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PubMed2004

Clinical features of sensitization to methamphetamine observed in patients with methamphetamine dependence and psychosis.

Methamphetamine (METH) has been the most popular drug of abuse in Japan for more than 50 years, resulting in serious health and social issues. Most adult abusers in Japan consume only METH; multiple-substance abusers are rare. This unusual aspect of drug abuse makes it possible to observe clearly the sequential alteration of psychiatric symptoms induced by METH without modification by other illegal drugs. Clinical investigation reveals three core characteristics of METH abuse: (1) progressive qualitative alteration in mental symptoms from a nonpsychotic to a prepsychotic to a severely psychotic state; (2) enhanced vulnerability to relapse of psychosis; and (3) very long duration of the vulnerability to relapse. These findings indicate that the phenomenon of sensitization to METH develops during abuse and plays a key role in the susceptibility to and onset of psychosis and in the refractory process. Molecular findings using animal sensitization models may facilitate a better understanding of, and open the way for innovative therapies for, METH psychosis and also chronic schizophrenia.

Adult↗

PubMed2006

Methamphetamine induces autophagy and apoptosis in a mesencephalic dopaminergic neuronal culture model: role of cathepsin-D in methamphetamine-induced apoptotic cell death.

Autophagy is a phylogenetically conserved process that plays a critical role in the degradation of oxidatively damaged proteins and organelle turnover. The role of oxidative stress and apoptosis in methamphetamine (METH)-induced neurotoxicity is well known; however, the potential contribution of autophagy to METH-induced oxidative damage in dopaminergic neuronal systems remains unclear. The goals of the present article were twofold: (a) to develop an in vitro dopaminergic cell culture model to study cellular and molecular mechanisms underlying METH-induced autophagy and apoptosis, and (b) to determine whether lysosomal protease cathepsin-D activation, resulting from the loss of lysosomal membrane integrity, contributes to METH-induced apoptosis. To accomplish these goals, we characterized morphological and biochemical changes in an immortalized mesencephalic dopaminergic neuronal cell line (N27 cells) following treatment with METH. Exposure of METH (2 mM) to N27 cells resulted in the appearance of cytoplasmic vacuolar structures reminiscent of autophagic vacuoles within 3 h. In order to ascertain the identity of the vacuolar structures that are formed following METH exposure, immunohistochemical staining for markers of autophagy were performed. LAMP 2, a classical marker of autophagolysosomes, revealed an extensive punctuate pattern of distribution on the vacuolar membrane surface, with exclusive localization in the cytoplasm. Additionally, using DNA fragmentation analysis we showed a dose-dependent increase in fragmented DNA in METH treated N27 cells. Since METH-induced autophagy preceded DNA fragmentation, we tested whether dysfunction of the autophagolysosomal system contributes to nuclear damage. Immunofluorescence studies with cathepsin-d demonstrated a granular pattern of staining in untreated cells, whereas an increased cathepsin- D immunoreactivity with a globular pattern of staining was observed in METH-treated cells. Nevertheless, blockade of cathepsin-D activation by pepstatin-A, cathepsin-D inhibitor, failed to alter METH-induced DNA fragmentation. Collectively, these results demonstrate that N27 dopaminergic neuronal cell model may serve as an excellent in vitro model to study the mechanisms of METH-induced autophagy and apoptosis. Furthermore, it is less likely that cathepsin-D may serve as a trigger for the induction of apoptosis subsequent to exposure of N27 dopaminergic neuronal cells to METH.

Animals↗

PubMed1996

Abuse of smoking methamphetamine mixed with tobacco. V. Plasma metabolites of N-cyanomethylmethamphetamine, a pyrolysis product formed by smoking methamphetamine in tobacco, and the species difference between mouse and rat.

N-Cyanomethylmethamphetamine (CMMA), N-formylmethamphetamine (FMA) and methamphetamine (MA) were given intraperitoneally to mouse and rat in doses of 3 mg/kg. The major metabolites of CMMA, FMA and MA in plasma were determined at short intervals after administration by GC-MS to obtain the area under the concentration-time curve (AUC). Regarding the plasma concentration of FMA after CMMA administration, a definite species difference was observed between mouse and rat. In rats given CMMA, FMA was the major component, followed by MA, amphetamine (AP), CMMA and N-formylamphetamine (FAP). In mice given CMMA, MA was a major component, followed by AP, FMA, CMMA and FAP. However, it was demonstrated that MA is also non-enzymatically produced from CMMA in plasma. Following FMA administration to rats, FMA was the major component in the plasma, showing the largest AUC value of the four metabolites, FMA, FAP, MA and AP. Following FMA administration to mice, MA showed the largest AUC value, followed by FMA, FAP and AP which were present at low levels even 5 min after injection and were scarcely detectable at 60 min. These results suggest two main mechanisms involved in the metabolism of the N-cyanomethyl group, one of which is the formation of MA by elimination of cyanoformaldehyde from N-alpha-hydroxylated CMMA and the other which is the formation of FMA by elimination of hydrogen cyanide from N-alpha-hydroxylated CMMA. The formation of FMA from CMMA was the predominant pathway in rats but not in mice.

Amphetamines↗

PubMed2001

[Positron emission tomography (PET) study of the alterations in brain pharmacokinetics of methamphetamine in methamphetamine sensitized animals].

I investigated the differences in brain pharmacokinetics of [11C]methamphetamine ([11C]MAP) in normal and MAP sensitized animals using positron emission tomography (PET). [11C]MAP was synthesized by an automated on-line [11C]methylation system. I newly produced MAP sensitized dog and monkey by repeated MAP treatment. The maximal level of accumulation of [11C]MAP in the sensitized dog brain was 1.4 times higher than that in the control. This result suggests the changes in the pharmacokinetic profile of MAP in the brain affect the development or expression of MAP-induced behavioral sensitization. However, the overaccumulation of [11C]MAP in the sensitized monkey brain was not observed due to the influence of anesthesia.

Animals↗

PubMed1983

Methamphetamine-induced behavioral effects and releases of brain catecholamines and brain concentrations of methamphetamine in mice.

The characteristic behavioral effect of methamphetamine (MA) at 2.5 mg/kg was enhanced locomotor activity which lasted over 2.5 hr. At 10.0 mg/kg MA, stereotyped behavior was predominant and lasted over 3 hr. The behavioral effect of 5.0 mg/kg MA was of the mixed type. MA at 5.0 and 10.0 mg/kg lowered the brain NE level from 2 hr after drug treatment, while the accumulation of MHPG-SO4 was increased over 2 hr at 2.5 and 5.0 mg/kg MA. The accumulation of HVA was significantly increased at 10.0 mg/kg MA over 3 hr. Accordingly, the behavioral effects of MA at the earlier period were compatible with the biochemical effects of MA. The behavioral effects during the 2- to 4-hr period, however, seem to be unrelated to the actions on brain catecholamines. Measurement of brain MA concentrations revealed that approx. 2 micrograms/g in the brain may be necessary to produce enhanced locomotor activity and the increased accumulation of brain MHPG-SO4. It appeared that approx. 8 to 9 micrograms/g MA in the brain was required to produce characteristic stereotyped behavior and the increased accumulation of HVA. Therefore, the behavioral and biochemical effects of MA were correlated with the brain MA concentrations.

Amphetamine↗

PubMed1986

Methamphetamine-induced behavioral alterations following repeated administration of methamphetamine.

Repeated administration of a large dose of methamphetamine (MA) (25 mg/kg, i.p. twice daily for 4 days) to mice enhanced locomotor activity and decreased stereotyped behavior following a subsequent injection of MA. Simultaneous determinations of catecholamines revealed a depletion of brain dopamine. The moderate doses of haloperidol significantly enhanced MA-induced locomotor activity in mice. A significant enhancement of MA-induced locomotor activity was observed in the rats pretreated with 6-hydroxydopamine into the striatum, and this effect correlated negatively with the striatal dopamine level. These results suggest that hypofunction of striatal dopaminergic neuron systems induced by repeated administration of MA may be one of possible mechanisms of the enhancement of MA-induced locomotor activity due to the decrease of stereotyped behavior.

Animals↗

PubMed1994

Effects of methamphetamine, dopamine and noradrenaline administered into the nucleus accumbens of rats discriminating subcutaneous methamphetamine.

Since the nucleus accumbens has been hypothesized to centrally mediate the discriminative effects of psychomotor stimulants, the discriminative effects of methamphetamine (MA) as well as dopamine (DA) and noradrenaline (NA) were observed by intracerebral administration of these drugs into the nucleus accumbens in rats discriminating subcutaneous MA from saline. These rats were trained and maintained to discriminate between MA at 0.5 mg/kg, s.c. and saline under a fixed ratio 10 schedule for food reinforcement in a 2-lever operant chamber situation. Guide cannulae were implanted bilaterally into the nucleus accumbens. In the substitution tests, the drug was administered into the nucleus accumbens. MA at 10 micrograms per rat substituted for subcutaneous MA in 4 out of 5 rats but neither DA at 10-40 micrograms per rat (n = 7) nor NA at 10-40 micrograms per rat (n = 4) substituted for subcutaneous MA. On the other hand, the same drugs administered into the nucleus accumbens induced increased spontaneous motor activity as also observed in six other untrained rats. MA, DA or NA alone each at 10 micrograms per rat increased spontaneous motor activity. The discriminative effects of MA are considered to be mediated in the nucleus accumbens of rats. Although DA or NA alone administered into the nucleus accumbens showed similar increasing motor activity effects as those of MA, the discriminative effects of exogenous DA or NA alone administered into the same brain area were different from those of MA in the present experimental condition.

Animals↗

PubMed2003

Methamphetamine and amphetamine pharmacokinetics in oral fluid and plasma after controlled oral methamphetamine administration to human volunteers.

BACKGROUND: Methamphetamine (METH) and amphetamine (AMP) concentrations in 200 plasma and 590 oral fluid specimens were used to evaluate METH pharmacokinetics and pharmacodynamics after oral administration of sustained-release METH. METHODS: Eight participants received four oral 10-mg S-(+)-METH hydrochloride sustained-release tablets within 7 days. Three weeks later, five participants received four oral 20-mg doses. Blood samples were collected for up to 24 h and oral fluid for up to 72 h after drug administration. RESULTS: After the first oral dose, initial plasma METH detection was within 0.25-2 h; c(max) was 14.5-33.8 micro g/L (10 mg) and 26.2-44.3 micro g/L (20 mg) within 2-12 h. In oral fluid, METH was detected as early as 0.08-2 h; c(max) was 24.7-312.2 micro g/L (10 mg) and 75.3-321.7 micro g/L (20 mg) and occurred at 2-12 h. The median oral fluid-plasma METH concentration ratio was 2.0 across 24 h and was highly variable. Neutral cotton swab collection yielded significantly higher METH and AMP concentrations than citric acid candy-stimulated expectoration. Mean (SD) areas under the curve for AMP were 21% +/- 25% and 24% +/- 11% of those observed for METH in plasma and oral fluid, respectively. After a single low or high dose, plasma METH was >2.5 micro g/L for up to 24 h in 9 of 12 individuals (mean, 7.3 +/- 5.5 micro g/L at 24 h); in oral fluid the detection window was at least 24 h (mean, 18.8 +/- 18.0 micro g/L at 24 h). The plasma and oral fluid 24-h METH detection rates were 54% and 60%, respectively. After four administrations, METH was measurable for 36-72 h (mean, 58.3 +/- 14.5 h). CONCLUSIONS: Perceived advantages of oral fluid for verifying METH exposure compared with urine include simpler specimen collection and reduced potential for adulteration, but urine offers higher analyte concentrations and a greater window of detection.

Administration, Oral↗

PubMed1995

Abuse of smoking methamphetamine mixed with tobacco. III. Urinary metabolites of N-cyanomethylmethamphetamine, a pyrolysis product formed by smoking methamphetamine in tobacco, and species difference in its metabolism between rat and mouse.

1. N-cyanomethylmethamphetamine (CMMA) or methamphetamine (MA) was given intraperitoneally to rat and mouse (1, 3, 10 mg/kg). The basic urinary metabolites of CMMA were determined by mass spectrometry (MS) and compared with those of MA. 2. N-formylmethamphetamine (FMA), a specific metabolite of CMMA, was found in both rat and mouse urine. However, the dose percentage of FMA excreted in mouse urine was less than one-quarter of that in rat urine. 3. No CMMA was detected in rat or mouse urine collected within 72 h after dosing. All other basic metabolites of CMMA except FMA, i.e. MA, amphetamine (AP), p-hydroxymethamphetamine (OHMA) and p-hydroxyamphetamine (OHAP), were the same as those of MA in both species. 4. The excretion pattern of the urinary metabolites of CMMA was similar to that of MA except FMA in both species, though the amount of each metabolite of MA administration was larger than that of CMMA administration. However, in urinary excretion of FMA and hydroxylated metabolites, definite species differences were observed between rat and mouse. 5. A trace amount of FMA was identified in the urine of an abuser who had smoked MA with tobacco.

Amphetamines↗

PubMed2000

Effect of temperature on dopamine transporter function and intracellular accumulation of methamphetamine: implications for methamphetamine-induced dopaminergic neurotoxicity.

Hyperthermia exacerbates and hypothermia attenuates methamphetamine (METH)-induced dopamine (DA) neurotoxicity. The mechanisms underlying these temperature effects are unknown. Given the essential role of the DA transporter (DAT) in the expression of METH-induced DA neurotoxicity, we hypothesized that the effect of temperature on METH-induced DA neurotoxicity is mediated, at least in part, at the level of the DAT. To test this hypothesis, the effects of small, physiologically relevant temperature changes on DAT function were evaluated in two types of cultured neuronal cells: (1) a neuroblastoma cell line stably transfected with human DAT cDNA and (2) rat embryonic mesencephalic primary cells that naturally express the DAT. Temperatures for studies of DAT function were selected based on core temperature measurements in animals exposed to METH under usual ambient (22 degrees C) and hypothermic (6 degrees C) temperature conditions, where METH neurotoxicity was fully expressed and blocked, respectively. DAT function, determined by measuring accumulation of radiolabeled DA and 1-methyl-4-phenylpyridinium (MPP(+)), was found to directly correlate with temperature, with higher levels of substrate uptake at 40 degrees C, intermediate levels at 37 degrees C, and lower levels at 34 degrees C. DAT-mediated accumulation of METH also directly correlated with temperature, with greater accumulation at higher temperatures. These findings indicate that relatively small, physiologically relevant changes in temperature significantly alter DAT function and intracellular METH accumulation, and suggest that the effect of temperature on METH-induced DA neurotoxicity is mediated, at least in part, at the level of the DAT.

1-Methyl-4-phenylpyridinium↗

PubMed2001

[Pharmacokinetic behavioral changes of methamphetamine in methamphetamine-sensitized animal model].

There has been an increased population of users and abusers of amphetamines, including methamphetamines (METH), in the past two decades, and this has become a crucial social problem in Japan. METH abusers show a paranoid schizophrenia-like syndrome, including paranoid hallucination and delusion, and repeated exposure to these drugs will enhance their effects; i.e. the behavioral and reinforcing effects of abusing drugs became progressively and irreversibly developed (behavioral sensitization) in humans and in experimental animals. Although numerous neuropsychopharmacological/neurochemical studies on behavioral sensitization were conducted, few reports are available to understand the pharmacokinetic aspect of METH, including the brain penetration of METH, in this phenomenon. The present report reviews previous pharmacokinetic studies for METH and our findings in rats having behavioral sensitization to METH, especially from the point of view regarding the relationship of drug transporters.

Animals↗

PubMed2002

Duration of detectable methamphetamine and amphetamine excretion in urine after controlled oral administration of methamphetamine to humans.

BACKGROUND: Confirmation of a workplace drug test requires urinary methamphetamine (MAMP) and amphetamine (AMP) concentrations > or = 500 and 200 micro g/L, respectively, but cutoffs at half those values (250/100 micro g/L) have been proposed. We determined the urinary excretion of MAMP after oral ingestion and examined the effect of using lower cutoffs on detection of exposure. METHODS: Volunteers (n = 8) ingested four 10-mg doses of MAMP. HCl daily over 7 days, and five of them ingested four 20-mg doses 4 weeks later. After ingestion, the volunteers collected all urine specimens for 2 weeks. After solid-phase extraction, MAMP and AMP were measured by gas chromatography-positive chemical ionization mass spectrometry with dual silyl derivatization. RESULTS: MAMP and AMP were generally detected in the first or second void (0.7-11.3 h) collected after drug administration, with concentrations of 82-1827 and 12-180 micro g/L, respectively. Peak MAMP concentrations (1871-6004 micro g/L) after single doses occurred within 1.5-60 h. MAMP > or = 500 micro g/L was first detected in the first or second void (1-11 h) at 524-1871 micro g/L. Lowering the MAMP cutoff to 250 micro g/L changed the initial detection time little. AMP > or = 200 micro g/L was first detected in the 2nd-13th (7-20 h) post-administration voids. At a cutoff of 100 micro g/L, AMP was first confirmed in the second to eighth void (4-13 h). Reducing the cutoff to 250/100 micro g/L extended terminal MAMP detection by up to 24 h, increased total detection time by up to 34 h, and increased the total number of positive specimens by 48%. CONCLUSIONS: At the lower cutoff, initial detection times are earlier, detection windows are longer, and confirmation rates are increased. Elimination of the AMP requirement would increase detection rates and allow earlier detection.

Administration, Oral↗

PubMed2002

Enantiomeric separation of methamphetamine and related analogs by capillary zone electrophoresis: intelligence study in routine methamphetamine seizures.

A method for simultaneous enantiomeric separation of ephedrine, pseudoephedrine, and methamphetamine (MA) in a single run by simple capillary zone electrophoresis (CZE) with beta-cyclodextrin as a chiral selector is described. The effects of the buffer pH, phosphate concentration, beta-cyclodextrin concentration, voltage and temperature on the peak resolution were examined. Good enantiomeric resolution was attained for each analyte under our optimized conditions: 15 mM beta-cyclodextrin, 300 mM NaH2PO4 at pH 2.5 with an uncoated capillary (64.5 cm x 50 microm), applied potential at 20 kV and temperature at 30 degrees C. Ultraviolet (UV) detection at a fixed wavelength (200 nm) was employed using a diode array detector. Using phentermine as an internal standard, migration times for all analytes are reproducible within 0.16% for intra-day and 0.6% for inter-day runs. Application of this method to the analysis of confiscated drugs is discussed.

Cyclodextrins↗

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↗

PubMed1994

Stereotyped behavioral responses to an auditory stimulus in the course of repeated treatment with methamphetamine plus scopolamine and methamphetamine in rats.

The present experiment was designed to study the effects of an auditory stimulus with 300 Hz, 100 dB on gradual emergence of behavioral sensitization in the course of repeated administration of methamphetamine (MAP) in combination with scopolamine (SCOP) and MAP. Repeated intraperitoneal injection of MAP (4.0 mg/kg) plus SCOP (0.5 mg/kg) induced significantly progressive and enduring enhancement of stereotyped behavior, resulting in intense, focussed stereotypy intermingled with gnawing and licking compared to repeated MAP treatment. Vigorous stereotyped behavior induced by repeated MAP plus SCOP was progressively attenuated by the tone, resulting in attenuation of the development of behavioral sensitization. Conversely, the tone had no invariable effects on behavioral sensitization induced by repeated MAP treatment. The present findings indicate that repeated MAP plus SCOP treatment progressively induced attenuating effects of tone as low as 300 Hz on MAP plus SCOP-induced intense stereotypy and vigorous behavioral sensitization. These findings suggest that a reciprocal balance between dopaminergic and cholinergic inhibitory systems may be involved in producing behavioral sensitization, and in the attenuating effects of the tone on MAP plus SCOP-induced vigorous behavioral sensitization.

Acoustic Stimulation↗

PubMed1996

[Alterations in brain distribution of methamphetamine in methamphetamine-sensitized animals].

[11C]Methamphetamine ([11C]MAP) was synthesized by an automated on-line [11C]methylation system for a position emission tomography (PET) study. The author newly prepared a MAP-sensitized dog by repeated treatment of MAP, and studied the brain distribution of [11C]MAP in normal and MAP.sensitized dogs. The maximal level of accumulation of [11C]MAP in the sensitized dog brain was 1.4 times higher than that in the control. No difference was found in the metabolism of MAP between the two conditions. A significant increase in [11C]MAP uptake into the sensitized dog brain was prevented by haloperidol and cocaine pretreatments. These results suggest that changes in the pharmacokinetic profile of MAP in the brain affect the development or expression of MAP-induced behavioral sensitization.

Animals↗

PubMed1997

[Experimental study of methamphetamine psychosis--role of glutamate and nitric oxide in methamphetamine-induced dopaminergic and serotonergic neurotoxicity in the rat brain].

The present study examined effects of a high dose of methamphetamine (MA) (5mg/kg, s.c., x 4) on extracellular concentrations of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic acid (5-HIAA) and glutamate in rat striatum (ST) and nucleus accumbens (NA) using microdialysis. The toxic dose of MA markedly increased extracellular DA, and decreased DOPAC and 5-HIAA in both ST and NA. The increase in DA release was not different in magnitude between ST and NA. Extracellular glutamate showed a delayed increase in ST, but not in NA. Tissue contents of serotonin (5-HT) and 5-HIAA significantly decreased in both ST and NA, whereas those of DA, DOPAC and HVA decreased in ST but did not change in NA. These data suggest that the marked increase of DA release is not directly related to the MA-induced dopaminergic neurotoxicity. The increase in glutamate release found only in ST may be related to the dopaminergic damage in ST. However, enhancement in glutamate release did not appear to be essential for the serotonergic neurotoxicity. Nitric oxide (NO) has recently been recognized as a novel neuronal messenger. Taking into account the relationship between NMDA receptor activation and NO formation, the present study examined effects of a NO synthesis inhibitor, N omega-nitro-L-arginine methyl ester (LNAME) on MA-induced decreases in contents of the monoamines and their metabolites, in order to clarify whether the MA-induced dopaminergic and serotonergic neurotoxicity would be mediated by NO synthesis. Coadministration with LNAME (30 mg/kg, i.p., x2), reduced the MA-induced decreases in contents of DA, DOPAC and HVA in ST, but not reduced the MA-induced decreases in contents of 5-HT in ST and NA. These findings suggest that the MA-induced dopaminergic, but not serotonergic neurotoxicity, may be related to the neural process such as NO formation caused by the activation of postsynaptic DA receptor.

3,4-Dihydroxyphenylacetic Acid↗