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At least 667 records · Page 37Linked to original sources

PubMed1994

Methamphetamine protects against MPTP neurotoxicity in C57BL mice.

Methamphetamine (5 mg/kg) administered 30 min prior to each injection with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (3 x 30 mg/kg, at 24 h intervals) prevents the reduction of striatal levels of dopamine and its metabolites in C57BL mice. Methamphetamine and amphetamine inhibit the uptake of 1-methyl-4-phenylpyridinium (MPP+) by striatal synaptosomes of rats. A 30-min post-treatment with methamphetamine or amphetamine also prevents the MPTP-induced dopamine depletion, suggesting that their protective effect is related to the blockade of MPP+ uptake into dopaminergic neurons. Since amphetamine and methamphetamine are themselves neurotoxins at higher doses, this work demonstrated the protection against the actions of one neurotoxin by the administration of another.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1990

The effect of SCH 23390 against toxic doses of cocaine, d-amphetamine and methamphetamine.

The effect of SCH 23390, a dopamine-one (D1) antagonist, in preventing acute toxicity induced by lethal doses of cocaine, d-amphetamine, and methamphetamine was studied in the rat. Animals were first pretreated with SCH 23390 (0.0, 0.5, 1.0, and 2.5 mg/kg, i.p.) and then were challenged with cocaine (70 mg/kg, i.p., an LD85), d-amphetamine (75 mg/kg, i.p., an LD95), and methamphetamine (100 mg/kg, i.p., an LD90). SCH 23390 did not alter the incidence of stimulant-induced seizures compared to the vehicle controls. Significant protection against cocaine-induced death was afforded only by the lowest dose of SCH 23390 tested. Significant protection against d-amphetamine-induced death was provided by all doses, with a dose dependent effect noted so that the incidence decreased from 95% for vehicle to 30% (p less than or equal to 0.01) with 2.5 mg/kg SCH 23390 pretreatment. No statistically significant reduction in the incidence of methamphetamine-induced death was seen with SCH 23390 pretreatment. The ability of SCH 23390 to protect against d-amphetamine, but apparently not against methamphetamine-induced death, suggests that different mechanisms of toxicity may exist between these drugs at high doses.

Animals↗

PubMed1994

The role of delta-opioid receptor subtypes in cocaine- and methamphetamine-induced place preferences.

The effects of delta-receptor antagonists on cocaine- and methamphetamine-induced place preferences were examined in rats. Cocaine- and methamphetamine-induced place preferences were significantly attenuated by naltrindole (NTI: a non-selective delta-opioid receptor antagonist). Furthermore, naltriben (NTB: a selective delta 2-opioid receptor antagonist), but not 7-benzylidenenaltrexone (BNTX: a selective delta 1-opioid receptor antagonist), attenuated the cocaine- and methamphetamine-induced place preferences. These results suggest that delta-opioid receptors, particularly delta 2-opioid receptors, may be involved in the reinforcing effects of cocaine and methamphetamine.

Animals↗

PubMed1986

Disorganization of the rat activity rhythm by chronic treatment with methamphetamine.

Remarkable changes in the circadian activity rhythm of rats were observed when they were chronically treated with methamphetamine dissolved in drinking water. The circadian rhythm was phase-delayed with respect to the light-dark (LD) cycle, and showed signs of relative coordination. In some rats, the circadian organization was disturbed and two activity components appeared, with one component free-running and the other entrained by the LD cycle. After methamphetamine withdrawal, these changes disappeared rapidly but there were transient periods of 2-3 days before establishment of a stable entrainment to the LD cycle. The changes in the circadian rhythm persisted even in constant darkness (DD). The period around 24 hr in DD was significantly shorter during methamphetamine treatment than after the drug withdrawal. These results indicate that neither alteration of the sensitivity to light nor lengthening of the intrinsic period is involved in the methamphetamine induced disorganization of the circadian rhythm. Possible mechanisms are discussed in terms of a multi-oscillatory system.

Animals↗

PubMed1984

Circadian variation in susceptibility to methamphetamine after repeated administration in mice.

Since repeated administration of methamphetamine sometimes induces an augmentation in susceptibility, i.e., a reverse tolerance, to the stimulant drug effect in animals, the circadian variation in susceptibility to the ambulation-increasing effect of methamphetamine after repeated administration was investigated in mice. The ambulatory activity of each mouse was measured by a tilting-type round activity cage of 25 cm in diameter. Mice, which had been housed under a 12 hr light-dark schedule (light period; 6:00-18:00) for 5 weeks, were administered methamphetamine 1 or 2 mg/kg SC at one of 6 times of day (3:00, 7:00, 11:00, 15:00, 19:00 and 23:00) for 5 times at intervals of 7 days, and their ambulatory activities were measured for 3 hr after each administration. The repeated administration of methamphetamine induced a reverse tolerance to the ambulation-increasing effect of the drug, and the mean overall ambulatory activity counts on the 5th session were estimated to be 2-4 times as high as the corresponding activity counts on the 1st session. However, the circadian variation in susceptibility, which was at maximum during the late dark period (administration at 3:00) and at minimum during the late light period (administration at 15:00), was well maintained even after the repeated administration. When the time of day of the drug administration were changed by 12 hr on the 6th session, a marked increase in the activity counts was observed in the mice changed from 15:00 to 3:00, while a marked decrease was observed in the mice changed from 3:00 to 15:00.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Effects of methamphetamine and morphine on the vertical and horizontal motor activities in mice.

The effects of methamphetamine and morphine on the vertical (VMA) and the horizontal motor activities (HMA) in male ddY mice (six weeks of age) was investigated between 9:00 and 13:00, using an apparatus which can differentiate spontaneous motor activity into VMA and HMA, measuring their activities simultaneously. VMA and HMA were evaluated by counting the number of times that an infrared ray was blocked by the mouse in the activity cage. Nine infrared photo-couplers were used to measure the VMA and one to measure the HMA. All measurements were taken at 10 min intervals during the 180 min period after subcutaneous injection of methamphetamine (0.1, 1 and 10 mg/kg) or morphine (2, 10 and 50 mg/kg). A small dose of methamphetamine (0.1 mg/kg) did not exert influence on the counts of the VMA and the HMA, whereas a large dose enhanced both activities, especially at 10 mg/kg, where each activity showed qualitatively different biphasic patterns. On the other hand, three doses of morphine significantly inhibited the VMA for 20 min after administration, while morphine at 2 mg/kg depressed the HMA for 10 min after administration and at 10 mg/kg or more markedly enhanced it during the 180 min observation period. These results show that different doses of methamphetamine and morphine exert different effects on the VMA and the HMA in mice.

Animals↗

PubMed1993

Effects of the dopamine release inhibitor, CGS 10746B, on the locomotor stimulant and discriminative stimulus effects of cocaine and methamphetamine.

CGS 10746B or 5-(4-methyl-1 piperazinyl)-imadazo[2,1-b]1,3,5]benzothiadiazepine maleate is a clozapine analog that, unlike clozapine, produces decreases in neostriatal dopamine release without changing dopamine metabolism or occupying D2 receptors. CGS 10746B also blocks neuronal impulse flow. The ability of this atypical antipsychotic candidate to alter the discriminative stimulus effects induced by cocaine or methamphetamine in rats or the stimulation of locomotor activity in mice was evaluated. A range of doses of CGS 10746B was tested against maximally effective doses of the psychomotor stimulants. Although CGS 10746B completely blocked the locomotor stimulant effects of cocaine and methamphetamine, it also decreased spontaneous activity in mice over the same dose range. Rats were trained to discriminate 10 mg/kg cocaine or 1 mg/kg methamphetamine from saline. The discriminative stimulus effects of cocaine or methamphetamine were not blocked by CGS 10746B. Thus, in contrast to other potential atypical antipsychotic compounds (e.g., D1 receptor antagonists), CGS 10746B does not appear to produce selective blockade of these behavioral effects of psychomotor stimulant compounds.

Animals↗

PubMed1990

The long-term effects of neurotoxic doses of methamphetamine on the extracellular concentration of dopamine measured with microdialysis in striatum.

The extracellular concentrations of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) in the striatum were measured by in vivo microdialysis in freely moving rats one week after the animals were treated with neurotoxic doses of methamphetamine. Methamphetamine produced a marked depletion of striatal DA measured in postmortem tissue, and in the extracellular concentrations of DOPAC, HVA and 5-HIAA. In contrast, the resting extracellular concentration of DA in striatum was the same as in saline-pretreated controls. Furthermore, methamphetamine-pretreated rats were able to increase their concentration of extracellular DA to the same extent as controls in response to a (+)-amphetamine challenge. It is suggested that this adaptive response is probably responsible, at least in part, for the absence of obvious behavioral deficits in animals exposed to neurotoxic doses of methamphetamine.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1996

Blockade by ginseng total saponin of methamphetamine-induced hyperactivity and conditioned place preference in mice.

Ginseng total saponin (GTS) inhibited methamphetamine-induced hyperactivity and conditioned place preference (CPP). Dopamine (DA) receptor supersensitivity was developed in methamphetamine-induced CPP mice and it was inhibited by GTS. GTS also inhibited apomorphine-induced climbing behavior, showing the antidopaminergic activity of GTS. These results suggest that GTS inhibition of the methamphetamine-induced hyperactivity and CPP may be closely related with the inhibition of dopaminergic activation induced by methamphetamine.

Animals↗

PubMed1987

Methamphetamine-induced reduction in D1 and D2 dopamine receptors as evidenced by autoradiography: comparison with tyrosine hydroxylase activity.

As determined by autoradiographic techniques, multiple high doses of methamphetamine elicited a reduction in dopamine receptor population (both D1 and D2) in several areas of the rat central nervous system. D1 receptors were labeled with the D1-selective antagonist, [3H]SCH 23390, and D2 receptors were labeled with the D2-selective neuroleptic, [3H]sulpiride. Scatchard analysis, obtained from saturation data in caudate-putamen, indicated that the receptor alterations were due to a decrease in the number of receptors (Bmax) without an apparent change in affinity (Kd). A time course demonstrated that five doses of methamphetamine were required to elicit significant changes in receptors in most brain areas examined. The onset of the receptor alterations in various brain regions correlated with the development of methamphetamine-induced depression of striatal tyrosine hydroxylase activity. In most brain areas, the dopamine receptors returned to normal within 7 days following methamphetamine.

Animals↗

PubMed1990

Involvement of the entopeduncular nucleus and the habenula in methamphetamine-induced inhibition of dopamine neurons in the substantia nigra of rats.

The lateral habenula receives massive afferents from dopamine-rich forebrain areas through the stria medullaris and sends efferents to mesencephalic dopaminergic systems through the fasciculus retroflexus. In the present study, effects of electrolytic lesions of the habenula, transections of the stria medullaris, and kainic acid-induced lesions of the entopeduncular nucleus on methamphetamine-induced inhibition of substantia nigra dopamine neurons were investigated in rats. Following these lesions or transections the methamphetamine-induced inhibition on the dopamine neuronal activity was significantly attenuated compared to those in control animals with sham lesions or sham transections. Intravenous administration of methamphetamine at a dosage of 6.4 mg/kg produced only a 62.7 to 71.2% inhibition in lesioned or transected animals, whereas in control animals the activity of dopamine neurons was almost completely inhibited with this dose. The amounts of methamphetamine required to induce 50% inhibition of dopamine neurons in lesioned or transected animals was 3.3 to 4.7 times greater than those in control animals. There was no significant difference in cumulative dose-response curves between habenular-lesioned, stria medullaris-transected and entopeduncular-lesioned animals. These results, along with other findings, indicate possibly that the pathways running through the entopeduncular nucleus, the stria medullaris, the habenula, probably the lateral habenula, and the fasciculus retroflexus are involved in a feedback loop from the striatum to the substantia nigra and regulate the activity of dopamine neurons.

Animals↗

PubMed1984

Nails as useful materials for detection of methamphetamine or amphetamine abuse.

Methamphetamine and amphetamine could be demonstrated in nail clippings obtained from methamphetamine users by sensitive gas chromatography/chemical ionization mass spectrometry with N-methylbenzylamine as an internal standard. The methamphetamine levels in fingernails were comparable to those in hair. Both stimulants were more concentrated in toenails than in fingernails. The detection of methamphetamine and amphetamine in nails provides an alternative information to that in hair on their past abuse.

Amphetamine↗

PubMed1984

Articles found in the possession of a methamphetamine abuser.

A plastic syringe containing bloody fluid, 2 ampules of 20% glucose, and ampule containing diphenhydramine hydrochloride and calcium bromide, powder in a plastic bag and powder wrapped in paper were among the articles found in the possession of a 42-year-old male methamphetamine abuser, who had been taken to a mental hospital owing to his hallucinations. Examination of the patient revealed several recent needle punctures on the left forearm. The concentration of methamphetamine and its metabolite, amphetamine, in blood collected 1 day following the last intake was 76 nmol/100 g. Analysis of the powder and of the contents of the syringe revealed methamphetamine hydrochloride at a concentration of 99.0-99.5% and 7.4%, respectively. Neither glucose nor diphenhydramine were detected in the contents of the syringe. It would seem that the patient abused methamphetamine hydrochloride by intravenous injection after dissolving it in city water or distilled water.

Adult↗

PubMed1986

Detection of methamphetamine and amphetamine in a skeletonized body buried for 5 years.

A 28-year-old male methamphetamine abuser, who had been buried for 5 years after being killed by strangulation, was found skeletonized. Methamphetamine and amphetamine in the significantly denatured fatty material of the bone marrow were analyzed by gas chromatography and gas chromatography-mass spectrometry. The confirmation of the chemicals was carried out by chemical ionization (CI) mass chromatography, CI mass spectrometry and CI mass fragmentography. The concentrations of methamphetamine and amphetamine determined by CI mass fragmentography were 1.0 mumol/100 g and 0.1 mumol/100 g, respectively. The method used would seem to be very useful for determination of methamphetamine and amphetamine in marked putrefied biological materials.

Adipose Tissue↗

PubMed1990

Methamphetamine and amphetamine concentrations in postmortem rabbit tissues.

The feasibility of detecting methamphetamine and its major metabolite, amphetamine, in postmortem tissues over a 2-year period was examined. It is important to determine if the abuse and toxic effects of drugs can be proved from evidence found in decayed, submerged, or stained tissue materials. The blood, urine, liver, skeletal muscle, skin and extremity bones from rabbits given methamphetamine intravenously were kept at room temperature, under 4 different conditions: sealed in a test tube, dried in the open air, submerged in tap water and stained on gauze. Methamphetamine was present in all the samples, with slight change in concentration in case of sealed and air dried tissues. Changes varied in bones kept in water. There were considerable decreases in methamphetamine in blood and urine stains. Despite long term storage, drug abuse and/or toxicity could be determined, in all tissues examined.

Amphetamine↗

PubMedDate not supplied

A biotin-avidin based screening test for methamphetamine in urine.

A biotin-avidin based screening test for methamphetamine in urine samples has been developed. The assay method utilizes the immunoprecipitin reaction between an antibody to methamphetamine and a conjugate prepared by complexing avidin with a biotinyl amphetamine derivative. The rates of the immunoprecipitin reaction is monitored on the Beckman ARRAY 360 nephelometer. Methamphetamine inhibits the precipitin reaction, and the extent of inhibition allows the quantitation of methamphetamine in the urine samples. Using a cut-off value of 0.7 microgram ml-1, the assay correctly predicted 83 of 84 samples (98.8%) confirmed to be positive by GC-MS (> 500 ng ml-1). Of 59 GC-MS confirmed negative samples, 46 samples were found to be negative by this method as compared to 34 samples determined with the EMIT assay. Within-run and between-run relative standard deviations near the cut-off value were less than 4%. Cross-reactivity with amphetamine was < 7%.

Antibodies↗

PubMed2004

The anxiogenic drug yohimbine reinstates methamphetamine seeking in a rat model of drug relapse.

BACKGROUND: Brain noradrenaline is involved in footshock stress-induced reinstatement of drug seeking in a rat relapse model. We studied whether yohimbine, an alpha-2 adrenoceptor antagonist that increases noradrenaline release and induces anxiety-like responses in human and nonhuman subjects, would reinstate methamphetamine seeking in rats. METHODS: In experiment 1, the effect of yohimbine (1.25-2.5 mg/kg) on reinstatement was compared with that of intermittent footshock (5 min;.2-.6 mA) in rats that were trained to lever press for intravenous methamphetamine (9-11 days) and subsequently underwent 7 days of extinction training. In experiment 2, the effect of yohimbine on reinstatement of drug seeking was determined during early (1 day) and late (21 or 51 days) withdrawal periods. On the test days, rats were first given 3-hour extinction sessions and were then tested for reinstatement induced by yohimbine. RESULTS: In experiment 1, both yohimbine and footshock stress reinstated methamphetamine seeking after extinction. In experiment 2, extinction responding was higher after 21 or 51 withdrawal days than after 1 withdrawal day. In contrast, no significant time-dependent changes in yohimbine-induced reinstatement were observed. CONCLUSIONS: Results indicate that yohimbine is a potent stimulus for reinstatement of methamphetamine seeking in a rat relapse model.

Adrenergic alpha-Antagonists↗

PubMed2005

Cerebral metabolic dysfunction and impaired vigilance in recently abstinent methamphetamine abusers.

BACKGROUND: Methamphetamine (MA) abusers have cognitive deficits, abnormal metabolic activity and structural deficits in limbic and paralimbic cortices, and reduced hippocampal volume. The links between cognitive impairment and these cerebral abnormalities are not established. METHODS: We assessed cerebral glucose metabolism with [F-18]fluorodeoxyglucose positron emission tomography in 17 abstinent (4 to 7 days) methamphetamine users and 16 control subjects performing an auditory vigilance task and obtained structural magnetic resonance brain scans. Regional brain radioactivity served as a marker for relative glucose metabolism. Error rates on the task were related to regional radioactivity and hippocampal morphology. RESULTS: Methamphetamine users had higher error rates than control subjects on the vigilance task. The groups showed different relationships between error rates and relative activity in the anterior and middle cingulate gyrus and the insula. Whereas the MA user group showed negative correlations involving these regions, the control group showed positive correlations involving the cingulate cortex. Across groups, hippocampal metabolic and structural measures were negatively correlated with error rates. CONCLUSIONS: Dysfunction in the cingulate and insular cortices of recently abstinent MA abusers contribute to impaired vigilance and other cognitive functions requiring sustained attention. Hippocampal integrity predicts task performance in methamphetamine users as well as control subjects.

Adult↗