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At least 649 records · Page 36Linked to original sources

PubMed1982

Small doses of apomorphine induce catalepsy and antagonize methamphetamine stereotypy in rats.

Small doses of apomorphine (AP, 31.25-125 micrograms/ kg IP) induced dose-dependent catalepsy in rats. However, unlike the stereotyped behavior induced by high doses of AP which has a rapid onset and is short-lasting, the cataleptic effect induced by small doses of AP was evident 30 min after AP injection and was unusually long-lasting. Further, AP (31.25-125 micrograms/kg) administered 60 min before methamphetamine was found to significantly antagonize the methamphetamine-induced stereotyped behavior. Pretreatment with molindone (0.45 and 0.8 mg/kg IP), in doses reported to selectively block the presynaptic DA receptors, not only decreased the cataleptic effect of AP but also reversed the AP antagonism of methamphetamine stereotypy. The results suggest that small doses of AP induce catalepsy and antagonize methamphetamine stereotypy probably by an action at presynaptic DA receptor sites.

Animals↗

PubMed1976

Measurement of acute and chronic behavioural effects of methamphetamine in the mouse.

A simple and reliable method was developed for rating the dose-related behavioural effects of methamphetamine in male Swiss Albino mice for acute or chronic drug treatment. This procedure was based on a frequency count of certain behaviours made at 15-min intervals over a 90-min period following drug administration. The Fisher Randomization procedure was adapted to analyze behavioural data for the chronic studies. Clear-cut, dose-related behavioural responses occurred following acute (+)-methamphetamine administration and ranged from decreased quiescence (0.64 mg/kg) through increased locomotor activity (2.5 mg/kg), a mixture of stereotyped behaviour and increased locomotor activity (5.0 and 7.5 mg/kg), to primarily stereotyped gnawing, licking or sniffing (10 mg/kg). In studies involving chronic administration of (+)-methamphetamine at 0.64, 2.5 and 10 mg/kg conducted over six and seven weeks, behavioural responses were more exaggerated than in acute studies. All behaviours returned to normal levels in the recovery week except for locomotor activity at the 10 mg/kg dosage. In some animals, chronic treatment with 10 mg/kg (+)-methamphetamine led to protracted self-tearing that replaced the gnawing, licking, sniffing stereotype.

Animals↗

PubMed1986

Comparison of effects of phencyclidine and methamphetamine on body temperature in mice: a possible role for histamine neurons in thermoregulation.

We compared the effects of phencyclidine (PCP) and methamphetamine on body temperature and brain histamine turnover in mice. Methamphetamine at 5 and 10 mg/kg produced dose-related increases in rectal temperature, whereas PCP given in the same doses had no significant effect. In mice pretreated with alpha-fluoromethylhistidine, an inhibitor of histidine decarboxylase, PCP produced a marked hyperthermia. PCP markedly accelerated brain histamine turnover, as measured by the accumulation of tele-methylhistamine, a predominant metabolite of brain histamine, following administration of pargyline. Methamphetamine had no significant effect on the histamine dynamics. These results suggest involvement of brain histaminergic neurons in the action of PCP but not methamphetamine, and the presence of a histaminergic thermoregulatory mechanism.

Animals↗

PubMed1993

Differential modification of the rewarding effects of methamphetamine and cocaine by opioids and antihistamines.

We previously reported that the reinforcing effects of opioids are enhanced in combination with antihistamines. In the present study, effects of opioids and antihistamines on the reinforcing effects of psychostimulants such as methamphetamine and cocaine were investigated by utilizing the conditioned place preference procedure in rats. The place preference induced by methamphetamine was enhanced in combination with either morphine or chlorpheniramine, which produced additive and potentiative effects, respectively. In contrast, although the preference for cocaine was also enhanced by combination with these two drugs, morphine caused a potentiative effect and chlorpheniramine an additive one. In other words, the reinforcing effect of methamphetamine was differentially enhanced by opioids and antihistamines as compared to that of cocaine. These results suggest that the mechanism of reinforcing effect of methamphetamine is different from that of cocaine, resembling rather those of opioids.

Animals↗

PubMed1990

D-2 but not D-1 dopamine agonists produce augmented behavioral response in rats after subchronic treatment with methamphetamine or cocaine.

A study was performed to examine behavioral response to a challenge of selective dopamine D-1 and D-2 agonists in rats previously sensitized by subchronic administration of methamphetamine or cocaine. Rats in three groups received repeated injections (IP) of saline, methamphetamine (4 mg/kg/day) or cocaine (20 mg/kg/day), respectively, for 14 days. After an abstinence period of 7-13 days, all groups were challenged with either a selective D-1 agonist (SKF 38393) or D-2 agonists (quinpirole or RU 24213). The ability of SKF 38393 (6 mg/kg or 18 mg/kg) to produce grooming behavior did not differ significantly among the saline-, methamphetamine- and cocaine-treated groups. In contrast, quinpirole (1 mg/kg) and RU 24213 (3 mg/kg) produced more intense stereotypy consisting of rearing, sniffing and repetitive head movement in the two psychostimulant-treated groups than in the saline-treated group. Such augmented response to selective D-2 agonists was observed even after a 1-month abstinence period. These results suggest that the enduring behavioral sensitization induced by two pharmacologically distinct psychostimulant agents, methamphetamine and cocaine, occurs through a common neurobiological mechanism of lasting supersensitivity in postsynaptic D-2, but not D-1 dopamine receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1999

A case of traumatic shock complicated by methamphetamine intoxication.

A case of a 38-year-old male with traumatic shock complicated by methamphetamine intoxication is presented. The patient was involved in an assault which resulted in cardiac tamponade and right ventricular outflow laceration. Pericardiocentesis was immediately performed. However, profound metabolic acidosis greatly in excess of that expected from the short duration of the shock was revealed by arterial blood gas analysis. Another cause of the metabolic acidosis was suspected. The patient subsequently admitted to intravenous use of methamphetamine. Following hemodynamic and metabolic stabilization by continuous pericardial drainage and intravenous administration of sodium bicarbonate, the patient underwent cardiac surgery. His postoperative course was uneventful. There is a substantial association between methamphetamine users and traumatic accidents. In such cases, early identification of drug use is important. Marked metabolic acidosis, which conflicts with the diagnosed cause of shock, may be a clinical clue to methamphetamine intoxication.

Acidosis↗

PubMed2003

Methamphetamine attenuates disruptions in performance and mood during simulated night-shift work.

RATIONALE: Increased sleepiness while working and sleep disruptions are common complaints among shift workers. Consequently, shift workers may be more susceptible to diminished performance and work-related accidents. OBJECTIVE: To examine the effects of the central nervous system stimulant methamphetamine on psychomotor task performance, subjective effects, and food intake during shift work under laboratory conditions. METHODS: Seven participants completed this 23-day, within-participant design, residential laboratory study. They received a single oral methamphetamine dose (0, 5, 10 mg) 1 h after waking for three consecutive days under two shift conditions: (1) during the day shift, participants performed computerized psychomotor tasks from 0830 hours to 1730 hours and went to bed at 2400 hours and (2) during the night shift, participants performed tasks from 0030 hours to 0930 hours and went to bed at 1600 hours. Shifts alternated three times during the study; shift conditions were separated by an "off" day during which participants were not on a schedule and data were not collected. RESULTS: When participants received placebo, psychomotor task performance and subjective effects were disrupted during the night shift, relative to the day shift. Changing shift conditions did not alter food intake significantly. Methamphetamine reversed performance and subjective-effects disruptions, and decreased food intake during the night shift. CONCLUSION: These data indicate that shift changes produce performance impairments and mood alterations, and that a single low to moderate dose of methamphetamine attenuates many shift change-related disruptions in performance and mood.

Adult↗

PubMed2003

Liquid chromatographic method for the determination of enantiomeric composition of amphetamine and methamphetamine in hair samples.

Interest in hair analysis as an alternative or complementary approach to urinalysis for drug abuse detection has grown in recent years. Hair analysis can be particularly advantageous for drugs such as amphetamine and methamphetamine that are rapidly excreted. Confirmation of abuse of these stimulants is complicated by the fact that some forms are found in legitimate medications. Examination of the enantiomeric composition of amphetamine and methamphetamine in hair samples can provide valuable assistance in interpreting drug testing results. In this work, we developed a liquid chromatographic method for the separation of amphetamine and methamphetamine enantiomers isolated from human hair samples. The drug enantiomers were separated on a chiral stationary phase after derivatization with an achiral fluorescent agent. The methodology was evaluated with a Standard Reference Material that contained several drugs of abuse including amphetamine and methamphetamine.

Amphetamine↗

PubMed2000

Sexual differences and estrous cycle in methamphetamine-induced dopamine and serotonin depletions in the striatum of mice.

Four consecutive doses (10 mg/kg) of methamphetamine, s.c., produced a substantial striatal dopamine depletion in both sexes of BALB/c and C57BL/6J mice. Male C57BL/6J mice exhibited greater dopamine depletions in the striatum compared to female C57BL/6J mice. In contrast, male and female BALB/c mice demonstrated an equivalent magnitude of striatal dopamine depletion. Regardless of sex, C57BL/6J mice demonstrated approximately 1.4 to 2.2 times greater dopamine depletions in the striatum compared to BALB/c mice. Moreover, methamphetamine caused 4 times greater serotonin depletions in male as opposed to female BALB/c mice while sparing either sex of the C57BL/6J mice. Furthermore, female mice of both strains appeared to have the greatest basal dopamine levels during proestrus and the lowest basal dopamine levels during diestrus. Likewise, female mice of both strains exhibited the lowest dopamine depletions in the striatum when the dosing regimen of methamphetamine started at proestrus whereas the greatest dopamine depletions in the striatum occurred when the regimen started during diestrus. These results suggest that sex hormones and other modulating factors may play a role in methamphetamine-induced dopamine and serotonin neurotoxicity.

Animals↗

PubMed1989

Selective reduction of serotonin immunoreactivity in some forebrain regions of rats induced by acute methamphetamine treatment; quantitative morphometric analysis by serotonin immunocytochemistry.

The influence of acute methamphetamine treatment on serotonin-like immunoreactive axons was studied in the rat forebrain. Animals, sacrificed 90 min after i.p. injection of methamphetamine (16 mg/kg) or saline, were processed for immunocytochemistry using serotonin antiserum. The numerical density of immunoreactive boutons of terminals and varicosities was quantitatively analyzed by a computer-assisted image analyzer. Compared with the control, administration of methamphetamine caused varying degrees of reduction in the numerical density in several forebrain regions. A high decrement (over -90%) was found in deep layers of the cerebral cortex, striatum and thalamic paraventricular nucleus, while a less prominent reduction (about -50%) was seen in such regions as the suprachiasmatic nucleus and basolateral amygdaloid nucleus. Moreover, superficial layers of the cerebral cortex contained uncommon features of immunopositive axons which were characterized by intensely stained fibers with large varicosities. The results suggest that the rat forebrain contains at least two types of serotonin nerves, one very sensitive to methamphetamine and another relatively insensitive or resistant to it.

Animals↗

PubMed1990

MK-801 antagonizes methamphetamine-induced decreases in hippocampal and striatal corticosteroid receptors.

Administration of methamphetamine (15 mg/kg) to adrenalectomized rats significantly decreased hippocampal type I and II corticosteroid receptors as well as type II receptors in the striatum. Type II receptors in the frontal cortex and hypothalamus were unaffected by methamphetamine administration. Pretreatment with MK-801, a non-competitive antagonist of N-methyl-D-aspartate receptors, antagonized the methamphetamine-induced decrease in hippocampal and striatal corticosteroid receptors. These results are in agreement with previous studies demonstrating that some of the neurobiological effects of methamphetamine may be mediated via a mechanism involving excitatory amino acids.

Adrenal Glands↗

PubMed1991

Amphetamine-antagonistic properties of 4-phenyl-1,2,3,4- tetrahydroisoquinoline: inhibition of spinal reflex-enhancing effects of methamphetamine, phenylethylamine and nomifensine.

The antagonistic effects of 4-phenyl-1,2,3,4-tetrahydroisoquinoline (4PTIQ) against S(+)-methamphetamine, phenylethylamine and nomifensine were studied by measurement of spinal monosynaptic reflex potential (MSR). S(+)-Methamphetamine, phenylethylamine and nomifensine enhanced the amplitude of MSR in C1-spinalized rats through release of noradrenaline from the terminals of descending fibers and consequent activation of alpha 1-adrenoceptors. Although 4PTIQ alone did not change the amplitude of the MSR, 4PTIQ inhibited the enhancement of MSR induced by S(+)-methamphetamine and related compounds. The MSR of rats with an intact spinal cord was enhanced by conditioning stimulation of the ipsilateral locus ceruleus. The MSR enhancement produced by the stimulation was blocked by prazosin but unaffected by 4PTIQ, showing that 4PTIQ does not have an alpha 1-blocking action. These results suggest that the antagonistic effects of 4PTIQ on MSR enhancement by S(+)-methamphetamine, phenylethylamine and nomifensine are due to its blocking of noradrenaline release produced by these amphetamine-like agents.

Amphetamine↗

PubMed1981

Methamphetamine-induced depression of tryptophan hydroxylase: recovery following acute treatment.

Acute administration of methamphetamine produced a dose-dependent depression of tryptophan hydroxylase (TPH) activity. The depression was observed in several serotonergic nerve terminal regions of the rat brain and spinal cord. Complete recovery of TPH activity following methamphetamine treatment occurred in all regions, but the time to recovery varied with the dose administered. In contrast to TPH, tyrosine hydroxylase (TH) was not affected by a single injection of methamphetamine. The data are discussed in the context of the effects of single versus repeated doses of methamphetamine on tryptophan and tyrosine hydroxylase.

Amphetamine↗

PubMed1982

Reduction in brain serotonin synthesis rate following chronic methamphetamine administration in rats.

Chronic administration of methamphetamine (20 mg/kg i.p., every 12 h for 6 days) produced significant decreased in brain 5-hydroxytryptophan accumulation following decarboxylase inhibition and 5-hydroxyindoleacetic acid accumulation following probenecid treatment in rats. Administration of fluoxetine prior to each methamphetamine injection prevented these neurochemical changes. Acute methamphetamine treatment produced no changes in these neurochemical measures. These data demonstrate that chronic, but not acute, methamphetamine treatment reduces brain serotonin synthesis rate.

5-Hydroxytryptophan↗

PubMed1992

The substituted amphetamines 3,4-methylenedioxymethamphetamine, methamphetamine, p-chloroamphetamine and fenfluramine induce 5-hydroxytryptamine release via a common mechanism blocked by fluoxetine and cocaine.

The abilities of the substituted amphetamines 3,4-methylenedioxymethamphetamine (MDMA), methamphetamine, p-chloroamphetamine (PCA) and fenfluramine to induce synaptosomal [3H]serotonin (5-HT) release were compared using a novel microassay system. The rank order of release potencies was found to be (+/-)PCA congruent to (+)-fenfluramine greater than (+)-MDMA much greater than (+)-methamphetamine. Combination of two drugs at their EC50 did not cause more release than either drug alone at an equivalent concentration. In addition, the 5-HT uptake blockers fluoxetine and cocaine inhibited the release induced by MDMA, methamphetamine, PCA and fenfluramine to the same percentage. However, threshold concentrations of the substituted amphetamines known to inhibit uptake did not attenuate the release caused by higher concentrations of these compounds. These results suggests that MDMA, methamphetamine, PCA and fenfluramine cause 5-HT release via a common mechanism. Furthermore, these results indicate that the 5-HT uptake blockade induced by these substituted amphetamines in vitro is different from that induced by either fluoxetine or cocaine.

3,4-Methylenedioxyamphetamine↗

PubMed1993

Methamphetamine antagonistic property of (+)- and (-)-4-phenyltetrahydroisoquinoline in rat anococcygeus muscle.

The antagonistic effects of (+)- and (-)-4-phenyl-1,2,3,4-tetrahydroisoquinoline (4PTIQ) on methamphetamine in the rat anococcygeus muscle were compared with those of cocaine and nomifensine. Methamphetamine contracted the anococcygeus muscle through the release of norepinephrine from noradrenergic nerve terminals. (+)-4PTIQ inhibited the methamphetamine-induced contractions more strongly than cocaine and nomifensine. (+)-4PTIQ had no potentiating effects on exogenous norepinephrine-induced contraction, which was considered to be an index of amine neuronal uptake blockade. On the other hand, (-)-4PTIQ, cocaine and nomifensine produced a significant leftward shift of the norepinephrine concentration-response curve, i.e. they showed a strong blocking effect on amine neuronal uptake. These results suggest that the inhibitory effects of (+)-4PTIQ on the action of methamphetamine are mediated by a mechanism other than inhibition of amine neuronal uptake.

Animals↗

PubMed1993

4-Phenyltetrahydroisoquinoline, but not nomifensine or cocaine, inhibits methamphetamine-induced dopamine release.

The inhibitory effect of 4-phenyltetrahydroisoquinoline (4-PTIQ) on methamphetamine-induced dopamine release in the rat nucleus accumbens was investigated using a brain microdialysis method. Methamphetamine (10(-6) M) infusion through a microdialysis probe induced the release of dopamine. Although the uptake inhibitors, cocaine (3 x 10(-6) M) and nomifensine (10(-6) M), failed to block dopamine release, 4-PTIQ (10(-6 M) inhibited the dopamine-releasing effect of methamphetamine. 4-PTIQ did not affect the elevation of the extracellular dopamine level induced by high concentrations of nomifensine (10(-5) M) and cocaine (3 x 10(-5) M). 4-PTIQ was the weakest inhibitor of [3H]dopamine uptake by rat striatal synaptosomes. These results suggest that 4-PTIQ is a selective antagonist against the dopamine-releasing effect of methamphetamine in the nucleus accumbens.

Animals↗

PubMed1994

Effects of N-ethylmaleimide on dopamine release in the rat striatum after repeated treatment with methamphetamine.

Effects of N-ethylmaleimide or forskolin on electrically evoked dopamine release were investigated in striatal slices of rats pretreated with methamphetamine. N-Ethylmaleimide and forskolin both enhanced the evoked dopamine release in a concentration-dependent manner. The enhancement by N-ethylmaleimide of spontaneous dopamine release was not abolished by tetrodotoxin; the electrically evoked release was abolished, irrespective of its magnitude. Moreover, N-ethylmaleimide prevented the inhibitory effect of the dopamine receptor agonist, 2-amino-6-allyl- 5,6,7,8-tetrahydro-4H-thiazolo(5,4-d)-azepine dihydrochloride (B-HT 920) and the stimulatory effect of the dopamine receptor antagonist, (-)-sulpiride, on the evoked dopamine release. In contrast, forskolin had no effect on the B-HT 920-induced inhibition and (-)-sulpiride-induced enhancement of the evoked dopamine release. These data indicate that release-modulating dopamine autoreceptors are N-ethylmaleimide-sensitive and forskolin-insensitive. As N-ethylmaleimide has been reported to inactivate Gi protein and to block the regulation of noradrenaline release by alpha 2-adrenoceptors, the present results suggest that N-ethylmaleimide inactivates inhibitory GTP binding proteins to block the regulation by dopamine autoreceptors of evoked dopamine release. Methamphetamine pretreatment, which caused behavioral sensitization to a challenge dose of methamphetamine, attenuated the stimulatory effect of N-ethylmaleimide but not forskolin on the evoked dopamine release. The data indicate that the repeated administration of methamphetamine reduces a function of N-ethylmaleimide sensitive signal transduction system, probably including inhibitory GTP binding protein.

Animals↗