methamphetamine, but abnormalities in thought subject may be deeply influenced by the patient's "feeling of social wrong". Emotional exhilaration and euphoria decreased as the number of years of methamphetamine use increased. These phenomena may be an indication of tolerance. The symptoms that were seen with high frequency at the last examination were hypobulia, affective disorder, personality change, insomnia, anxiety and fretfulness. The symptoms that were highly resistant to treatment were hypobulia, affective disorder, personality change, general malaise, hypochondriasis, insomnia, anxiety and fretfulness. It was suggested that five years of methamphetamine use may be a turning point in the residual rate of symptoms at the last examination after treatment, and also the resistance rate to treatment. Hypobulia and personality change became more evident during treatment.

Adolescent↗
PubMedDate not supplied

Detection of D,L-amphetamine, D,L-methamphetamine, and illicit amphetamine analogs using diagnostic products corporation's amphetamine and methamphetamine radioimmunoassay.

Cross-reactivity with Diagnostic Products Corporation (DPC) amphetamine and methamphetamine radioimmunoassay (RIA) reagents was determined for amphetamine, methamphetamine, and a number of amphetamine analogs. Concentrations from 100 to 100,000 ng/mL were assayed. 3,4-Methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA) showed significant cross-reactivity for the amphetamine and methamphetamine reagents respectively. 4-Hydroxymethamphetamine, 3,4-methylenedioxyethylamphetamine (MDEA), and N,N-dimethyl-MDA also showed significant cross-reactivity with the methamphetamine reagents, but less than MDMA. None of the other analogs showed a positive result with the amphetamine or methamphetamine reagents at even the highest concentration, although several did show measurable cross-reactivity. The L isomers of amphetamine and methamphetamine showed substantially less cross-reactivity than the D forms to which the respective antibody systems are targeted.

3,4-Methylenedioxyamphetamine↗
PubMed1992

[Three cases of acute methamphetamine intoxication--analysis of optically active methamphetamine].

Three typical cases of acute methamphetamine intoxication are reported. The concentrations of methamphetamine in the blood were 27.2, 6.43 and 0.60 micrograms/ml, respectively. All three victims had been exposed to high temperature in a bathroom or a closed room in summer at the time of death. Macroscopic autopsy revealed hemorrhagic pulmonary edema, and histologically, diffuse contraction-band necrosis was evident in the myocardium in all cases. The absolute structures of six illegally available methamphetamine showed an (S)-configuration with an optical purity of > 99% in enantiomeric excess and four were racemic form.

Adult↗
PubMed1989

Subchronic methamphetamine treatment enhances methamphetamine- or cocaine-induced dopamine efflux in vivo.

Intracerebral dialysis was used to study the mechanism underlying behavioral sensitization. Rats were divided into two groups: a control group that received intraperitoneal injections of saline and an experimental group that was given methamphetamine (MAP) (4 mg/kg) once a day for 14 days. Seven days after the last injection, dopamine (DA) and its metabolites were measured in striatal dialysates obtained from awake freely moving rats. A challenge injection of MAP (4 mg/kg) caused a marked increase in the extracellular concentrations of DA, and the extent of the increase was significantly greater in MAP-pretreated rats than in the saline-pretreated controls. A challenge injection of cocaine (20 mg/kg) also caused a significantly greater increase in extracellular DA levels in MAP-pretreated rats than in saline-pretreated rats. These results suggest that an enhancement in striatal DA efflux may play an important role in MAP-induced behavioral sensitization and cross-sensitization to cocaine.

Animals↗
PubMed1991

Co-administration of either a selective D1 or D2 dopamine antagonist with methamphetamine prevents methamphetamine-induced behavioral sensitization and neurochemical change, studied by in vivo intracerebral dialysis.

Repeated administration of amphetamine or methamphetamine (MAP) causes behavioral sensitization in animals. Recently, several studies have revealed that in vivo release of dopamine from presynaptic nerve terminals of mesotelencephalic dopamine neurons is enhanced when sensitized animals are rechallenged with a psychostimulant. The present study investigated the effect of co-administration of SCH 23390 (a selective D1 dopamine receptor antagonist) or YM-09151-2 (a selective D2 dopamine receptor antagonist) prior to each MAP injection for 14 days on dopamine efflux in the striatal perfusates using in vivo dialysis. After 3 months drug abstinence, MAP challenge alone produced augmented stereotypy in the MAP group, but not in the control, the SCH 23390 + MAP or the YM-09151-2 + MAP group. In parallel with this behavioral observation, the degree to which dopamine efflux increased following the MAP challenge was significantly greater in the MAP group than that in the control, SCH 23390 + MAP group and the YM-09151-2 + MAP groups. While dopamine efflux after MAP challenge did not differ between the control and the YM-09151-2 + MAP group, it was greater in the SCH 23390 + MAP group than the control group. These results indicate that both D1 and D2 dopamine receptors play a role in the formation of behavioral sensitization, but with different mechanisms.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

The acute effects of methamphetamine, amphetamine and p-chloroamphetamine on the cortical serotonergic system of the rat brain: evidence for differences in the effects of methamphetamine and amphetamine.

Cortical tryptophan hydroxylase (TPH) activity was reduced 3 h after a 10 or 15 mg/kg i.p. dose of either amphetamine (AMP), methamphetamine (METH), or p-chloroamphetamine (PCA). These injections of METH or PCA also decreased cortical serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations; none of the four doses of AMP decreased indoleamine concentrations. The time course of the effects following a 15 mg/kg dose of each amine was also different. Cortical TPH activity was reduced by all three amines for periods up to 24 h, whereas only METH and PCA significantly decreased 5-HT and 5-HIAA concentrations for long periods. These data suggest that each of the amphetamines may inhibit TPH activity, whereas only METH and PCA produced long-lasting decreases in indoleamine concentrations, reflecting either varying degrees of toxicity or differential effects of AMP on enzyme activity and neurotransmitter concentrations.

Amphetamine↗
PubMedDate not supplied

Simultaneous HPLC analysis of optical isomers of methamphetamine and its metabolites, and stereoselective metabolism of racemic methamphetamine in rat urine.

Simultaneous identification of optical isomers (D and L) of methamphetamine (MAMP), amphetamine (AMP), para(p)-hydroxy(OH)-MAMP, and para(p)-hydroxy(OH)-AMP in rat urine was attempted by high-performance liquid chromatography (HPLC). They were determined as benzoyl derivatives. After administration of D- or L-isomer (15 mg/kg), only D- or L-isomers of the above mentioned metabolites were found in rat urine. In rats administered racemic MAMP (15 mg/kg), each percent dose of L-isomers of MAMP or AMP excreted at four collection times up to 24 h was less than that of the D-isomer (L/D less than 1.00), but the doses of L-isomers of p-OH-MAMP and p-OH-AMP excreted were higher than those of D-isomers (L/D greater than 1.00). Simultaneous analysis within 36 minutes showed good peak resolution. The L/D ratio for each metabolite decreased with time. The total percent doses of D- or L-isomer excreted by 24 hours were about 50% of the administered dose, 23.70 +/- 1.45% for the D-isomer, 25.70 +/- 1.54% for the L-isomers. The total L/D ratio was 1.08 +/- 0.03. These results indicated that Wistar rats have no chiral isomerization enzyme of MAMP, and show stereoselective metabolism of DL-MAMP. In the optical isomer analysis of 11 MAMP powder samples and 28 human urine specimens obtained from Japanese abusers, only D-MAMP was detected in the powder, and D-MAMP and D-AMP were detected in urine, respectively. This suggested that humans have no chiral isomerization enzyme of D-MAMP.

Adolescent↗
PubMed1992

[Studies on origin of illicit methamphetamine. I. The relationship of enantiomeric compositions between methamphetamine and its raw material (ephedrine)].

In order to elucidate the relationship of enantiomeric compositions between methamphetamine (MA) and its raw materials, ephedrine (EP) enantiomers, commercial EP samples and MA samples prepared from them were analyzed by HPLC using GITC-prelabeling. The GITC derivatives were separated on ODS column using methanol-water-acetic acid (45:54:1) at a flow rate of 1.2 ml/min for EP and tetrahydrofuran-water-acetic acid (29:70:1) at a flow rate of 1 ml/min for MA. The chromatographic conditions resulted in such a good separation of four EP and two MA enantiomers that 1/1000 enantiomeric impurities could be detected and discriminated from the major enantiomer with good reproducibility. Moreover, it was demonstrated that the asymmetric center at alpha-position of amino group was entirely retained throughout the reductive reaction of the EP samples, and that the MA samples inherited the enantiomeric character from the EP samples used. This method was applied to discriminative analysis of MA samples seized in Japan.

Chromatography, High Pressure Liquid↗
PubMed1978

Methamphetamine-induced behavioural effects and brain concentrations of methamphetamine and its metabolite amphetamine in mice.

(+)-Methamphetamine (MA) produced dose-related behavioural changes in mice. There was a correlation between the type of behavioural response and the peak brain MA concentration after the i.p. administration of each of the following doses of (+)-MA: 0.64 mg/kg (decreased quiescence--0.738 microgram/g MA), 2.5 mg/kg (increased locomotor activity--3.148 microgram/g MA) and 10.0 mg/kg (stereotyped behaviour--12.608 microgram/g MA). During the 90-min experimental period, there was no positive correlation between the magnitude of each type of drug-induced behaviour and the brain MA concentration. For 10.0 mg/kg (+)-MA, there was a negative correlation between the drug-induced stereotyped behaviour and the brain MA concentration. The apparent disappearance half-life of MA from brain was dependent on the dose of (+)-MA: 0.64 mg/kg (t1/2 56.6 min), 2.5 mg/kg (t1/2 66.6 min), 10.0 mg/kg (42.2 min). For the three (+)-MA doses, the metabolite amphetamine (A) also was present in the brain and the A/MA + A brain concentration ratio was 0.11--0.14. This metabolite appeared to have only a small involvement in the MA-induced behavioural effects.

Amphetamine↗
PubMedDate not supplied

Methamphetamine in antemortem blood and urine by radioimmunoassay and GC/MS.

Methamphetamine abuse is increasing and methamphetamine is second only to alcohol as a positive finding in cases submitted to the San Diego Sheriff's Crime Laboratory. In general, whole blood specimens are submitted more often than urine. A modified version of a commercially available radioimmunoassay, Coat-A-Count (CAC) Methamphetamine, was investigated as a screen for methamphetamine in whole blood and urine. The assay was modified by using 100 microL of sample, making up standards in whole beef blood, extending the incubation time to 2 h or overnight, and using a cutoff reference of 50 ng/mL methamphetamine. The detection limit for the CAC Methamphetamine kit was 20 ng/mL methamphetamine in whole blood. The CAC Methamphetamine results were compared to Abuscreen Amphetamine High Specificity results and to gas chromatography/mass spectrometry (GC/MS) quantitation of amphetamine and methamphetamine for 157 positive and 48 negative blood specimens. With the CAC Methamphetamine assay there were 2 false negatives detected, both less than the 50 ng/mL cutoff level. There were 12 (6%) false positives with the CAC Methamphetamine assay and 29 (14%) false positives with the Abuscreen Amphetamine assay. Of the positive samples, 95% contained only methamphetamine, with an average concentration of 308 ng/mL, range 25-2030 ng/mL.

Evaluation Studies as Topic↗
PubMed1985

Studies on the mechanism of tolerance to methamphetamine.

We have reported that the ability of high doses of methamphetamine to impair dopamine and serotonin synthesis in the rat brain is attenuated when animals are pretreated with gradually increasing doses of methamphetamine. To examine the mechanism of this tolerance phenomenon, the effect of methamphetamine on several neurochemical parameters was determined in naive and methamphetamine-pretreated rats. The elevation of nigral substance P concentrations by methamphetamine was attenuated in pretreated compared to naive rats. The methamphetamine-induced reduction in [3H]sulpiride binding in the rat neostriatum and nucleus accumbens was similarly attenuated in animals pretreated with methamphetamine. Determination of brain concentrations of methamphetamine and amphetamine revealed significantly lower concentrations of both compounds in the brains of pretreated compared to naive animals. The results indicate a reduction in the ability of methamphetamine to increase dopamine transmission in the brains of methamphetamine-pretreated rats. Furthermore, this effect appears to be due, at least in part, to a change in the disposition of methamphetamine in pretreated animals.

Amphetamine↗
PubMed1992

Sigma (sigma) antagonist BMY 14802 prevents methamphetamine-induced sensitization.

We have demonstrated for the first time that the sigma antagonist BMY 14802 prevents the development of behavioral sensitization induced by repeated administration of methamphetamine. Rats received an intraperitoneal injection of 15 or 30 mg/kg BMY 14802 followed by 2 mg/kg methamphetamine 30 min later. Unlike dopamine antagonists, BMY 14802 did not induce major changes in the acute motor effects of 2 mg/kg methamphetamine. Repeated administration of methamphetamine induced progressive augmentation of stereotyped behaviors and resulted in behavioral sensitization. However, repeated administration of methamphetamine in combination with BMY 14802 at either dose produced no increase in the intensity of stereotypy when compared with the first treatment. After a 7-day abstinence period, a challenge test with methamphetamine alone revealed supersensitivity of methamphetamine-sensitized rats to subsequent methamphetamine, whereas rats pretreated with repeated methamphetamine in combination with BMY 14802 exhibited no difference in the intensity of stereotypy from rats pretreated with repeated saline. These results suggest that sigma receptors play a crucial role in the induction of methamphetamine-induced sensitization.

Animals↗
PubMed1990

Potentiating effect of morphine upon d-methamphetamine-induced hyperthermia in mice. Effects of naloxone and haloperidol.

We have examined changes in rectal temperature of mice after subcutaneous administrations of d-methamphetamine alone or methamphetamine plus morphine. Methamphetamine 5 mg/kg produced slight hyperthermia, while simultaneous administration of morphine (25-100 mg/kg), which alone produces hypothermia, potentiated markedly the increase in body temperature by methamphetamine. Methamphetamine showed a hyperthermic effect in a dose-dependent manner in the presence of morphine. The hyperthermia due to methamphetamine plus morphine was avoided by pretreatment with 10 mg/kg naloxone. When animals were pretreated with 2.5 mg/kg haloperidol, hyperthermia due to methamphetamine alone was completely abolished, while that due to methamphetamine plus morphine was still observed. These results showed that dopamine may be implicated in methamphetamine hyperthermia and a haloperidol-nonsensitive mechanism may be involved in the methamphetamine-morphine hyperthermia.

Animals↗
PubMed1989

Enhancement of dopamine actions on rat nucleus accumbens neurones in vitro after methamphetamine pre-treatment.

1. Intracellular recordings were made from the nucleus accumbens neurons in brain slices from rats previously treated with saline or methamphetamine. 2. In neurones from both methamphetamine- and saline (control)-treated rats, dopamine (0.1 mM) produced three types of responses: a biphasic response consisting of an initial hyperpolarization followed by a depolarization, a monophasic hyperpolarization and a simple depolarization. 3. Haloperidol (1 microM) reversibly suppressed both responses to dopamine; (-)-sulpiride (1 microM) selectively abolished the depolarization and prolonged the hyperpolarization. Forskolin (10 microM) and dibutyryl adenosine 3',5'-cyclic monophosphate (1 mM) mimicked the hyperpolarization. Both of the latter two substances were more effective in neurones from methamphetamine-treated rats than in neurones from control rats. 4. In slices from methamphetamine-treated rats, the dose-response curve for the dopamine hyperpolarization was shifted to the left of that seen in neurones from control rats by a factor of approximately 100. The dose-response curve for the dopamine depolarization was shifted to the right about 10-fold in neurones from rats treated with methamphetamine. 5. In slices from control rats, dopamine (less than or equal to 0.1 mM) and methamphetamine (less than or equal to 1 microM) had no effect on the EPSPs evoked by focal electrical stimulation of the periaccumbens regions: dopamine (greater than or equal to 10 nM) and methamphetamine (1 microM) markedly depressed the EPSPs in slices from methamphetamine-treated rats. Depolarizations evoked by application of exogenous glutamate were unaffected by dopamine (less than 5 microM). 6. In slices from methamphetamine-treated rats, dopamine (greater than or equal to 10 nM), forskolin (greater than or equal to 1 microM) and dibutyryl adenosine 3',5'-cyclic monophosphate (1 mM) depressed Ca2+-dependent spikes as well as the EPSPs. Haloperidol (1 microM) completely reversed the depressions of the EPSPs and Ca2+-dependent spikes by dopamine, while (-)-sulpiride (1 microM) was only partially effective. 7. These results indicate that chronic methamphetamine administration leads to enhancement of the actions of dopamine at D1 receptors located on glutamate and/or aspartate nerve terminals and of the dopamine hyperpolarization of principal neurones, which is also mediated by D1 receptors.

Action Potentials↗
PubMed1978

Enhancement of morphine analgesia and brain levels by methamphetamine in mice.

Methamphetamine and morphine were approximately equipotent in producing analgesia in mice using the tail-flick assay. The ED50 for morphine analgesia was significantly reduced when 3.2 mg/kg of methamphetamine was given 5 or 60 min before morphine. Methamphetamine pretreatment increased the peak effect but did not alter the duration of morphine analgesia. Enhancement of morphine analgesia was apparent when methamphetamine was given up to 60 min before morphine and it did not coincide with analgesia produced by methamphetamine alone. Brain levels of morphine were found to be significantly higher in methamphetamine- compared to saline-pretreated mice, at times when enhanced analgesia was observed. Further studies showed that morphine brain levels were increased by methamphetamine pretreatment in an apparent dose-dependent manner. The analgesia observed at several morphine brain levels was compared in order to determine whether enhanced analgesia resulted from increased morphine brain levels. Methamphetamine administration 5 or 60 min before morphine shifted the log morphine brain level-response curves for morphine analgesia to the left and the morphine brain level at a given percent analgesia was significantly lower in methamphetamine- than in saline-pretreated mice. In addition, methamphetamine pretreatment enhanced methadone analgesia but had no effect on methadone brain levels.

Analgesia↗
PubMed1992

Competitive and non-competitive N-methyl-D-aspartate antagonists fail to prevent the induction of methamphetamine-induced sensitization.

In order to elucidate the possible roles of the glutamate system in the mechanisms underlying behavioral sensitization, which is used as an animal model for human psychosis, we investigated the effects of 3-((+/-)-2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) and MK-801 ((+)-dizocilpine), a competitive and noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, respectively, on methamphetamine-induced behavioral sensitization in rats. Administration of 0.5 mg/kg MK-801 enhanced 2 mg/kg methamphetamine-induced hyperactivity, whereas it reduced 6 mg/kg methamphetamine-induced stereotyped behavior markedly. CPP (10 mg/kg) reduced 2 mg/kg methamphetamine-induced stereotypy slightly. Repeated treatment with 2 and 6 mg/kg methamphetamine alone induced progressive augmentation of stereotypy, whereas combining either MK-801 or CPP with methamphetamine treatment abolished or attenuated this augmentation. However, when rats were challenged with methamphetamine after a 7-day period of abstinence, the intensity of stereotypy among the rats pretreated with repeated doses of methamphetamine alone or in combination with MK-801 or CPP did not differ significantly. These results indicate that competitive and non-competitive NMDA receptor antagonists modulate acute methamphetamine-induced abnormal behavior and sensitization expression, but they failed to prevent the induction of the neural mechanisms underlying behavioral sensitization.

Animals↗
PubMed1991

Selective effects of behaviorally active doses of methamphetamine on mRNA expression in the gerbil brain.

Administration of methamphetamine results in neuronal damage that may be mediated through the production of oxygen-free radicals and modulations in levels of calcium and glutamate in the brain. These changes have been associated with alterations in gene expression, which may play a role in cell damage. To assess the differences in gene expression related to treatment with methamphetamine, levels of mRNA were evaluated for the proto-oncogene c-fos, heat-shock protein (HSP 70) and actin. It was found that c-fos mRNA expression increased in a dose-dependent manner after administration of methamphetamine. Whereas, levels of HSP mRNA dropped at small doses of methamphetamine and increased dramatically at large doses. In addition, both c-fos and HSP mRNA showed increased levels throughout the brain. Actin mRNA expression was unaffected by any dose of the drug. At the doses that altered gene expression, methamphetamine produced dose-related behavioral changes. Spontaneous locomotor activity was increased at 1.0 mg/kg of methamphetamine, while, larger doses did not alter activity. The data demonstrated that effects of methamphetamine on gene expression occurred within the behaviorally-active dose range and might correlate with the degree of neuronal damage. Selective modulation of gene expression may have a role in determining the acute quantitative and qualitative effects of methamphetamine and the long-term changes that occur after administration of methamphetamine.

Animals↗