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PubMed1985

Neurochemical and functional consequences following 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) and methamphetamine.

The neurochemical and functional consequences following MPTP administration to the rat were evaluated and compared to similar effects following methamphetamine administration. It was observed that MPTP induced long lasting depletions of striatal dopamine concentrations and this neurotoxic effect could be prevented by pargyline pretreatment. The MPTP-induced neuronal damage produced a tolerance to the disruptive effects of amphetamine and a supersensitivity to the disruptive effects of apomorphine in rats responding in a schedule controlled paradigm. Methamphetamine, like MPTP, produced depletions of striatal dopamine but these actions were potentiated by pargyline pretreatment. These observations are discussed in reference to possible deleterious effects following the administration of pargyline to patients with Parkinson's Disease.

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

PubMed1993

Blockade of the locomotor stimulant effects of cocaine and methamphetamine by glutamate antagonists.

The AMPA antagonist, NBQX, produced dose-dependent blockade of the locomotor stimulant effects of cocaine and methamphetamine in male, Swiss-Webster mice at doses which did not alter spontaneous locomotion. A similar finding was obtained with the competitive NMDA antagonist, NPC 12626, although blockade was only observed at the highest dose studied. The NMDA antagonists, (+)-HA-966 and 7-chlorokynurenic acid (7-CKA), which act at the strychnine-insensitive modulatory site of the NMDA receptor, only blocked the stimulatory effects of methamphetamine and with (+)-HA-966, blockade was only achieved at a dose that decreased spontaneous locomotor activity. These results provide evidence for the involvement of glutamatergic input in the control of behavior involving mesolimbic dopamine. Along with other findings these results suggest that glutamate receptors may be a target for the development of pharmacological therapies for the treatment of psychomotor stimulant abuse and for other disorders involving hyperfunction of the mesolimbic dopamine system (eg. schizophrenia).

Amino Acids↗

PubMed1995

Sertindole antagonizes morphine-, cocaine-, and methamphetamine-induced place preference in the rat.

The motivational effect of sertindole, a limbic selective antipsychotic drug, was investigated in rats using a non-biased conditioned place preference method which could reliably detect the reinforcing effects of morphine, cocaine and methamphetamine. Sertindole (0.01-1.0 mg/kg, s.c.), like haloperidol and fluphenazine, produced neither place preference nor place aversion. However, sertindole, at a dose of 1.0 mg/kg, s.c., completely abolished the place preferences induced by morphine (8.0 mg/kg, i.p.), cocaine (4.0 mg/kg, i.p.) and methamphetamine (2.0 mg/kg i.p.). These results strongly suggest that sertindole itself does not induce a rewarding effect and may have therapeutic value in the treatment of drug abuse.

Animals↗

PubMed1988

Rhythms in behaviors, body temperature and plasma corticosterone in SCN lesioned rats given methamphetamine.

In aperiodic rats with lesions in the suprachiasmatic nuclei (SCN), rhythms with a circadian period in spontaneous locomotion, wheel-running, feeding, drinking, body temperature and plasma corticosterone were restored by chronic administration of methamphetamine. These rhythms were not entrained by a light-dark cycle. Wheel-running, feeding and drinking rhythms in individual rats were in phase in terms of ultradian bout as well as circadian fluctuation. Rhythms of the intraperitoneal temperature appeared accompanying the spontaneous locomotor rhythm. The phase relation between the two rhythms was similar to that of SCN dependent rhythms. Plasma corticosterone also fluctuated in a circadian fashion. The corticosterone peak preceded the activity onset of locomotor rhythm by a few hours, which was similar to the phase relation observed in the SCN intact animals. It is concluded that the oscillatory mechanism underlying the spontaneous locomotor rhythm in SCN lesioned and methamphetamine treated rats drives also other physiological rhythms. The phase-relations among them were similar to those of rhythms driven by the circadian pacemaker in the SCN.

Administration, Oral↗

PubMedDate not supplied

Tolerance and cross-tolerance to the effects of amphetamine, methamphetamine and fenfluramine on milk consumption in the rat.

It has been reported that rats develop tolerance to the milk intake suppressant effects of d-amphetamine, d-methamphetamine, and d, l-fenfluramine. However, it has been hypothesized that the mechanism of action of fenfluramine is different from that of the other two drugs. In the present experiment, rats were given one of these 3 phenylethylamine derivatives each day until tolerance developed to the suppression of milk intake. A second of these drug s was then substituted and milk intake measured. There was cross-tolerance to the drug-induced suppression between d-amphetamine and d-methamphetamine, but not between d-amphetamine and d,l-fenfluramine. The lack of cross tolerance suggests a different mechanism of action for these drugs.

Animals↗

PubMed1985

Cathinone, cocaine and methamphetamine: similarity of behavioral effects.

The discriminative stimulus properties of (+/-)-cathinone were tested by training eight rats to discriminate between the interoceptive cues produced by 0.6 mg/kg (+/-)-cathinone and saline in a food-reinforced, two lever operant task. Doses of cocaine and methamphetamine were observed to transfer to the cathinone cue and all three drugs exhibited decreased discriminative performance with decreasing doses. The ED50 for (+/-)-cathinone, (+/-)-methamphetamine and cocaine were 0.23, 0.17, and 1.97 mg/kg, respectively, and the three curves were shown to be parallel. These data indicate the possibility of a common mechanism/site of action for these three stimulants, presumably by their actions upon central dopaminergic neurons.

Alkaloids↗

PubMed1988

A preliminary behavioral investigation of PMMA, the 4-methoxy analog of methamphetamine.

The controlled-substance analog N-monomethyl-1-(4-methoxyphenyl)-2-aminopropane (PMMA) may be viewed as being either the 4-methoxy analog of methamphetamine or the N-methyl analog of 1-(4-methoxyphenyl)-2-aminopropane (PMA). Because of its abuse potential, PMMA was examined with regard to (a) its stimulus properties in rats trained to discriminate either 1.0 mg/kg of (+)amphetamine or (+/-)DOM from saline, (b) its toxicity (isolated and aggregated) in mice relative to (+/-)PMA, and (c) its locomotor stimulant activity in mice relative to (+/-)amphetamine, (+/-)methamphetamine, and (+/-)PMA. Racemic PMMA produced neither DOM-like nor, unlike PMA, amphetamine-like stimulus effects. There was no significant difference between the 24-hr isolated (LD50 = 63 mg/kg) and aggregated (LD50 = 53 mg/kg) toxicity, and PMMA did not produce significant locomotor stimulation at doses of up to 30 mg/kg. The present results suggest that while PMMA may produce central effects it does not appear to behave as a simple amphetamine-like agent.

Amphetamine↗

PubMed1995

Uridine reduces rotation induced by L-dopa and methamphetamine in 6-OHDA-treated rats.

The pyrimidine nucleoside uridine may reduce side effects associated with antipsychotic medication by interacting with dopamine or GABA neurotransmission. Male Sprague-Dawley rats were used to investigate coadministration of uridine with agents that alter food intake (amphetamine, haloperidol, and chlordiazepoxide) and locomotor activity (methamphetamine and L-dopa). Results indicated that chronic uridine [32.0 mg/kg, intraperitoneally (IP)] alone did not alter milk intake or reduction of milk intake induced by amphetamine (dose range 0.5-2.0 mg/kg, IP) or haloperidol (0.125-1.0 mg/kg, IP), nor did it alter the biphasic response induced by chlordiazepoxide (5.0-40.0 mg/kg, IP). However, uridine-treated animals with unilateral striatal lesions exhibited no rotational behavior in the absence of drug challenge, but showed decreased rotation induced by the dopamine agonist, L-dopa (50.0-200.0 mg/kg, IP) compared with controls. In addition, uridine-treated rats exhibited reduced rotation after repeated injections of methamphetamine (4.0 mg/kg, IP) in contrast to increasingly greater rotation observed in control animals. These results are further evidence that chronic uridine may alter drug-induced dopaminergic activity without exerting effects itself.

Animals↗

PubMed1993

Developmental dissociation of methamphetamine-induced depletion of dopaminergic terminals and astrocyte reaction in rat striatum.

In 60- and 80-day-old rats, TH-positive terminal depletion occurred simultaneously with increased glial fibrillary acid protein (GFAP)-containing astrocytes in the caudate-putamen nucleus following four 10 or 20 mg/kg methamphetamine treatments. At 40 days, astrocytes were increased without depletion of TH-positive terminals. At younger ages (20 days old) neither marker was altered. Processes leading to methamphetamine-induced gliosis and TH-positive terminal depletion may not be present in rats prior to 40 and 60 days, respectively. The data suggest that factors other than degenerated dopaminergic terminals, such as increased glutamate release and/or production of free radicals may be involved in triggering striatal gliosis.

Animals↗

PubMed1994

Acute amphetamine or methamphetamine alters opioid peptide mRNA expression in rat striatum.

The effects of a single dose of amphetamine or methamphetamine on opioid peptide gene expression in the dorsal and ventral striatum of rats were investigated by quantitative in situ hybridization 3, 6, or 18 h after injection. Although amphetamine-treated rats exhibited significantly different behaviors than those treated with methamphetamine, both drugs caused a patchy increase in preprodynorphin, but not preproenkephalin, mRNA in the caudate at all 3 time points. No changes were detected in the nucleus accumbens. These data indicate that prolonged elevation of preprodynorphin expression may alter the responsiveness of striatonigral neurons to subsequent amphetamine exposure.

Amphetamine↗

PubMed1992

Crystal methamphetamine abuse: a concern to oral and maxillofacial surgeons.

Synthetically manufactured methamphetamine ("ice," "crystal") appears to be undergoing a rebirth in popularity because experienced drug users are reportedly unable to distinguish between the qualities of the cocaine and methamphetamine euphoria. Like cocaine, adverse drug reactions with therapeutic drugs used in dentistry have been reported, ranging from mild intoxication to sudden death. This article discusses the pharmacology of this illicit drug and the problems associated with its use in patients undergoing oral and maxillofacial surgery.

Administration, Oral↗

PubMed1988

Neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and methamphetamine in several strains of mice.

We previously reported that C57 black mice were more sensitive than several other strains of mice to the neurotoxic actions of MPTP. We now report that a significantly higher amount of the 1-methyl-4-phenylpyridinium species, a very toxic metabolite of MPTP, was found in the brains of C57 black mice than in the brains of CF-W or CD-1 mice, two strains of mice which are less sensitive to MPTP. In addition, we also found that there were strain differences in the response of mice to the neurotoxic actions of methamphetamine with CF-W mice being more sensitive to methamphetamine than C57 black mice.

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

PubMed1988

Habenular lesion attenuates methamphetamine-induced inhibition of dopamine neuronal activity in the substantia nigra pars compacta of rats.

The relation between the habenula and central dopaminergic system was investigated by examining the inhibitory effects of methamphetamine on the firing rate of dopamine neurons in the substantia nigra of habenular lesioned and unlesioned rats. Electrolytic lesions of the habenula attenuated the methamphetamine-induced inhibition of dopamine neurons in the substantia nigra. This, along with other findings, indicates possibly that the habenula is involved in a feedback pathway from the striatum to the substantia nigra and regulates the activity of dopamine neurons in the substantia nigra.

Action Potentials↗

PubMed1988

Effects of methamphetamine upon circadian rhythms in multiple unit activity inside and outside the suprachiasmatic nucleus in the golden hamster (Mesocricetus auratus).

To investigate the circadian system of the golden hamster, multiple unit activity (MUA) was recorded inside and outside the suprachiasmatic nucleus (SCN). MUA inside the SCN showed a daily rhythm with a daytime peak during a 24 h light-dark cycle (LD, 12:12), whereas MUA outside the SCN revealed a nighttime peak. The phase reversal of MUA between inside and outside the SCN in the golden hamster was similar to the rat which is also a nocturnal rodent. MUA rhythms to the lighting cycle started to freerun after methamphetamine administration. This result indicates that methamphetamine may affect directly the neural circadian oscillator to induce behavioral change.

Action Potentials↗

PubMed1994

Omega-conotoxin GVIA inhibits the methylphenidate-induced but not methamphetamine-induced behavior.

We investigated the effects of antagonists for omega-conotoxin GVIA (omega-CTX)-sensitive N-type voltage-sensitive calcium channels (N-channels) on methylphenidate- and methamphetamine-induced behavior. I.c.v. injection of omega-CTX or neomycin, both N-channel antagonists, caused a dose-dependent inhibition of methylphenidate-induced hypermotility in mice but failed to inhibit methamphetamine-induced hyperactivity. Further, omega-CTX inhibited the circling behavior induced by methylphenidate in rats that had kainic acid-induced unilateral striatal lesions. These results suggest that calcium influx through omega-CTX-sensitive N-channels plays an important role in methylphenidate-induced behavior.

Animals↗

PubMed1987

Tyrosine hydroxylase immunochemistry and quantitative light microscopic studies of the mesolimbic dopamine system in rat brain: effects of chronic methamphetamine administration.

Long-term treatment of rats with methamphetamine (20 mg/kg, IP, every 12 hours for 10 days) resulted in a large decrease in tyrosine hydroxylase staining axons and terminal boutons in the nucleus accumbens and frontal cortex, as well as the ventral tegmental area of the midbrain, when examined 60 days following termination of the drug treatment regimen. Quantitative analysis showed a 71 and 78% decrease in tyrosine hydroxylase staining processes in the nucleus accumbens and frontal cortex, respectively, and a 90% decrease in tyrosine hydroxylase positive material in the ventral tegmental area. Thus, tyrosine hydroxylase enzyme in both the cell bodies of the midbrain ventral tegmental area as well as in the nerve terminals in post-synaptic target regions of the forebrain is depleted by chronic methamphetamine administration.

Animals↗

PubMed1995

Gas chromatographic determination of methamphetamine and its metabolite amphetamine in human plasma and urine following conversion to N-propyl derivatives.

A gas chromatographic method for the simultaneous determination of methamphetamine and its metabolite amphetamine in human plasma and urine is described. The method utilizes reductive alkylation with propionaldehyde and sodium borohydride to produce N-propyl derivatives, which have excellent chromatographic properties. Structural analogs of the analytes, p-methylmethamphetamine and p-methylamphetamine, are used as internal standards. The method has good precision and accuracy for concentrations ranging from less than 10 ng/ml to 5000 ng/ml and has been used to measure plasma concentrations as part of a pharmacokinetic/pharmacodynamic study of methamphetamine in humans.

Aldehydes↗

PubMed1984

A high selective screening test for methamphetamine in human urine.

A high selective screening test (Ad-Tip method) for methamphetamine in human urine has been devised. The method involves a brief extraction from a urine sample with an Ad-Tip (ODS-silica minicolumn), washing, eluting with modified Simon's reagent, and coloration with carbonate buffer. Detection limit of methamphetamine in urine is 1 microgram/ml and the test takes within 3 min/sample. The results of the Ad-Tip method were almost identical to those of laboratory analyses.

Acetates↗