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Results for “Methamphetamine”

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PubMed1991

Evaluation of the effects of inhibition of monoamine oxidase and senescence on methamphetamine-induced neuronal damage.

The administration of high doses of methamphetamine causes long lasting damage to central dopaminergic and serotonergic neurons through a mechanism known to involve presynaptic, cytoplasmic stores of those transmitters and thought to be dependent upon a free radical reaction. The following studies were designed to determine if differential inhibition of the subtypes of monoamine oxidase would alter the magnitude of the methamphetamine induced neuronal damage. In addition, since monoamine oxidase type B increases with age, the effects of high dose administration of methamphetamine were evaluated in senescent mice. It was observed that inhibition of monoamine oxidase type A, and to a lesser degree, type B, increased the magnitude of methamphetamine-induced neuronal damage and that aged mice were more sensitive to the toxic action of methamphetamine. These results are interpreted with respect to the use of monoamine oxidase inhibitors in the treatment of Parkinson's disease.

Aging↗

PubMed1993

Dopamine D2 and serotonin S2 receptors in susceptibility to methamphetamine psychosis detected by positron emission tomography.

Positron emission tomography (PET) was used to assess the role of dopamine D2 receptors in the striatum and serotonin S2 receptors in the frontal cortex in the susceptibility to methamphetamine-induced psychosis. Subjects were six men who had previously experienced methamphetamine psychosis (methamphetamine subjects) and 10 age- and sex-matched control subjects. The radiotracer used was 11C-N-methylspiperone. Although binding availability, assessed by dynamic analysis, in the two regions did not differ between the two groups, the ratio of binding availability in the striatum to that in the frontal cortex significantly decreased in the methamphetamine subjects as compared with the control subjects. These findings suggest that an imbalance in the activity of these two receptors may be related to the susceptibility to methamphetamine psychosis.

Adult↗

PubMed1993

Distribution of carbon-11 labeled methamphetamine and the effect of its chronic administration in mice.

[11C]Methamphetamine, a psychotropic agent, was synthesized by N-methylation of amphetamine with [11C]CH3 I in hopes that it could be applied in the near future to assist positron emission tomography (PET) in the imaging of its distribution in the human brain. The regional distribution of [11C]methamphetamine was investigated in the mice brain at various intervals after an intravenous (i.v.) injection. Radioactivity was higher in the hypothalamus, cortex, striatum and hippocampus. Furthermore, in chronically administered mice, the uptake of [11C]methamphetamine was higher in the striatum than those in other regions. The regional differences in the distribution of methamphetamine in the mice brain may enable the imaging of its distribution by PET using [11C]methamphetamine.

Animals↗

PubMed2005

Methamphetamine and alcohol abuse and dependence symptoms: associations with affect lability and impulsivity in a rural treatment population.

The present study examined associations between impulsivity and affect lability and methamphetamine and alcohol abuse and dependence symptoms in a rural inpatient treatment population (N=235). Thirty-two percent of participants reported methamphetamine use in the past 90 days prior to admission. Amphetamine use disorders were found to be more common among younger participants whereas alcohol use disorders were more common among older and Native American participants. After controlling for age, gender, use frequency, and injection use, impulsivity but not affect lability was associated with methamphetamine abuse but not dependence symptoms. Lability but not impulsivity was associated with alcohol dependence but not abuse symptoms after controlling for age, gender, and use frequency. Consistent with past epidemiological studies, results indicate that methamphetamine use is a prominent problem facing rural substance use treatment facilities. Affect lability and impulsivity are associated with methamphetamine and alcohol-related problems in this population.

Adolescent↗

PubMed2005

Psychological differences between binge and chronic methamphetamine using gay and bisexual men.

Methamphetamine use among gay and bisexual men in New York City continues to pervade the psychological and physical well being of those who engage in its use. While the behavioral and contextual factors associated with methamphetamine use have been examined, there is a paucity of literature examining the psychological and psychosocial correlates associated with varying levels of addiction to the substance. We assessed these correlates among 49 methamphetamine-using gay and bisexual men in New York City. Findings suggest that "Chronic" users report higher levels of avoidant coping and are more likely to use methamphetamine to avoid unpleasant emotions, to avoid physical pain, and to engage in pleasant times with others than those who are "Binge" users. While previous research demonstrates the value of treatment approaches that consider the synergy of mental health, drug use, and sexual-risk taking, our findings suggest the importance of identifying the frequency and current progression of methamphetamine use when addressing the psychological meanings it has for the individual user.

Adult↗

PubMed2006

Risk and protective factors for methamphetamine use and nonmedical use of prescription stimulants among young adults aged 18 to 25.

This article reports on correlates of past-year nonmedical use of prescription stimulants and methamphetamine among young adults aged 18 to 25. Data from the 2002 National Survey on Drug Use and Health (NSDUH) were used to conduct logistic regression analyses of the demographic, psychosocial, and behavioral correlates of nonmedical stimulant use. The sample size was 23,645. Multivariate analyses revealed that selling drugs and using marijuana and other illegal drugs were associated with increased odds of both methamphetamine and nonmedical prescription stimulant use. Females, individuals not enrolled in college, and those who had been arrested were more likely than their counterparts to have used methamphetamine, whereas black individuals and less religious individuals were less likely than their counterparts to have used methamphetamine. Psychological distress, sensation seeking, binge drinking, and college enrollment were associated with increased risks of nonmedical prescription stimulant use, whereas Hispanic and other ethnic identification were associated with decreased risks of nonmedical prescription stimulant use. Different intervention strategies are needed to prevent methamphetamine use versus nonmedical prescription stimulant use.

Adolescent↗

PubMed2005

Effect of MS-153, a glutamate transporter activator, on the conditioned rewarding effects of morphine, methamphetamine and cocaine in mice.

There is a body of evidence implying the involvement of the glutamatergic system in the conditioned rewarding effects of drugs of abuse. It is recognized that the release of extracellular glutamate from nerve terminals is counterbalanced by the functions of neuronal and glial glutamate transporters. In the present study, we investigated the effects of (R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline (MS-153), a glutamate transporter activator, on the induction of the conditioned place preference to morphine, methamphetamine and cocaine in mice. In the conditioned place preference paradigm, mice were conditioned with repeated subcutaneous injections of morphine (5 mg/kg), methamphetamine (2 mg/kg) or cocaine (8 mg/kg) in combination with or without MS-153 (3 and 10 mg/kg). Co-administration of MS-153 at a dose of 10 mg/kg, but not 3 mg/kg, significantly attenuated the induction of conditioned place preference to morphine, methamphetamine and cocaine. However, MS-153 itself produced neither conditioned place preference nor aversion. On the other hand, co-administration of MS-153 (10 mg/kg) did not alter the acute locomotor activation elicited by a single injection of morphine, methamphetamine and cocaine. These results suggest that MS-153, a glutamate transporter activator, has an inhibitory effect on the conditioned rewarding effects of morphine, methamphetamine and cocaine without affecting their acute locomotor responses.

Amino Acid Transport System X-AG↗

PubMed2006

A sensitizing regimen of methamphetamine causes impairments in a novelty preference task of object recognition.

A neurotoxic regimen of methamphetamine impairs object recognition (OR) in rats. The present study investigated whether neurotoxicity is a necessary component of methamphetamine's effect on OR. Animals were exposed to a sensitizing regimen of methamphetamine, and were tested for OR one week, and locomotor behavior two weeks, later. Quantitative autoradiography was used to measure [(125)I]RTI-55 binding to forebrain dopaminergic and serotonergic transporters. Methamphetamine treatment produced significant OR impairments (and increased locomotion), without reducing dopamine or serotonin transporter binding. This study supports the conclusion that factors other than monoamine terminal injury contribute to the methamphetamine-induced cognitive impairments.

Animals↗

PubMed2005

MK-801 and dextromethorphan block microglial activation and protect against methamphetamine-induced neurotoxicity.

Methamphetamine causes long-term toxicity to dopamine nerve endings of the striatum. Evidence is emerging that microglia can contribute to the neuronal damage associated with disease, injury, or inflammation, but their role in methamphetamine-induced neurotoxicity has received relatively little attention. Lipopolysaccharide (LPS) and the neurotoxic HIV Tat protein, which cause dopamine neuronal toxicity after direct infusion into brain, cause activation of cultured mouse microglial cells as evidenced by increased expression of intracellular cyclooxygenase-2 and elevated secretion of tumor necrosis factor-alpha. MK-801, a non-competitive NMDA receptor antagonist that is known to protect against methamphetamine neurotoxicity, prevents microglial activation by LPS and HIV Tat. Dextromethorphan, an antitussive agent with NMDA receptor blocking properties, also prevents microglial activation. In vivo, MK-801 and dextromethorphan reduce methamphetamine-induced activation of microglia in striatum and they protect dopamine nerve endings against drug-induced nerve terminal damage. The present results indicate that the ability of MK-801 and dextromethorphan to protect against methamphetamine neurotoxicity is related to their common property as blockers of microglial activation.

Animals↗

PubMed2004

Methamphetamine sensitization in nociceptin receptor knockout mice: locomotor and c-fos expression.

The role of endogenous nociceptin in the development and expression of sensitization to repeated methamphetamine administration in a novel environment was studied in nociceptin receptor knockout mice. No differences in acute or sensitized locomotor responses were found in nociceptin receptor knockout mice. However, analysis of c-fos expression revealed significant interactions between chronic methamphetamine treatment and genotype in the nucleus accumbens and lateral septum. This was due to increased c-fos expression in chronically methamphetamine-treated nociceptin receptor knockout mice contrasted with reduced c-fos expression in chronically vehicle-treated nociceptin receptor knockout mice. Two further regions (nucleus accumbens core and ventromedial caudate putamen) showed significant interactions between genotype, chronic, and acute methamphetamine treatment due to accentuated c-fos expression in nociceptin receptor knockout mice sensitized and challenged with methamphetamine. These findings suggest endogenous nociceptin modulates the response of the central nervous system to repeated psychostimulant administration, although this is little reflected in locomotion.

Animals↗

PubMed2006

Risk and protective factors for nonmedical use of prescription stimulants and methamphetamine among adolescents.

PURPOSE: This article reports on correlates of past-year nonmedical use of prescription stimulants and methamphetamine among adolescents aged 12 to 17 years. METHODS: Data from the 2002 National Survey of Drug Use and Health (NSDUH) were used to conduct logistic regression analyses of the demographic, psychosocial, and behavioral correlates of illicit stimulant use. The sample size was 17,709. RESULTS: Analyses revealed that mental health treatment utilization and use of marijuana and other illegal drugs were correlated with nonmedical use of prescription stimulants and methamphetamine among adolescents. Females and adolescents who reported low religiosity, binge drinking, and selling drugs were more likely to use methamphetamine than were males or individuals who did not report these attitudes or behaviors. Additionally, black adolescents were less likely than white adolescents to use methamphetamine. Alternatively, adolescents who reported high family conflict and sensation-seeking were more likely than their counterparts to use prescription stimulants nonmedically, and Hispanic adolescents were less likely to use prescription stimulants nonmedically than white adolescents. CONCLUSIONS: Risk for illicit use of stimulants varies by demographic, psychosocial, and behavioral factors. Different intervention mechanisms, populations, and settings should be targeted to prevent nonmedical use of prescription stimulants versus methamphetamine among adolescents.

Adolescent↗

PubMed2005

Methamphetamine stimulates interferon inducible genes in HIV infected brain.

OBJECTIVE: To study the synergism of HIV and methamphetamine. DESIGN AND METHODS: We undertook a microarray study using RNA from the frontal cortex of 15 individuals with HIV infection to initially identify genes that are differentially regulated by HIV encephalitis (HIVE). From the analysis of the microarray data, we identified candidate genes to be validated by quantitative real time PCR (qRT-PCR) and to assess if these genes were differentially modulated in individuals with HIVE and documented methamphetamine use. RESULTS: Analysis of microarray data revealed that genes involved in several categories were dysregulated in HIVE. We then chose 15 candidate genes for validation by qRT-PCR and analyzed the tissue concentration of these genes across three groups: those with HIV infection and no brain pathology, those with HIVE, and those with both HIVE and a history of methamphetamine use. We noted that there was upregulation of interferon inducible genes in the HIVE with methamphetamine using group, which together as a gene group was highly statistically significant (p=0.0064). CONCLUSION: These findings indicate that dysregulation of interferon inducible genes may underlie the pathogenic mechanism resulting in greater neurodegenerative and neurocognitive burden that occurs in methamphetamine using HIV infected individuals.

Adult↗

PubMed2005

High concentrations of plasma brain-derived neurotrophic factor in methamphetamine users.

Methamphetamine is a highly addictive drug that has a neurotoxic effect on the brain. A growing body of evidence suggests that brain-derived neurotrophic factor (BDNF) is associated with addictive behavior. The present study investigated the changes in plasma BDNF concentration that were induced by chronic methamphetamine use. Using an enzyme-linked immunosorbent assay (ELISA), we measured peripheral BDNF levels in methamphetamine users and in a control group. The plasma BDNF concentrations of methamphetamine users were significantly higher compared with those of controls (2536.3 pg/ml versus 1352.6 pg/ml). This finding suggests that BDNF plays some role in the neurotoxicity of methamphetamine.

Adult↗

PubMed2005

Ghrelin precursor gene polymorphism and methamphetamine dependence in the Korean population.

Ghrelin is a recently isolated brain-gut peptide that has growth hormone-releasing and appetite-inducing activities. Several recent studies have suggested that ghrelin plays a major role in the pathophysiology of drug-seeking behavior and anxiety. Therefore, we assessed the effect of the ghrelin precursor polymorphism on methamphetamine dependence in the Korean population. One hundred and eighteen patients with methamphetamine dependence, according to the Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV) criteria, and the 144 healthy controls were enrolled in this study. Genotyping for the ghrelin precursor polymorphism was performed by the polymerase chain reaction-restriction fragment length polymorphism-based technique. The genotypic and allelic distributions of the ghrelin precursor polymorphism in the patients with methamphetamine dependence were not significantly different from those of the control subjects. However, the Met72 carriers were associated with the emotional problems of methamphetamine dependence. The patients with the Met72 allele were more depressed and anxious than the homozygous patients with the wild Leu72 allele. The present study suggests that the ghrelin precursor polymorphism may not confer a susceptibility to the development of methamphetamine dependence in the Korean population. However, the Leu72Met polymorphism could have a potential role in the emotional problems that are associated with this disease.

Adult↗

PubMed2005

Neither non-contingent electric footshock nor administered corticosterone facilitate the acquisition of methamphetamine self-administration.

Previous research has indicated a role for the hypothalamo-pituitary-adrenal (HPA) axis in the acquisition of intravenous cocaine self-administration since both exposure to stressors and exogenous injections of corticosterone facilitate this behavior. The present experiment was designed to determine whether electric footshock or pretreatment with corticosterone would produce similar effects on the acquisition of methamphetamine self-administration in male Wistar rats. Following initial food training, the rats were allowed to self-administer methamphetamine in ascending doses (0.0075-0.12 mg/kg/infusion) that were doubled weekly. Neither non-contingent electric footshock nor treatment with corticosterone (2.0 mg/kg, i.p.) affected the lowest dose at which the rats first acquired methamphetamine self-administration (0.015 mg/kg/infusion). The treatment groups all had similar inverted "U"-shaped acquisition curves typical of psychostimulants. Although these experiments do not indicate a major role for the HPA axis in the acquisition of methamphetamine self-administration, more studies need to be conducted to further evaluate the effects of the HPA axis on the acquisition of methamphetamine self-administration before a potential role can be ruled out.

Animals↗

PubMed2005

Combined effects of methamphetamine and zolpidem on performance and mood during simulated night shift work.

Individuals who work irregular or rotating shifts often use stimulants and sedatives to offset shift-change-related mood and performance decrements. During this simulated shift work study the acute effects of the stimulant, methamphetamine were examined, and the effects of the hypnotic, zolpidem, and the combination were assessed during the shift after drug administration. Eight volunteers completed this 21-day, within-participant, residential laboratory study during which they received a single oral methamphetamine dose (0 or 10 mg) 1 h after waking, i.e., before task performance, and a single oral zolpidem dose (0 or 10 mg) 1 h before bedtime under 2 shift conditions: day shift and night shift. When participants received placebo at both dosing times, performance on some psychomotor tasks (e.g., the digit-symbol substitution task) and on some measures of mood (e.g., ratings of "Energetic") were disrupted during the night shift, relative to the day shift. Methamphetamine alone eliminated virtually all shift-related disruptions, while zolpidem alone and the drug combination produced few effects. These data indicate that shift changes produce performance impairments and mood alterations that are improved by a single low to moderate dose of methamphetamine. Zolpidem, given alone or in combination with methamphetamine, did not alleviate most shift-change mood and performance effects.

Adult↗

PubMed1994

The ovine fetal sympathoadrenal response to the maternal administration of methamphetamine.

OBJECTIVE: We hypothesized that maternally administered methamphetamine would alter fetal sympathoadrenal activity. STUDY DESIGN: Six chronically catheterized near-term pregnant ewes received an intravenous bolus injection of methamphetamine (1.25 mg/kg). Maternal and fetal arterial blood gas values, glucose, insulin, lactate, and catecholamines were measured in the control period and at 15, 30, 60, 90, 120, and 180 minutes after methamphetamine. RESULTS: Fetal PO2 decreased from 21.4 +/- 1.9 mm Hg at control measurement to 15.3 +/- 3.3 mm Hg after 60 minutes (p < 0.05). Fetal pH declined from 7.35 +/- 0.014 at control to 7.29 +/- 0.024 after 180 minutes. Fetal plasma glucose rose from 15.3 +/- 2.4 mg/dl at control to peak at 51.2 +/- 6.8 mg/dl at 120 minutes. Insulin levels increased from a control of 40.5 +/- 8.06 to a peak of 128 +/- 46 microIU/ml at 180 minutes (p < 0.05). Lactate levels increased from a baseline of 33.5 +/- 2.0 mg/dl to 92.3 +/- 22.8 mg/dl at 180 minutes. Fetal catecholamines rose from a baseline of 153 +/- 20.2 pg/ml for epinephrine and 226 +/- 18.5 pg/ml for norepinephrine to maximum values of 518 +/- 87.3 and 661 +/- 59.3 pg/ml at 15 minutes (p < 0.05), declining thereafter. CONCLUSIONS: Maternal administration of methamphetamine is associated with a short-term increase in circulating fetal catecholamines followed by hyperglycemia, lactacidemia, and hyperinsulinemia. These findings suggest that the alteration of fetal sympathoadrenal activity may contribute to the various perinatal complications associated with methamphetamine use.

Animals↗

PubMed2000

Methamphetamine selectively alters brain glutathione.

As methamphetamine-induced neurotoxicity has been proposed to involve oxidative stress, reduced and oxidized glutathione (GSH and GSSG, respectively), vitamin E and ascorbate were measured in the striata of rats killed 2 or 24 h after a neurotoxic regimen of methamphetamine. At 2 h, methamphetamine increased GSH and GSSG (32. 5% and 43.7%, respectively) compared to controls at 2 h. No difference was seen in glutathione at 24 h, and in vitamin E and ascorbate at either time point. These findings indicate selectivity of methamphetamine for the glutathione system and a role for methamphetamine in inducing oxidative stress.

Animals↗